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Reticular formation
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Reticular formation
Axial section of the pons, at its upper part. (Formatio reticularis labeled at left.)
Section of the medulla oblongata at about the middle of the olive. (Formatio reticularis grisea and formatio reticularis alba labeled at left.)
Details
Identifiers
Latin
formatio reticularis
MeSH
D012154
NeuroNames
1223
NeuroLex ID
nlx_143558
TA
A14.1.00.021
A14.1.05.403
A14.1.06.327
FMA
77719
Anatomical terms of neuroanatomy
[edit on Wikidata]
The reticular formation is a set of interconnected nuclei that are located throughout the brainstem. The reticular formation is not anatomically well defined because it includes neurons located in diverse parts of the brain. The neurons of the reticular formation make up a complex set of networks in the core of the brainstem that stretches from the upper part of the midbrain to the lower part of the medulla oblongata.[1] The reticular formation includes ascending pathways to the cortex in the ascending reticular activating system (ARAS) and descending pathways to the spinal cord via the reticulospinal tracts of the descending reticular formation.[2][3][4][5]
Neurons of the reticular formation, particularly those of the ascending reticular activating system, play a crucial role in maintaining behavioral arousal and consciousness. The functions of the reticular formation are modulatory and premotor. The modulatory functions are primarily found in the rostral sector of the reticular formation and the premotor functions are localized in the neurons in more caudal regions.
The reticular formation is divided into three columns: raphe nuclei (median), gigantocellular reticular nuclei (medial zone), and parvocellular reticular nuclei (lateral zone). The raphe nuclei are the place of synthesis of the neurotransmitter serotonin, which plays an important role in mood regulation. The gigantocellular nuclei are involved in motor coordination. The parvocellular nuclei regulate exhalation.[6]
The reticular formation is essential for governing some of the basic functions of higher organisms and is one of the phylogenetically oldest portions of the brain.
Contents
[hide]
1 General structure
1.1 Medial and lateral reticular formation
2 General functions
3 Major subsystems
3.1 Ascending reticular activating system
3.1.1 Structure of the ARAS
3.1.2 Functions of the ARAS
3.1.2.1 Consciousness
3.1.2.2 Regulating sleep-wake transitions
3.1.2.3 Attention
3.1.3 Clinical significance of the ARAS
3.1.3.1 Pathologies
3.1.3.1.1 Developmental influences
3.2 Descending reticulospinal tracts
3.2.1 Components of the reticulospinal tracts
3.2.2 Functions of the reticulospinal tracts
3.2.3 Clinical significance of the reticulospinal tracts
4 History
5 See also
6 References
7 External links
General structure[edit]
This section needs expansion with: content from these[2][3] references. You can help by adding to it. (September 2017)
A cross section of the lower part of the pons showing the pontine reticular formation labeled as #9
The human reticular formation is composed of almost 100 brain nuclei and contains many projections into the forebrain, brainstem, and cerebellum, among other regions.[2] It includes the reticular nuclei, reticulothalamic projection fibers, diffuse thalamo-cortical projections, ascending cholinergic projections, descending non-cholinergic projections, and descending reticulospinal projections.[3] The reticular formation also contains two major neural subsystems, the ascending reticular activating system and descending reticulospinal tracts, which mediate distinct cognitive and physiological proceses.[2][3] It has been functionally cleaved both sagittally and coronally.
Traditionally the reticular nuclei are divided into three columns:
In the median column – the raphe nuclei
In the medial column – gigantocellular nuclei (because of larger size of the cells)
In the lateral column – parvocellular nuclei (because of smaller size of the cells)
The original functional differentiation was a division of caudal and rostral. This was based upon the observation that the lesioning of the rostral reticular formation induces a hypersomnia in the cat brain. In contrast, lesioning of the more caudal portion of the reticular formation produces insomnia in cats. This study has led to the idea that the caudal portion inhibits the rostral portion of the reticular formation.
Sagittal division reveals more morphological distinctions. The raphe nuclei form a ridge in the middle of the reticular formation, and, directly to its periphery, there is a division called the medial reticular formation. The medial RF is large and has long ascending and descending fibers, and is surrounded by the lateral reticular formation. The lateral RF is close to the motor nuclei of the cranial nerves, and mostly mediates their function.
Medial and lateral reticular formation [edit]
The medial reticular formation and lateral reticular formation are two columns of neuronal nuclei with ill-defined boundaries that send projections through the medulla and into the mesencephalon (midbrain). The nuclei can be differentiated by function, cell type, and projections of efferent or afferent nerves. Moving caudally from the rostral midbrain, at the site of the rostral pons and the midbrain, the medial RF becomes less prominent, and the lateral RF becomes more prominent.[7]
Existing on the sides of the medial reticular formation is its lateral cousin, which is particularly pronounced in the rostral medulla and caudal pons. Out from this area spring the cranial nerves, including the very important vagus nerve. The Lateral RF is known for its ganglions and areas of interneurons around the cranial nerves, which serve to mediate their characteristic reflexes and functions.
General functions[edit]
The reticular formation consists of more than 100 small neural networks, with varied functions including the following:
Somatic motor control – Some motor neurons send their axons to the reticular formation nuclei, giving rise to the reticulospinal tracts of the spinal cord. These tracts function in maintaining tone, balance, and posture—especially during body movements. The reticular formation also relays eye and ear signals to the cerebellum so that the cerebellum can integrate visual, auditory, and vestibular stimuli in motor coordination. Other motor nuclei include gaze centers, which enable the eyes to track and fixate objects, and central pattern generators, which produce rhythmic signals of breathing with swallowing, and with dedication and urination.
Cardiovascular control – The reticular formation includes the cardiac and vasomotor centers of the medulla oblongata.
Pain modulation – The reticular formation is one means by which pain signals from the lower body reach the cerebral cortex. It is also the origin of the descending analgesic pathways. The nerve fibers in these pathways act in the spinal cord to block the transmission of some pain signals to the brain.
Sleep and consciousness – The reticular formation has projections to the thalamus and cerebral cortex that allow it to exert some control over which sensory signals reach the cerebrum and come to our conscious attention. It plays a central role in states of consciousness like alertness and sleep. Injury to the reticular formation can result in irreversible coma.
Habituation – This is a process in which the brain learns to ignore repetitive, meaningless stimuli while remaining sensitive to others. A good example of this is a person who can sleep through loud traffic in a large city, but is awakened promptly due to the sound of an alarm or crying baby. Reticular formation nuclei that modulate activity of the cerebral cortex are part of the ascending reticular activating system.[8][9]
Major subsystems[edit]
Ascending reticular activating system[edit]
Ascending reticular activating system. Reticular formation labeled near center.
The ascending reticular activating system (ARAS), also known as the extrathalamic control modulatory system or simply the reticular activating system (RAS), is a set of connected nuclei in the brains of vertebrates that is responsible for regulating wakefulness and sleep-wake transitions. The ARAS is a part of the reticular formation and is mostly composed of various nuclei in the thalamus and a number of dopaminergic, noradrenergic, serotonergic, histaminergic, cholinergic, and glutamatergic brain nuclei.[2][10][11][12]
Structure of the ARAS[edit]
The ARAS is composed of several neuronal circuits connecting the dorsal part of the posterior midbrain and anterior pons to the cerebral cortex via distinct pathways that project through the thalamus and hypothalamus.[2][11][12] The ARAS is a collection of different nuclei – more than 20 on each side in the upper brainstem, the pons, medulla, and posterior hypothalamus. The neurotransmitters that these neurons release include dopamine, norepinephrine, serotonin, histamine, acetylcholine, and glutamate.[2][10][11][12] They exert cortical influence through direct axonal projections and indirect projections through thalamic relays.[11][12][13]
The thalamic pathway consists primarily of cholinergic neurons in the pontine tegmentum, whereas the hypothalamic pathway is composed primarily of neurons that release monoamine neurotransmitters, namely dopamine, norepinephrine, serotonin, and histamine.[2][10] The glutamate-releasing neurons in the ARAS were identified much more recently relative to the monoaminergic and cholinergic nuclei;[14] the glutamatergic component of the ARAS includes one glutamatergic nucleus in the hypothalamus and various glutamatergic brainstem nuclei.[11][14][15] The orexin neurons of the lateral hypothalamus innervate every component of the ascending reticular activating system and coordinate activity within the entire system.[12][16][17]
The key components of the ARAS are listed in the table below.
Key components of the ascending reticular activating system
Nucleus type
Corresponding nuclei that mediate arousal
Sources
Dopaminergic nuclei
Ventral tegmental area
Substantia nigra pars compacta
[2][10][11][12]
Noradrenergic nuclei
Locus coeruleus
Related noradrenergic brainstem nuclei
[2][10][12]
Serotonergic nuclei
Dorsal raphe nucleus
Median raphe nucleus
[2][10][12]
Histaminergic nuclei
Tuberomammillary nucleus
[2][10][18]
Cholinergic nuclei
Forebrain cholinergic nuclei
Pontine tegmental nuclei: laterodorsal and pedunculopontine tegmental nucleus
[2][11][12][14]
Glutamatergic nuclei
Brainstem nuclei: parabrachial nucleus, precoeruleus, and pedunculopontine tegmental nucleus
Hypothalamic nuclei: supramammillary nucleus
[11][12][14][15][18][19]
Thalamic nuclei
Thalamic reticular nucleus
Intralaminar nucleus, including the centromedian nucleus
[2][11][20]
The ARAS consists of evolutionarily ancient areas of the brain, which are crucial to survival and protected during adverse periods. As a result, the ARAS still functions during inhibitory periods of hypnosis.[21]
The ascending reticular activating system which sends neuromodulatory projections to the cortex - mainly connects to the prefrontal cortex.[22] There is seen to be low connectivity to the motor areas of the cortex.[22]
Functions of the ARAS[edit]
Consciousness[edit]
The ascending reticular activating system is an important enabling factor for the state of consciousness.[23] The ascending system is seen to contribute to wakefulness as characterised by cortical and behavioural arousal.[5]
Regulating sleep-wake transitions[edit]
Further information: Neuroscience of sleep
The main function of the ARAS is to modify and potentiate thalamic and cortical function such that electroencephalogram (EEG) desynchronization ensues.[24][25] There are distinct differences in the brain’s electrical activity during periods of wakefulness and sleep: Low voltage fast burst brain waves (EEG desynchronization) are associated with wakefulness and REM sleep (which are electrophysiologically similar); high voltage slow waves are found during non-REM sleep. Generally speaking, when thalamic relay neurons are in burst mode the EEG is synchronized and when they are in tonic mode it is desynchronized.[25] Stimulation of the ARAS produces EEG desynchronization by suppressing slow cortical waves (0.3–1 Hz), delta waves (1–4 Hz), and spindle wave oscillations (11–14 Hz) and by promoting gamma band (20 – 40 Hz) oscillations.[16]
The physiological change from a state of deep sleep to wakefulness is reversible and mediated by the ARAS.[26] Inhibitory influence from the brain is active at sleep onset, likely coming from the preoptic area (POA) of the hypothalamus. During sleep, neurons in the ARAS will have a much lower firing rate; conversely, they will have a higher activity level during the waking state.[27] Therefore, low frequency inputs (during sleep) from the ARAS to the POA neurons result in an excitatory influence and higher activity levels (awake) will have inhibitory influence. In order that the brain may sleep, there must be a reduction in ascending afferent activity reaching the cortex by suppression of the ARAS.[26]
Attention[edit]
The ARAS also helps mediate transitions from relaxed wakefulness to periods of high attention.[20] There is increased regional blood flow (presumably indicating an increased measure of neuronal activity) in the midbrain reticular formation (MRF) and thalamic intralaminar nuclei during tasks requiring increased alertness and attention.
Clinical significance of the ARAS[edit]
Mass lesions in brainstem ARAS nuclei can cause severe alterations in level of consciousness (e.g., coma).[28] Bilateral damage to the reticular formation of the midbrain may lead to coma or death.[29]
Direct electrical stimulation of the ARAS produces pain responses in cats and educes verbal reports of pain in humans.[citation needed] Additionally, ascending reticular activation in cats can produce mydriasis,[citation needed] which can result from prolonged pain. These results suggest some relationship between ARAS circuits and physiological pain pathways.[30]
Pathologies[edit]
Given the importance of the ARAS for modulating cortical changes, disorders of the ARAS should result in alterations of sleep-wake cycles and disturbances in arousal.[31] Some pathologies of the ARAS may be attributed to age, as there appears to be a general decline in reactivity of the ARAS with advancing years.[32] Changes in electrical coupling have been suggested to account for some changes in ARAS activity: If coupling were down-regulated, there would be a corresponding decrease in higher-frequency synchronization (gamma band). Conversely, up-regulated electrical coupling would increase synchronization of fast rhythms that could lead to increased arousal and REM sleep drive.[33] Specifically, disruption of the ARAS has been implicated in the following disorders:
Narcolepsy: Lesions along the PPT/LDT nuclei are associated with narcolepsy.[34] There is a significant down-regulation of PPN output and a loss of orexin peptides, promoting the excessive daytime sleepiness that is characteristic of this disorder.[16]
Schizophrenia: Intractable schizophrenic patients have a significant increase (> 60%) in the number of PPN neurons[31] and dysfunction of NO signaling involved in modulating cholinergic output of the ARAS.[35]
Post-traumatic stress disorder, Parkinson's disease, REM behavior disorder: Patients with these syndromes exhibit a significant (>50%) decrease in the number of locus coeruleus (LC) neurons, resulting is increased disinhibition of the PPN.[31]
Progressive supranuclear palsy (PSP): Dysfunction of NO signaling has been implicated in the development of PSP.[35]
Depression, autism, Alzheimer's disease, attention deficit disorder: The exact role of the ARAS in each of these disorders has not yet been identified. However, it is expected that in any neurological or psychiatric disease that manifests disturbances in arousal and sleep-wake cycle regulation, there will be a corresponding dysregulation of some elements of the ARAS.[31]
Parkinson's disease: REM sleep disturbances are common in Parkinson's. It is mainly a dopaminergic disease, but cholinergic nuclei are depleted as well. Degeneration in the ARAS begins early in the disease process.[34]
Developmental influences[edit]
There are several potential factors that may adversely influence the development of the ascending reticular activating system:
Preterm birth:[36] Regardless of birth weight or weeks of gestation, premature birth induces persistent deleterious effects on pre-attentional (arousal and sleep-wake abnormalities), attentional (reaction time and sensory gating), and cortical mechanisms throughout development.
Smoking during pregnancy:[37] Prenatal exposure to cigarette smoke is known to produce lasting arousal, attentional and cognitive deficits in humans. This exposure can induce up-regulation of nicotinic receptors on α4b2 subunit on Pedunculopontine nucleus (PPN) cells, resulting in increased tonic activity, resting membrane potential, and hyperpolarization-activated cation current. These major disturbances of the intrinsic membrane properties of PPN neurons result in increased levels of arousal and sensory gating deficits (demonstrated by a diminished amount of habituation to repeated auditory stimuli). It is hypothesized that these physiological changes may intensify attentional dysregulation later in life.
Descending reticulospinal tracts[edit]
Spinal cord tracts - reticulospinal tract labeled in red, near-center at left in figure.
The reticulospinal tracts, also known as the descending or anterior reticulospinal tracts, are extrapyramidal motor tracts that descend from the reticular formation[38] in two tracts to act on the motor neurons supplying the trunk and proximal limb flexors and extensors. The reticulospinal tracts are involved mainly in locomotion and postural control, although they do have other functions as well.[39] The descending reticulospinal tracts are one of four major cortical pathways to the spinal cord for musculoskeletal activity. The reticulospinal tracts works with the other three pathways to give a coordinated control of movement, including delicate manipulations.[40] The four pathways can be grouped into two main system pathways – a medial system and a lateral system. The medial system includes the reticulospinal pathway and the vestibulospinal pathway, and this system provides control of posture. The corticospinal and the rubrospinal tract pathways belong to the lateral system which provides fine control of movement.[41]
Components of the reticulospinal tracts[edit]
The tract is divided into two parts, the medial (or pontine) and lateral (or medullary) reticulospinal tracts (MRST and LRST).
The MRST is responsible for exciting anti-gravity, extensor muscles. The fibers of this tract arise from the caudal pontine reticular nucleus and the oral pontine reticular nucleus and project to the lamina VII and lamina VIII of the spinal cord (BrainInfo)
The LRST is responsible for inhibiting excitatory axial extensor muscles of movement. It is also responsible for automatic breathing. The fibers of this tract arise from the medullary reticular formation, mostly from the gigantocellular nucleus, and descend the length of the spinal cord in the anterior part of the lateral column. The tract terminates in lamina VII mostly with some fibers terminating in lamina IX of the spinal cord.
The ascending sensory tract conveying information in the opposite direction is known as the spinoreticular tract.
Functions of the reticulospinal tracts[edit]
Integrates information from the motor systems to coordinate automatic movements of locomotion and posture
Facilitates and inhibits voluntary movement; influences muscle tone
Mediates autonomic functions
Modulates pain impulses
Influences blood flow to lateral geniculate nucleus of the thalamus.
Clinical significance of the reticulospinal tracts[edit]
The reticulospinal tracts are mostly inhibited by the corticospinal tract; if damage occurs at the level of or below the red nucleus (e.g. to the superior colliculus), it is called decerebration, and causes decerebrate rigidity: an unopposed extension of the head and limbs.[citation needed] The reticulospinal tracts also provide a pathway by which the hypothalamus can control sympathetic thoracolumbar outflow and parasympathetic sacral outflow.[citation needed]
History[edit]
The term "reticular formation" was coined in the late 19th century by Otto Deiters, coinciding with Ramon y Cajal’s neuron doctrine. Allan Hobson states in his book The Reticular Formation Revisited that the name is an etymological vestige from the fallen era of the aggregate field theory in the neural sciences. The term "reticulum" means "netlike structure", which is what the reticular formation resembles at first glance. It has been described as being either too complex to study or an undifferentiated part of the brain with no organization at all. Eric Kandel describes the reticular formation as being organized in a similar manner to the intermediate gray matter of the spinal cord. This chaotic, loose, and intricate form of organization is what has turned off many researchers from looking farther into this particular area of the brain.[citation needed] The cells lack clear ganglionic boundaries, but do have clear functional organizations and distinct cell types. The term "reticular formation" is seldom used anymore except to speak in generalities. Modern scientists usually refer to the individual nuclei that compose the reticular formation.[citation needed]
Moruzzi and Magoun first investigated the neural components regulating the brain’s sleep-wake mechanisms in 1949. Physiologists had proposed that some structure deep within the brain controlled mental wakefulness and alertness.[24] It had been thought that wakefulness depended only on the direct reception of afferent (sensory) stimuli at the cerebral cortex.
The direct electrical stimulation of the brain could simulate electrocortical relays. Magoun used this principle to demonstrate, on two separate areas of the brainstem of a cat, how to produce wakefulness from sleep. First the ascending somatic and auditory paths; second, a series of "ascending relays from the reticular formation of the lower brain stem through the midbrain tegmentum, subthalamus and hypothalamus to the internal capsule."[42] The latter was of particular interest, as this series of relays did not correspond to any known anatomical pathways for the wakefulness signal transduction and was coined the ascending reticular activating system (ARAS).
Next, the significance of this newly identified relay system was evaluated by placing lesions in the medial and lateral portions of the front of the midbrain. Cats with mesancephalic interruptions to the ARAS entered into a deep sleep and displayed corresponding brain waves. In alternative fashion, cats with similarly placed interruptions to ascending auditory and somatic pathways exhibited normal sleeping and wakefulness, and could be awakened with somatic stimuli. Because these external stimuli would be blocked by the interruptions, this indicated that the ascending transmission must travel through the newly discovered ARAS.
Finally, Magoun recorded potentials within the medial portion of the brain stem and discovered that auditory stimuli directly fired portions of the reticular activating system. Furthermore, single-shock stimulation of the sciatic nerve also activated the medial reticular formation, hypothalamus, and thalamus. Excitation of the ARAS did not depend on further signal propagation through the cerebellar circuits, as the same results were obtained following decerebellation and decortication. The researchers proposed that a column of cells surrounding the midbrain reticular formation received input from all the ascending tracts of the brain stem and relayed these afferents to the cortex and therefore regulated wakefulness.[42][26]
See also[edit]
This article uses anatomical terminology; for an overview, see Anatomical terminology.
Locus coeruleus
Pedunculopontine nucleus
Medial pontine reticular formation
Midbrain reticular formation
References[edit]
Jump up ^ Purves, Dale (2011). Neuroscience (5. ed.). Sunderland, Mass.: Sinauer. pp. 390–395. ISBN 978-0-87893-695-3.
^ Jump up to: a b c d e f g h i j k l m n Iwańczuk W, Guźniczak P (2015). "Neurophysiological foundations of sleep, arousal, awareness and consciousness phenomena. Part 1". Anaesthesiol Intensive Ther. 47 (2): 162–167. doi:10.5603/AIT.2015.0015. PMID 25940332. The ascending reticular activating system (ARAS) is responsible for a sustained wakefulness state. It receives information from sensory receptors of various modalities, transmitted through spinoreticular pathways and cranial nerves (trigeminal nerve — polymodal pathways, olfactory nerve, optic nerve and vestibulocochlear nerve — monomodal pathways). These pathways reach the thalamus directly or indirectly via the medial column of reticular formation nuclei (magnocellular nuclei and reticular nuclei of pontine tegmentum). The reticular activating system begins in the dorsal part of the posterior midbrain and anterior pons, continues into the diencephalon, and then divides into two parts reaching the thalamus and hypothalamus, which then project into the cerebral cortex (Fig. 1). The thalamic projection is dominated by cholinergic neurons originating from the pedunculopontine tegmental nucleus of pons and midbrain (PPT) and laterodorsal tegmental nucleus of pons and midbrain (LDT) nuclei [17, 18]. The hypothalamic projection involves noradrenergic neurons of the locus coeruleus (LC) and serotoninergic neurons of the dorsal and median raphe nuclei (DR), which pass through the lateral hypothalamus and reach axons of the histaminergic tubero-mamillary nucleus (TMN), together forming a pathway extending into the forebrain, cortex and hippocampus. Cortical arousal also takes advantage of dopaminergic neurons of the substantia nigra (SN), ventral tegmenti area (VTA) and the periaqueductal grey area (PAG). Fewer cholinergic neurons of the pons and midbrain send projections to the forebrain along the ventral pathway, bypassing the thalamus [19, 20].
^ Jump up to: a b c d Augustine JR (2016). "Chapter 9: The Reticular Formation". Human Neuroanatomy (2nd ed.). John Wiley & Sons. pp. 141–153. ISBN 9781119073994. Retrieved 4 September 2017.
Jump up ^ "the definition of reticular activating system". Dictionary.com.
^ Jump up to: a b Jones, BE (2008). "Modulation of cortical activation and behavioral arousal by cholinergic and orexinergic systems". Annals of the New York Academy of Sciences. 1129: 26–34. Bibcode:2008NYASA1129...26J. doi:10.1196/annals.1417.026. PMID 18591466.
Jump up ^ "The Brain From Top To Bottom". Thebrain.mcgill.ca. Retrieved 2016-04-28.
Jump up ^ "The Benefits of Midbrain Activation". 2014-09-15. Retrieved 2017-07-05.
Jump up ^ "Anatomy of the Brain - Reticular Formation". Biology.about.com. 2015-07-07. Retrieved 2016-04-28.
Jump up ^ Saladin, Kenneth S. Anatomy & Physiology the Unity of Form and Function. Dubuque: McGraw-Hill, 2009. Print.
^ Jump up to: a b c d e f g Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 12: Sleep and Arousal". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York, USA: McGraw-Hill Medical. p. 295. ISBN 9780071481274. The RAS is a complex structure consisting of several different circuits including the four monoaminergic pathways ... The norepinephrine pathway originates from the locus ceruleus (LC) and related brainstem nuclei; the serotonergic neurons originate from the raphe nuclei within the brainstem as well; the dopaminergic neurons originate in ventral tegmental area (VTA); and the histaminergic pathway originates from neurons in the tuberomammillary nucleus (TMN) of the posterior hypothalamus. As discussed in Chapter 6, these neurons project widely throughout the brain from restricted collections of cell bodies. Norepinephrine, serotonin, dopamine, and histamine have complex modulatory functions and, in general, promote wakefulness. The PT in the brain stem is also an important component of the ARAS. Activity of PT cholinergic neurons (REM-on cells) promotes REM sleep. During waking, REM-on cells are inhibited by a subset of ARAS norepinephrine and serotonin neurons called REM-off cells.
^ Jump up to: a b c d e f g h i Brudzynski SM (July 2014). "The ascending mesolimbic cholinergic system--a specific division of the reticular activating system involved in the initiation of negative emotional states". Journal of Molecular Neuroscience : MN. 53 (3): 436–445. doi:10.1007/s12031-013-0179-1. PMID 24272957. Understanding of arousing and wakefulness-maintaining functions of the ARAS has been further complicated by neurochemical discoveries of numerous groups of neurons with the ascending pathways originating within the brainstem reticular core, including pontomesencephalic nuclei, which synthesize different transmitters and release them in vast areas of the brain and in the entire neocortex (for review, see Jones 2003; Lin et al. 2011). They included glutamatergic, cholinergic, noradrenergic, dopaminergic, serotonergic, histaminergic, and orexinergic systems (for review, see Lin et al. 2011). ... The ARAS represented diffuse, nonspecific pathways that, working through the midline and intralaminar thalamic nuclei, could change activity of the entire neocortex, and thus, this system was suggested initially as a general arousal system to natural stimuli and the critical system underlying wakefulness (Moruzzi and Magoun 1949; Lindsley et al. 1949; Starzl et al. 1951, see stippled area in Fig. 1). ... It was found in a recent study in the rat that the state of wakefulness is mostly maintained by the ascending glutamatergic projection from the parabrachial nucleus and precoeruleus regions to the basal forebrain and then relayed to the cerebral cortex (Fuller et al. 2011). ... Anatomical studies have shown two main pathways involved in arousal and originating from the areas with cholinergic cell groups, one through the thalamus and the other, traveling ventrally through the hypothalamus and preoptic area, and reciprocally connected with the limbic system (Nauta and Kuypers 1958; Siegel 2004). ... As counted in the cholinergic connections to the thalamic reticular nucleus ...
^ Jump up to: a b c d e f g h i j Schwartz MD, Kilduff TS (December 2015). "The Neurobiology of Sleep and Wakefulness". The Psychiatric Clinics of North America. 38 (4): 615–644. doi:10.1016/j.psc.2015.07.002. PMC 4660253  . PMID 26600100. This ascending reticular activating system (ARAS) is comprised of cholinergic laterodorsal and pedunculopontine tegmentum (LDT/PPT), noradrenergic locus coeruleus (LC), serotonergic (5-HT) Raphe nuclei and dopaminergic ventral tegmental area (VTA), substantia nigra (SN) and periaqueductal gray projections that stimulate the cortex directly and indirectly via the thalamus, hypothalamus and BF.6, 12-18 These aminergic and catecholaminergic populations have numerous interconnections and parallel projections which likely impart functional redundancy and resilience to the system.6, 13, 19 ... More recently, the medullary parafacial zone (PZ) adjacent to the facial nerve was identified as a sleep-promoting center on the basis of anatomical, electrophysiological and chemo- and optogenetic studies.23, 24 GABAergic PZ neurons inhibit glutamatergic parabrachial (PB) neurons that project to the BF,25 thereby promoting NREM sleep at the expense of wakefulness and REM sleep. ... The Hcrt neurons project widely throughout the brain and spinal cord92, 96, 99, 100 including major projections to wake-promoting cell groups such as the HA cells of the TM,101 the 5-HT cells of the dorsal Raphe nuclei (DRN),101 the noradrenergic cells of the LC,102 and cholinergic cells in the LDT, PPT, and BF.101, 103 ... Hcrt directly excites cellular systems involved in waking and arousal including the LC,102, 106, 107 DRN,108, 109 TM,110-112 LDT,113, 114 cholinergic BF,115 and both dopamine (DA) and non-DA neurons in the VTA.116, 117
Jump up ^ Squire L (2013). Fundamental neuroscience (4th ed.). Amsterdam: Elsevier/Academic Press. p. 1095. ISBN 978-0-12-385-870-2.
^ Jump up to: a b c d Saper CB, Fuller PM (June 2017). "Wake-sleep circuitry: an overview". Current Opinion in Neurobiology. 44: 186–192. doi:10.1016/j.conb.2017.03.021. PMC 5531075  . PMID 28577468. Parabrachial and pedunculopontine glutamatergic arousal system
Retrograde tracers from the BF have consistently identified one brainstem site of input that is not part of the classical monoaminergic ascending arousal system: glutamatergic neurons in the parabrachial and pedunculopontine nucleus ... Juxtacellular recordings from pedunculopontine neurons have found that nearly all cholinergic neurons in this region, as well as many glutamatergic and GABAergic neurons, are most active during wake and REM sleep [25], although some of the latter neurons were maximally active during either wake or REM, but not both. ... [Parabrachial and pedunculopontine glutamatergic neurons] provide heavy innervation to the lateral hypothalamus, central nucleus of the amygdala, and BF
^ Jump up to: a b Pedersen NP, Ferrari L, Venner A, Wang JL, Abbott SG, Vujovic N, Arrigoni E, Saper CB, Fuller PM (November 2017). "Supramammillary glutamate neurons are a key node of the arousal system". Nature Communications. 8 (1): 1405. doi:10.1038/s41467-017-01004-6. PMC 5680228  . PMID 29123082. Basic and clinical observations suggest that the caudal hypothalamus comprises a key node of the ascending arousal system, but the cell types underlying this are not fully understood. Here we report that glutamate-releasing neurons of the supramammillary region (SuMvglut2) produce sustained behavioral and EEG arousal when chemogenetically activated.
^ Jump up to: a b c Burlet, S., Tyler, C. J., & Leonard, C. S. (2002). "Direct and indirect excitation of laterodorsal tegmental neurons by hypocretin/orexin peptides: Implications for wakefulness and narcolepsy". Journal of Neuroscience. 22 (7): 2862–2872. PMID 11923451. CS1 maint: Multiple names: authors list (link)
Jump up ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 12: Sleep and Arousal". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York, USA: McGraw-Hill Medical. p. 295. ISBN 9780071481274. Orexin neurons are located in the lateral hypothalamus. They are organized in a widely projecting manner, much like the monoamines (Chapter 6), and innervate all of the components of the ARAS. They excite the REM-off monoaminergic neurons during wakefulness and the PT cholinergic neurons during REM sleep. They are inhibited by the VLPO neurons during NREM sleep.
^ Jump up to: a b Cherasse Y, Urade Y (November 2017). "Dietary Zinc Acts as a Sleep Modulator". International Journal of Molecular Sciences. 18 (11): 2334. doi:10.3390/ijms18112334. PMC 5713303  . PMID 29113075. The regulation of sleep and wakefulness involves many regions and cellular subtypes in the brain. Indeed, the ascending arousal system promotes wakefulness through a network composed of the monaminergic neurons in the locus coeruleus (LC), histaminergic neurons in the tuberomammilary nucleus (TMN), glutamatergic neurons in the parabrachial nucleus (PB) ...
Jump up ^ Fuller PM, Fuller P, Sherman D, Pedersen NP, Saper CB, Lu J (April 2011). "Reassessment of the structural basis of the ascending arousal system". The Journal of Comparative Neurology. 519 (5): 933–956. doi:10.1002/cne.22559. PMC 3119596  . PMID 21280045.
^ Jump up to: a b Kinomura, S., Larsson, J., Gulyas, B., & Roland, P. E. (January 1996). "Activation by attention of the human reticular formation and thalamic intralaminar nuclei". Science. 271 (5248): 512–515. doi:10.1126/science.271.5248.512. PMID 8560267. This corresponds to the centro-median and centralis lateralis nuclei of the intralaminar group CS1 maint: Multiple names: authors list (link)
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^ Jump up to: a b Jang, SH; Kwon, HG (8 October 2015). "The direct pathway from the brainstem reticular formation to the cerebral cortex in the ascending reticular activating system: A diffusion tensor imaging study". Neuroscience Letters. 606: 200–3. doi:10.1016/j.neulet.2015.09.004. PMID 26363340.
Jump up ^ Squire, Larry Squire (2013). Fundamental neuroscience (4th ed.). Amsterdam: Elsevier/Academic Press. p. 1095. ISBN 978-0-12-385-870-2.
^ Jump up to: a b Steriade, M. (1996). "Arousal: Revisiting the reticular activating system". Science. 272 (5259): 225–226. Bibcode:1996Sci...272..225S. doi:10.1126/science.272.5259.225. PMID 8602506.
^ Jump up to: a b Reiner, P. B. (1995). "Are mesopontine cholinergic neurons either necessary or sufficient components of the ascending reticular activating system?". Seminars in the Neurosciences. 7 (5): 355–359. doi:10.1006/smns.1995.0038.
^ Jump up to: a b c Evans, B.M. (2003). "Sleep, consciousness and the spontaneous and evoked electrical activity of the brain. Is there a cortical integrating mechanism?". Neurophysiologie clinique. 33 (1): 1–10. doi:10.1016/s0987-7053(03)00002-9. PMID 12711127.
Jump up ^ Kumar, V. M., Mallick, B. N., Chhina, G. S., & Singh, B. (1984). "INFLUENCE OF ASCENDING RETICULAR ACTIVATING SYSTEM ON PREOPTIC NEURONAL-ACTIVITY". Experimental Neurology. 86 (1): 40–52. doi:10.1016/0014-4886(84)90065-7. PMID 6479280. CS1 maint: Multiple names: authors list (link)
Jump up ^ Tindall SC (1990). "Chapter 57: Level of Consciousness". In Walker HK, Hall WD, Hurst JW. Clinical Methods: The History, Physical, and Laboratory Examinations. Butterworth Publishers. Retrieved 2008-07-04.
Jump up ^ The Human Brain: An Introduction to its Functional Anatomy 5th ed by J Nolte chpt 11 pp. 262–290
Jump up ^ Ruth, R. E., & Rosenfeld, J. P. (1977). "TONIC RETICULAR ACTIVATING SYSTEM - RELATIONSHIP TO AVERSIVE BRAIN-STIMULATION EFFECTS". Experimental Neurology. 57 (1): 41–56. doi:10.1016/0014-4886(77)90043-7. PMID 196879. CS1 maint: Multiple names: authors list (link)
^ Jump up to: a b c d GarciaRill, E. (1997). "Disorders of the reticular activating system". Medical Hypotheses. 49 (5): 379–387. doi:10.1016/S0306-9877(97)90083-9. PMID 9421802.
Jump up ^ Robinson, D. (1999). "The technical, neurological and psychological significance of `alpha', `delta' and `theta' waves confounded in EEG evoked potentials: a study of peak latencies". Clinical Neurophysiology. 110 (8): 1427–1434. doi:10.1016/S1388-2457(99)00078-4. PMID 10454278.
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^ Jump up to: a b Schwartz JR, Roth T (December 2008). "Neurophysiology of sleep and wakefulness: basic science and clinical implications". Curr Neuropharmacol. 6 (4): 367–78. doi:10.2174/157015908787386050. PMC 2701283  . PMID 19587857.
^ Jump up to: a b Vincent, S. R. (2000). "The ascending reticular activating system - from aminergic neurons to nitric oxide". Journal of Chemical Neuroanatomy. 18 (1–2): 23–30. doi:10.1016/S0891-0618(99)00048-4. PMID 10708916.
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External links[edit]
Look up reticular formation in Wiktionary, the free dictionary.
[show]
v
t
e
The spinal cord
General features
Cervical enlargement
Lumbar enlargement
Conus medullaris
Filum terminale
Cauda equina
Meninges
Grey matter
Posterior grey column
Marginal nucleus
Substantia gelatinosa of Rolando
Nucleus proprius
Spinal lamina V
Spinal lamina VI
Lateral grey column
Intermediolateral nucleus
Posterior thoracic nucleus
Anterior grey column
Interneuron
Alpha motor neuron
Onuf's nucleus
Gamma motor neuron
Other
Rexed laminae
Central gelatinous substance
Gray commissure
Central canal
Terminal ventricle
White matter
Sensory
Posterior
Posterior column-medial lemniscus pathway:
Gracile
Cuneate
Lateral:
Spinocerebellar
dorsal
ventral
Spinothalamic
lateral
anterior
Posterolateral
Spinotectal
Spinoreticular tract
Spino-olivary tract
Motor
Lateral
Corticospinal
Lateral
Extrapyramidal
Rubrospinal
Olivospinal
Raphespinal
Anterior
Corticospinal
Anterior
Extrapyramidal
Vestibulospinal
Reticulospinal
Tectospinal
Both
Anterior white commissure
External features
Ventral
Anterior median fissure
Anterolateral sulcus
Dorsal
Posterior median sulcus
Posterolateral sulcus
[show]
v
t
e
Anatomy of the medulla
Grey matter
Cranial nuclei
afferent:
Solitary nucleus
tract
Dorsal respiratory group
Gustatory nucleus
Vestibular nuclei
Lateral
Medial
Inferior
efferent:
Hypoglossal nucleus
Nucleus ambiguus
Dorsal nucleus of vagus nerve
Inferior salivatory nucleus
Dorsal
Gracile nucleus
Cuneate nucleus
Accessory cuneate nucleus
Ventral
Ventral respiratory group
Arcuate nucleus of medulla
Rostral ventromedial medulla
Botzinger complex
Pre-Bötzinger complex
White matter
Dorsal
Sensory
Sensory decussation
Medial lemniscus
Juxtarestiform body
Ascending dorsal longitudinal fasciculus
Medial longitudinal fasciculus
Motor
Descending dorsal longitudinal fasciculus
Medial longitudinal fasciculus
Ventral
Descending tracts
Olivocerebellar tract
Rubro-olivary tract
Surface
Front
Pyramid
Anterior median fissure
Anterolateral sulcus
Olive
Inferior olivary nucleus
Back
Posterior median sulcus
Posterolateral sulcus
Area postrema
Vagal trigone
Hypoglossal trigone
Medial eminence
Inferior cerebellar peduncle
Grey
Reticular formation
Gigantocellular
Parvocellular
Ventral
Lateral
Paramedian
Raphe nuclei
Obscurus
Magnus
Pallidus
Perihypoglossal nuclei
[show]
v
t
e
Anatomy of the pons
Dorsal/
(tegmentum)
Surface
Cerebellopontine angle
Superior medullary velum
Sulcus limitans
Medial eminence
Facial colliculus
White: Sensory
Trapezoid body
Trigeminal lemniscus
Dorsal trigeminal tract
Ventral trigeminal tract
Medial lemniscus
Lateral lemniscus
Medial longitudinal fasciculus
Vestibulo-oculomotor fibers
Anterior trigeminothalamic tract
Central tegmental tract
White: Motor
Inferior cerebellar peduncle
Vestibulocerebellar tract
Medial longitudinal fasciculus
Vestibulospinal tract
Medial vestibulospinal tract
Lateral vestibulospinal tract
Grey: Cranial nuclei
afferent:
GSA
Trigeminal
Principal
Spinal
Cochlear nucleus
Dorsal
Anterior
Vestibular nuclei
Superior
efferent:
SVE: Trigeminal motor nucleus
Facial motor nucleus
GSE: Abducens nucleus
GVE: Superior salivary nucleus
Inferior salivary nucleus
Other
Apneustic center
Pneumotaxic center
Parabrachial nuclei
Subparabrachial nucleus
Medial parabrachial nucleus
Lateral parabrachial nucleus
Superior olivary nucleus
Locus coeruleus
Ventral/
(base)
Grey
Pontine nuclei
White: Motor/descending
Corticospinal tract
Corticobulbar tract
Corticopontine fibers
MCP
Pontocerebellar fibers
Surface
Basilar sulcus
Other grey: Raphe/
reticular
Reticular formation
Caudal
Oral
Tegmental
Paramedian
Raphe nuclei
Median
[show]
v
t
e
Brain and spinal cord: neural tracts and fasciculi
Sensory/
ascending
PCML
1°:
Pacinian corpuscle/Meissner's corpuscle → Posterior column (Gracile fasciculus/Cuneate fasciculus) → Gracile nucleus/Cuneate nucleus
2°:
→ sensory decussation/arcuate fibers (Posterior external arcuate fibers, Internal arcuate fibers) → Medial lemniscus/Trigeminal lemniscus → Thalamus (VPL, VPM)
3°:
→ Posterior limb of internal capsule → Postcentral gyrus
Anterolateral/
pain
Fast/lateral
1° (Free nerve ending → A delta fiber) → 2° (Anterior white commissure → Lateral and Anterior Spinothalamic tract → Spinal lemniscus → VPL of Thalamus) → 3° (Postcentral gyrus) → 4° (Posterior parietal cortex)
2° (Spinomesencephalic tract → Superior colliculus of Midbrain tectum)
Slow/medial
1° (Group C nerve fiber → Spinoreticular tract → Reticular formation) → 2° (MD of Thalamus) → 3° (Cingulate cortex)
Motor/
descending
Pyramidal
flexion: Primary motor cortex → Posterior limb of internal capsule → Decussation of pyramids → Corticospinal tract (Lateral, Anterior) → Neuromuscular junction
Extrapyramidal
flexion:
Primary motor cortex → Genu of internal capsule → Corticobulbar tract → Facial motor nucleus → Facial muscles
flexion:
Red nucleus → Rubrospinal tract
extension:
Vestibulocerebellum → Vestibular nuclei → Vestibulospinal tract
extension:
Vestibulocerebellum → Reticular formation → Reticulospinal tract
Midbrain tectum → Tectospinal tract → muscles of neck
Basal ganglia
direct:
1° (Motor cortex → Striatum) → 2° (GPi) → 3° (Lenticular fasciculus/Ansa lenticularis → Thalamic fasciculus → VL of Thalamus) → 4° (Thalamocortical radiations → Supplementary motor area) → 5° (Motor cortex)
indirect:
1° (Motor cortex → Striatum) → 2° (GPe) → 3° (Subthalamic fasciculus → Subthalamic nucleus) → 4° (Subthalamic fasciculus → GPi) → 5° (Lenticular fasciculus/Ansa lenticularis → Thalamic fasciculus → VL of Thalamus) → 6° (Thalamocortical radiations → Supplementary motor area) → 7° (Motor cortex)
nigrostriatal pathway:
Pars compacta → Striatum
Cerebellar
Afferent
Vestibular nuclei → Vestibulocerebellar tract → ICP → Cerebellum → Granule cell
Pontine nuclei → Pontocerebellar fibers → MCP → Deep cerebellar nuclei → Granule cell
Inferior olivary nucleus → Olivocerebellar tract → ICP → Hemisphere → Purkinje cell → Deep cerebellar nuclei
Efferent
Dentate nucleus in Lateral hemisphere/pontocerebellum → SCP → Dentatothalamic tract → Thalamus (VL) → Motor cortex
Interposed nucleus in Intermediate hemisphere/spinocerebellum → SCP → Reticular formation, or → Cerebellothalamic tract → Red nucleus → Thalamus (VL) → Motor cortex
Fastigial nucleus in Flocculonodular lobe/vestibulocerebellum → Vestibulocerebellar tract → Vestibular nuclei
Bidirectional:
Spinocerebellar
Unconscious
proprioception
lower limb → 1° (muscle spindles → DRG) → 2° (Posterior thoracic nucleus → Dorsal/posterior spinocerebellar tract → ICP → Cerebellar vermis)
upper limb → 1° (muscle spindles → DRG) → 2° (Accessory cuneate nucleus → Cuneocerebellar tract → ICP → Anterior lobe of cerebellum)
Reflex arc
lower limb → 1° (Golgi tendon organ) → 2° (Ventral/anterior spinocerebellar tract→ SCP → Cerebellar vermis)
upper limb → 1° (Golgi tendon organ) → 2° (Rostral spinocerebellar tract → ICP → Cerebellum)
Retrieved from "https://en.wikipedia.org/w/index.php?title=Reticular_formation&oldid=835160696"
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Dirty Dancing (2017 film)
From Wikipedia, the free encyclopedia
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Dirty Dancing
Based on
Dirty Dancing
by Eleanor Bergstein
Written by
Jessica Sharzer
Directed by
Wayne Blair
Starring
Abigail Breslin
Colt Prattes
Sarah Hyland
Nicole Scherzinger
Tony Roberts
J. Quinton Johnson
Music by
Mark Isham
Country of origin
United States
Production
Executive producer(s)
Allison Shearmur
Producer(s)
Stephen Meinen
Judy Cairo
Bill Hill
Adam Anders
Cinematography
John Lindley
Editor(s)
Michael P. Shawver
Running time
130 minutes
Production company(s)
Allison Shearmur Productions
Lionsgate Television
Distributor
Lionsgate Television
Release
Original network
ABC
Original release
May 24, 2017 (2017-05-24)
Dirty Dancing is a 2017 American television film directed by Wayne Blair and written by Jessica Sharzer. It is a remake of the 1987 film of the same name. The film stars Abigail Breslin, Colt Prattes, Nicole Scherzinger, Bruce Greenwood, Debra Messing, Sarah Hyland, Tony Roberts, Billy Dee Williams, and J. Quinton Johnson. It aired on May 24, 2017, on ABC.[1] In its original broadcast, the film was seen by 6.61 million viewers with a 1.4 Nielsen rating in the 18-49 age demographic and a 5 share.[2]
It received negative reviews from a majority of critics.[3][4]
Contents
[hide]
1 Plot
2 Cast
3 Production
3.1 Casting
3.2 Filming
4 Marketing
5 Soundtrack
6 Reception
6.1 Critical reception
6.2 Viewership
7 References
8 External Links
Plot[edit]
In late summer 1963, affluent, college-bound Frances "Baby" Houseman visits Kellerman's Catskills resort with her family and falls in love with working-class dance instructor Johnny Castle. The film closely follows the plot of the original film; the following are notable changes:
Baby plans to study medicine, rather than economics.
The role of Marjorie Houseman is significantly expanded. Feeling alienated by Jake's lack of attention and affection, despite her active efforts to engage him, Marjorie contacts a divorce lawyer and suggests she and Jake live apart. As Kellerman's is where Marjorie and Jake met and fell in love, Jake romances Marjorie and they have sex, reconciling.
The role of Vivian Pressman is also expanded; now a divorcee who visits Kellerman's alone, she tells Marjorie of her intense loneliness at night. When Johnny is accused of theft, the stolen property is no longer Vivian's husband's wallet, but instead her ex-husband's watch, which Johnny earlier rejected as a gift and which Vivian apparently planted among his belongings.
Lisa rejects Robbie much earlier in the film. She befriends a new character, Marco, the resort's African-American pianist. Over his boss Tito's objections, Marco teaches Lisa to play the ukulele and performs with her in the talent show. Tito and Max acknowledge that the world is changing for the better.
A frame story is added. In 1975, Frances attends "Dirty Dancing," a Broadway show choreographed by Johnny and inspired by a book Frances wrote. Frances' faith in Johnny gave him the confidence to pursue a career. Frances is married and has a daughter. Frances takes a weekly dance lesson; she and Johnny encourage each other to continue dancing.
Cast[edit]
Abigail Breslin as Frances "Baby" Houseman
Colt Prattes as Johnny Castle
Debra Messing as Marjorie Houseman
Bruce Greenwood as Dr. Jake Houseman
Nicole Scherzinger as Penny
Sarah Hyland as Lisa Houseman
Tony Roberts as Max Kellerman
Trevor Einhorn as Neil Kellerman
Shane Harper as Robbie Gould
J. Quinton Johnson as Marco
Casper Smart as Billy Kostecki
Katey Sagal as Vivian Pressman
Billy Dee Williams as Tito Suarez
Production[edit]
In January 2011, Lionsgate announced that Kenny Ortega, the choreographer of the 1987 film Dirty Dancing, would direct its remake; however, the project was shelved the following year.[5] In December 2015, ABC and Lionsgate Television announced a three-hour remake of the movie which will not be live and would be in the same vein as The Rocky Horror Picture Show: Let's Do the Time Warp Again, a remake of the 1975 film of the same name. The remake was directed by Wayne Blair and the screenplay was written by Jessica Sharzer. Allison Shearmur was attached to the project as executive producer.[6]
Casting[edit]
Abigail Breslin had been officially attached as Baby, while the studio would green-light the project after further casting.[7] In January 2016, ABC officially green-lit the project after Debra Messing was cast as Baby's mother.[7] The following month, after a lengthy audition process, dancer Colt Prattes was announced as Johnny, the role originally played by Patrick Swayze.[8] In March 2016, it was announced that Nicole Scherzinger would co-star as Penny, Johnny's dance partner,[9] alongside Sarah Hyland as Lisa Houseman, Baby's sister,[10] and Bruce Greenwood as Dr. Jake Houseman, Baby's father.[11] Billy Dee Williams as Tito, the band leader,[12] Shane Harper as Robbie,[13] joined the cast of the movie alongside Beau “Casper” Smart and J. Quinton Johnson.[14] Later that month, Trevor Einhorn was tapped to play Neil Kellerman.[15] In April 2016, Katey Sagal and Tony Roberts were respectively cast as Vivian Pressman and Max Kellerman.[16][17]
Filming[edit]
Filming was based in Hendersonville, North Carolina. Most of the filming locations were across western North Carolina including Asheville, Cashiers and Saluda, with filming taking place in April and May 2016.[18][19] People living in the Hendersonville area served as crew members, extras and dancers, and they were invited to provide cars from the 1960s. Much of the filming took place at High Hampton Inn in Cashiers.[20] It created an estimated 1,225 jobs, including 900 extras, 30 cast members and 225 crew positions to support the project.[21]
Marketing[edit]
The official poster was unveiled in March 2017, and features Breslin and Prattes in an embrace from their final dance in the movie.[22] A 30-second teaser trailer was released a month before the television movie's release.[23]
Soundtrack[edit]
Dirty Dancing: Original Television Soundtrack
Soundtrack album by Various artists
Released
May 19, 2017 (2017-05-19)
Length
50:28
Label
Virgin
Deepwell
Dirty Dancing: Original Television Soundtrack[24]
No.
Title
Performer(s)
Length
1. "Be My Baby" Bea Miller 2:44
2. "Big Girls Don't Cry" Karmin 2:20
3. "Love Man" J. Quinton Johnson 2:19
4. "Do You Love Me" Colt Prattes, Nicole Scherzinger & Johnson 2:45
5. "Fever" Katey Sagal & Prattes 3:21
6. "When I’m Alone" Johnson 2:44
7. "Wipe Out" American Authors featuring Lindsey Stirling 2:31
8. "Hungry Eyes" Greyson Chance 3:42
9. "Hey Baby" Lady Antebellum 2:24
10. "Whole Lotta Shakin' Goin' On" Scherzinger & Abigail Breslin 3:07
11. "Cry To Me" Seal 2:50
12. "They Can't Take That Away From Me" Debra Messing 2:29
13. "Love Is Strange" Breslin & Prattes 3:01
14. "They Can’t Take That Away (Reprise)" Bruce Greenwood 2:00
15. "She's Like the Wind" Calum Scott 3:25
16. "Don’t Think Twice It’s Alright" Sarah Hyland & Johnson 3:39
17. "(I've Had) The Time of My Life" The Cast of Dirty Dancing featuring Prattes, Breslin, Johnson, Scherzinger, Messing & Greenwood 5:07
Total length: 50:28
Reception[edit]
Critical reception[edit]
The film has received negative reviews. Rotten Tomatoes gave the film a score of 22% "Rotten" based on 17 reviews.[3] On Metacritic, the film was given a score of 39 out of 100 based on 15 critics, indicating "generally unfavorable reviews".[4]
Kimberly Roots of TVLine gave Dirty Dancing a D, stating: "By adding unnecessary elements and turning Dirty Dancing into a musical, ABC proves that it wouldn't know what made the original film special if it hit them in the pachanga."[25]
Mae Abdulbaki of theyoungfolks.com gave Dirty Dancing a 3 (out of 10), stating "Remaking one of the most popular and beloved movies in the history of cinema feels almost disrespectful on many levels. Going into the TV movie remake of Dirty Dancing with a clear and open mind, I figured that if at least the dancing was good, then there was something to enjoy. However, the updated version doesn't even meet the lowest of expectations and blows past mediocre to land at downright terrible. The film is slow and dull, the lead actors have absolutely no chemistry, and the musical aspect doesn't add anything to the film."[26]
Sonia Saraiya of Variety stated in her negative review: "An ill-conceived remake of the 1987 film retains none of the passion, skill, or fun of the original."[27]
Viewership[edit]
Dirty Dancing averaged a 1.3 rating in adults 18-49 and 6.6 million viewers, airing from 8 p.m. to 11 p.m. The remake gave ABC its most-watched Wednesday in nearly seven months.[28][29]
References[edit]
Jump up ^ Association, Press (9 December 2015). "Dirty Dancing gets television remake". Retrieved 17 March 2016.
Jump up ^ Porter, Rick (May 25, 2017). "Empire finale and Dirty Dancing adjust up, Survivor reunion adjusts down: Wednesday final ratings". TV by the Numbers. Retrieved May 25, 2017.
^ Jump up to: a b "Dirty Dancing (2017)". Rotten Tomatoes. Retrieved April 22, 2017.
^ Jump up to: a b "Dirty Dancing (2017) - Season 1 Reviews - Metacritic". Metacritic. CBS Interactive Inc. Retrieved May 23, 2017.
Jump up ^ Goldberg, Lesley (December 8, 2015). "ABC Sets 'Dirty Dancing' Musical With Abigail Breslin". The Hollywood Reporter. Prometheus Global Media. Retrieved April 21, 2017.
Jump up ^ Prudom, Laura (January 14, 2016). "TV News Roundup: Debra Messing Cast in ABC’s ‘Dirty Dancing,’ LeBron James Nabs CNBC Unscripted Series". Variety. Retrieved May 2, 2017.
^ Jump up to: a b Andreeva, Nellie (December 8, 2015). "‘Dirty Dancing’ TV Remake Nears ABC Green Light With Abigail Breslin Starring". Deadline.com. Retrieved May 2, 2017.
Jump up ^ Andreeva, Nellie (February 23, 2016). "‘Dirty Dancing’: Dancer Colt Prattes To Play Johnny In ABC Remake". Deadline.com. Retrieved May 2, 2017.
Jump up ^ Goldberg, Lesley (March 1, 2016). "Nicole Scherzinger to Co-Star in ABC's 'Dirty Dancing' Reboot". The Hollywood Reporter. Prometheus Global Media. Retrieved March 3, 2016.
Jump up ^ Andreeva, Nellie (March 2, 2016). "‘Dirty Dancing’ ABC Remake Adds ‘Modern Family’s Sarah Hyland". Deadline.com. Retrieved May 2, 2017.
Jump up ^ Stanhope, Kate; Goldberg, Lesley (March 22, 2016). "Bruce Greenwood Boards ABC's 'Dirty Dancing' Remake". The Hollywood Reporter. Prometheus Global Media. Retrieved May 2, 2017.
Jump up ^ Goldberg, Lesley (March 3, 2016). "ABC's 'Dirty Dancing' Adds Billy Dee Williams". The Hollywood Reporter. Prometheus Global Media. Retrieved May 2, 2017.
Jump up ^ Stanhope, Kate (March 10, 2016). "ABC's 'Dirty Dancing' Remake Adds 'Awkward' Alum as Robbie (Exclusive)". The Hollywood Reporter. Prometheus Global Media. Retrieved May 2, 2017.
Jump up ^ Andreeva, Nellie (March 15, 2016). "‘Dirty Dancing’: Beau "Casper" Smart Joins ABC Remake; J. Quinton Johnson Cast Too". Deadline.com. Retrieved May 2, 2017.
Jump up ^ Hipes, Patrick (March 30, 2016). "Trevor Einhorn Joins ABC’s ‘Dirty Dancing’ Remake". Deadline.com. Retrieved May 2, 2017.
Jump up ^ Pedersen, Erik (April 4, 2016). "‘Dirty Dancing’: Katey Sagal Joins ABC Remake". Deadline.com. Retrieved May 2, 2017.
Jump up ^ Sandberg, Bryn Elise (April 8, 2016). "Tony Roberts Joins ABC's 'Dirty Dancing' Remake (Exclusive)". The Hollywood Reporter. Prometheus Global Media. Retrieved May 2, 2017.
Jump up ^ Kimzey, Kim (18 March 2016). "Dirty Dancing production sets up in Hendersonville". Fox Carolina. Retrieved 21 March 2016.
Jump up ^ Staff, Web (8 March 2016). "Casting agency seeks extras for ‘Dirty Dancing’ remake filmed in NC". Fox 8. Retrieved 17 March 2016.
Jump up ^ Benton, Hayley (22 March 2016). "'Dirty Dancing' sets up production HQ in Hendersonville". Asheville Citizen-Times. Retrieved 23 March 2016.
Jump up ^ Saylor, Jennifer (18 March 2016). "'Dirty Dancing' production HQ sets up--in Hendersonville". WLOS. Retrieved 23 March 2016.
Jump up ^ Li, Shirley (March 1, 2017). "Dirty Dancing remake: Abigail Breslin, Colt Prattes strike a pose in first poster". Entertainment Weekly. Time Inc. Retrieved May 2, 2017.
Jump up ^ Marquina, Sierra (April 25, 2017). "Watch the First Trailer for ABC’s ‘Dirty Dancing’ Remake — See Abigail Breslin as Baby!". Us Weekly. Retrieved May 2, 2017.
Jump up ^ "Dirty Dancing (Original Television Soundtrack) by Various Artists". iTunes Store (United States). Apple Inc. Retrieved May 11, 2017.
Jump up ^ Roots, Kimberly. (April 30, 2017). "Dirty Dancing Review: You Won't Have the Time of Your Life With ABC Remake.". Tvline.com. Retrieved May 1, 2017.
Jump up ^ Abdulbaki, Mae. (May 1, 2017). "'Dirty Dancing' Review: ABC Remake of Popular Film.". www.theyoungfolks.com. Retrieved May 1, 2017.
Jump up ^ Saraiya, Sonia (May 18, 2017). "TV Movie Review: ‘Dirty Dancing’ Rebooted on ABC". Variety. Retrieved May 18, 2017.
Jump up ^ Otterson, Joe (May 24, 2017). "TV Ratings: ABC’s ‘Dirty Dancing’ Remake Flounders Against ‘Survivor’ Season Finale". Variety. Retrieved May 25, 2017.
Jump up ^ O'connell, Michael (May 25, 2017). "TV Ratings: 'Empire' Finale Pops, 'Dirty Dancing' Does OK on ABC". The Hollywood Reporter. Retrieved May 25, 2017.
External Links[edit]
Dirty Dancing on IMDb
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