Reticular formation explained

Reticular formation
Latin:formatio reticularis
Location:Brainstem, hypothalamus and other regions

The reticular formation is a set of interconnected nuclei that are located in the brainstem, hypothalamus, and other regions. It is not anatomically well defined, because it includes neurons located in different parts of the brain. The neurons of the reticular formation make up a complex set of networks in the core of the brainstem that extend 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.[2] [3]

Neurons of the reticular formation, particularly those of the ascending reticular activating system, basically act as an “on/off” switch to the cerebral cortex and hence play a crucial role in maintaining behavioral arousal and consciousness. The overall functions of the reticular formation are modulatory and premotor,involving somatic motor control, cardiovascular control, pain modulation, sleep and consciousness, and habituation. 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.[4]

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.

Structure

The human reticular formation is composed of almost 100 brain nuclei and contains many projections into the forebrain, brainstem, and cerebellum, among other regions. It includes the reticular nuclei,reticulothalamic projection fibers, diffuse thalamocortical projections, ascending cholinergic projections, descending non-cholinergic projections, and descending reticulospinal projections.[5] The reticular formation also contains two major neural subsystems, the ascending reticular activating system and descending reticulospinal tracts, which mediate distinct cognitive and physiological processes. It has been functionally cleaved both sagittally and coronally.

Traditionally the reticular nuclei are divided into three columns:

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

The medial reticular formation and lateral reticular formation are two columns of nuclei with ill-defined boundaries that send projections through the medulla and into the 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.

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.

Function

The reticular formation consists of more than 100 small neural networks, with varied functions including the following:

  1. 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 postureespecially 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 and swallowing.
  2. Cardiovascular control – The reticular formation includes the cardiac and vasomotor centers of the medulla oblongata.
  3. 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.
  4. 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.
  5. 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.[6] [7]

Ascending reticular activating system

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/hypothalamus and a number of dopaminergic, noradrenergic, serotonergic, histaminergic, cholinergic, and glutamatergic brain nuclei.[8] [9] [10] [11]

Structure

The ARAS is composed of several neural 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. 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. They exert cortical influence through direct axonal projections and indirect projections through thalamic relays.[12]

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. The glutamate-releasing neurons in the ARAS were identified much more recently relative to the monoaminergic and cholinergic nuclei; the glutamatergic component of the ARAS includes one nucleus in the hypothalamus and various brainstem nuclei. The orexin neurons of the lateral hypothalamus innervate every component of the ascending reticular activating system and coordinate activity within the entire system.[13] [14]

Key components of the ascending reticular activating system
Nucleus typeCorresponding nuclei that mediate arousalSources
Dopaminergic nuclei
Noradrenergic nuclei
Serotonergic nuclei
Histaminergic nuclei
Cholinergic nuclei
Glutamatergic nuclei [15] [16] [17] [18]
Thalamic nuclei [19]

The ARAS consists of evolutionarily ancient areas of the brain, which are crucial to the animal's survival and protected during adverse periods, such as during inhibitory periods of Totstellreflex, aka, "animal hypnosis".[20] The ascending reticular activating system which sends neuromodulatory projections to the cortex - mainly connects to the prefrontal cortex.[21] There seems to be low connectivity to the motor areas of the cortex.[21]

Function

Consciousness

The ascending reticular activating system is an important enabling factor for the state of consciousness.[12] The ascending system is seen to contribute to wakefulness as characterised by cortical and behavioural arousal.[3]

Regulating sleep-wake transitions

The main function of the ARAS is to modify and potentiate thalamic and cortical function such that electroencephalogram (EEG) desynchronization ensues.[22] 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. 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.[13]

The physiological change from a state of deep sleep to wakefulness is reversible and mediated by the ARAS. The ventrolateral preoptic nucleus (VLPO) of the hypothalamus inhibits the neural circuits responsible for the awake state, and VLPO activation contributes to the sleep onset. 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.[23] In order that the brain may sleep, there must be a reduction in ascending afferent activity reaching the cortex by suppression of the ARAS. Dysfunction of the paraventricular nucleus of the hypothalamus can lead to drowsiness for up to 20 hours per day.[24]

Attention

The ARAS also helps mediate transitions from relaxed wakefulness to periods of high attention. 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

Mass lesions in brainstem ARAS nuclei can cause severe alterations in level of consciousness (e.g., coma).[25] Bilateral damage to the reticular formation of the midbrain may lead to coma or death.[26]

Direct electrical stimulation of the ARAS produces pain responses in cats and elicits verbal reports of pain in humans. Ascending reticular activation in cats can produce mydriasis, which can result from prolonged pain. These results suggest some relationship between ARAS circuits and physiological pain pathways.[27]

Pathology

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.[28] 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.[29] Specifically, disruption of the ARAS has been implicated in the following disorders:

Developmental influences

There are several potential factors that may adversely influence the development of the ascending reticular activating system:

History

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. The cells lack clear ganglionic boundaries, but do have clear functional organization 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.

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.[34] It had been thought that wakefulness depended only on the direct reception of afferent (sensory) stimuli at the cerebral cortex.

As 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. He first stimulated 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." 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 mesencephalic 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 physical stimuli. Because these external stimuli would be blocked on their way to the cortex 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.[35] [36]

See also

References

Other references

Systems of The Body (2010)
Neuroscience (2018)
Anatomy and Physiology (2018)

Notes and References

  1. Book: Purves. Dale. Neuroscience. 2011. Sinauer. Sunderland, Mass.. 978-0878936953. 390–395. 5..
  2. Web site: the definition of reticular activating system. Dictionary.com. live. https://web.archive.org/web/20170205234212/http://www.dictionary.com/browse/reticular-activating-system. 2017-02-05.
  3. Jones. BE. Barbara E. Jones. Modulation of cortical activation and behavioral arousal by cholinergic and orexinergic systems. Annals of the New York Academy of Sciences. 2008. 1129. 1. 26–34. 10.1196/annals.1417.026. 18591466. 2008NYASA1129...26J. 16682827.
  4. Web site: The Brain From Top To Bottom . Thebrain.mcgill.ca . 2016-04-28 . live . https://web.archive.org/web/20160423222339/http://thebrain.mcgill.ca/flash/a/a_11/a_11_cr/a_11_cr_cyc/a_11_cr_cyc.html . 2016-04-23 .
  5. Book: Augustine JR . Human Neuroanatomy . 2016 . John Wiley & Sons . 978-1119073994 . 141–153 . 2nd . https://books.google.com/books?id=5lvEDQAAQBAJ&q=%22descending%20reticular%20formation%22%20reticulospinal&pg=PT426 . 4 September 2017 . Chapter 9: The Reticular Formation . live . https://web.archive.org/web/20180504013716/https://books.google.com/books?id=5lvEDQAAQBAJ&pg=PT426&lpg=PT426&dq=%22descending%20reticular%20formation%22%20reticulospinal . 4 May 2018 .
  6. Web site: Anatomy of the Brain – Reticular Formation . Biology.about.com . 2015-07-07 . 2016-04-28 . live . https://web.archive.org/web/20030414030148/http://biology.about.com/library/organs/brain/blreticular.htm . 2003-04-14 .
  7. Book: Saladin . KS . 2018 . Anatomy and Physiology: The Unity of Form and Function . 8th . New York . McGraw-Hill . 978-1259277726 . Chapter 14 – The Brain and Cranial Nerves . The Reticular Formation, pp. 518–519 .
  8. Iwańczuk W, Guźniczak P . Neurophysiological foundations of sleep, arousal, awareness and consciousness phenomena. Part 1 . Anaesthesiol Intensive Ther . 47 . 2 . 162–167 . 2015 . 25940332 . 10.5603/AIT.2015.0015 . 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]..
  9. Book: Malenka RC, Nestler EJ, Hyman SE . Sydor A, Brown RY . Molecular Neuropharmacology: A Foundation for Clinical Neuroscience . 2009 . McGraw-Hill Medical . New York . 978-0071481274 . 295 . 2nd . Chapter 12: Sleep and Arousal . 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..
  10. Brudzynski SM . 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 . 53 . 3 . 436–445 . July 2014 . 24272957 . 10.1007/s12031-013-0179-1 . 14615039 . 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 ....
  11. Schwartz MD, Kilduff TS . The Neurobiology of Sleep and Wakefulness . The Psychiatric Clinics of North America . 38 . 4 . 615–644 . December 2015 . 26600100 . 4660253 . 10.1016/j.psc.2015.07.002 . This ascending reticular activating system (ARAS) is 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.
  12. Book: Squire L. Fundamental neuroscience. 2013. Elsevier/Academic Press. Amsterdam. 978-0123858702. 1095. 4th.
  13. Burlet S, Tyler CJ, Leonard CS . Direct and indirect excitation of laterodorsal tegmental neurons by Hypocretin/Orexin peptides: implications for wakefulness and narcolepsy . J. Neurosci. . 22 . 7 . 2862–2872 . April 2002 . 11923451 . 6758338 . 10.1523/JNEUROSCI.22-07-02862.2002 .
  14. Book: Malenka RC, Nestler EJ, Hyman SE . Sydor A, Brown RY . Molecular Neuropharmacology: A Foundation for Clinical Neuroscience . 2009 . McGraw-Hill Medical . New York . 978-0071481274 . 295 . 2nd . Chapter 12: Sleep and Arousal . 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..
  15. Saper CB, Fuller PM . Wake-sleep circuitry: an overview . Current Opinion in Neurobiology . 44 . 186–192 . June 2017 . 28577468 . 10.1016/j.conb.2017.03.021 . 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 . 5531075.
  16. Pedersen NP, Ferrari L, Venner A, Wang JL, Abbott SG, Vujovic N, Arrigoni E, Saper CB, Fuller PM . Supramammillary glutamate neurons are a key node of the arousal system . Nature Communications . 8 . 1 . 1405 . November 2017 . 29123082 . 5680228 . 10.1038/s41467-017-01004-6 . 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.. 2017NatCo...8.1405P .
  17. Cherasse Y, Urade Y . Dietary Zinc Acts as a Sleep Modulator . International Journal of Molecular Sciences . 18 . 11 . 2334 . November 2017 . 29113075 . 5713303 . 10.3390/ijms18112334 . 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) .... free .
  18. Fuller PM, Fuller P, Sherman D, Pedersen NP, Saper CB, Lu J . Reassessment of the structural basis of the ascending arousal system . The Journal of Comparative Neurology . 519 . 5 . 933–956 . April 2011 . 21280045 . 3119596 . 10.1002/cne.22559 .
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