Role of the Vestibular Nuclei in the Cerebral Eye Nystagmus

1969 ◽  
Vol 2 (2) ◽  
pp. 65-75 ◽  
Author(s):  
E. Manni ◽  
M.L. Giretti
Keyword(s):  
Vestibular Nuclei ◽  
Cerebral Eye

Influence of sex and estrous cycle on synaptic responses of the medial vestibular nuclei in rats: Role of circulating 17β-estradiol

2012 ◽  
Vol 87 (2-3) ◽  
pp. 319-327 ◽  
Author(s):  
Silvarosa Grassi ◽  
Adele Frondaroli ◽  
Mariangela Scarduzio ◽  
Cristina V. Dieni ◽  
Gabriele Brecchia ◽  
...  
Keyword(s):  
Estrous Cycle ◽  
Vestibular Nuclei ◽  
17Β Estradiol ◽  
Synaptic Responses

scholarly journals Spike burst–pause dynamics of Purkinje cells regulate sensorimotor adaptation

2018 ◽  
Author(s):  
Niceto R. Luque ◽  
Francisco Naveros ◽  
Richard R. Carrillo ◽  
Eduardo Ros ◽  
Angelo Arleo
Keyword(s):  
Purkinje Cell ◽  
Purkinje Cells ◽  
Vestibular Nuclei ◽  
Response Patterns ◽  
Spike Burst ◽  
Vor Adaptation ◽  
Cell Firing ◽  
Cerebellar Purkinje Cells ◽  
Oculomotor Adaptation

AbstractCerebellar Purkinje cells mediate accurate eye movement coordination. However, it remains unclear how oculomotor adaptation depends on the interplay between the characteristic Purkinje cell response patterns, namely tonic, bursting, and spike pauses. Here, a spiking cerebellar model assesses the role of Purkinje cell firing patterns in vestibular ocular reflex (VOR) adaptation. The model captures the cerebellar microcircuit properties and it incorporates spike-based synaptic plasticity at multiple cerebellar sites. A detailed Purkinje cell model reproduces the three spike-firing patterns that are shown to regulate the cerebellar output. Our results suggest that pauses following Purkinje complex spikes (bursts) encode transient disinhibition of targeted medial vestibular nuclei, critically gating the vestibular signals conveyed by mossy fibres. This gating mechanism accounts for early and coarse VOR acquisition, prior to the late reflex consolidation. In addition, properly timed and sized Purkinje cell bursts allow the ratio between long-term depression and potentiation (LTD/LTP) to be finely shaped at mossy fibre-medial vestibular nuclei synapses, which optimises VOR consolidation. Tonic Purkinje cell firing maintains the consolidated VOR through time. Importantly, pauses are crucial to facilitate VOR phase-reversal learning, by reshaping previously learnt synaptic weight distributions. Altogether, these results predict that Purkinje spike burst-pause dynamics are instrumental to VOR learning and reversal adaptation.Author SummaryCerebellar Purkinje cells regulate accurate eye movement coordination. However, it remains unclear how cerebellar-dependent oculomotor adaptation depends on the interplay between Purkinje cell characteristic response patterns: tonic, high-frequency bursting, and post-complex spike pauses. We explore the role of Purkinje spike burst-pause dynamics in VOR adaptation. A biophysical model of Purkinje cell is at the core of a spiking network model, which captures the cerebellar microcircuit properties and incorporates spike-based synaptic plasticity mechanisms at different cerebellar sites. We show that Purkinje spike burst-pause dynamics are critical for (1) gating the vestibular-motor response association during VOR acquisition; (2) mediating the LTD/LTP balance for VOR consolidation; (3) reshaping synaptic efficacy distributions for VOR phase-reversal adaptation; (4) explaining the reversal VOR gain discontinuities during sleeping.

Central nystagmus. III. Functional correlations of mesodiencephalic nystagmogenic center

1959 ◽  
Vol 197 (2) ◽  
pp. 454-460 ◽  
Author(s):  
F. Bergmann ◽  
J. Lachmann ◽  
M. Monnier ◽  
P. Krupp
Keyword(s):  
Electrical Stimulation ◽  
Eye Movements ◽  
Vestibular Nuclei ◽  
Rabbit Brain ◽  
Vestibular Nystagmus ◽  
Posterior Commissure ◽  
Common Substrate ◽  
The Common ◽  
Stimulation Of

Transverse cuts at various levels of the rabbit brain stem have different effects on vestibular nystagmus and on central nystagmus elicited by electrical stimulation of the mesodiencephalic nystagmogenic area. While transections rostral to the sensitive region enhance both, probably by elimination of inhibitory influences from cortex or retina, transections caudal to this region, but rostral to the colliculi, abolish central nystagmus only. Transections at the level of the inferior colliculus abolish vestibular nystagmus only, while intermediate cuts may eliminate either response. When central nystagmus alone survives, its character is changed in a specific way indicating the important role of the vestibular nuclei in normal central nystagmus. These observations lead to an approximate localization of the common substrate for conjugate eye movements involved both in central and vestibular nystagmus. Longitudinal cuts through the posterior commissure provoke a temporary disconjugated nystagmus not described hitherto.

scholarly journals Vestibular CCK neurons drive motion-induced malaise

2021 ◽  
Author(s):  
Pablo Machuca-Márquez ◽  
Laura Sánchez-Benito ◽  
Fabien Menardy ◽  
Andrea Urpi ◽  
Isabella Appiah ◽  
...  
Keyword(s):  
Motion Sickness ◽  
Sensory Information ◽  
Behavioral Responses ◽  
Vestibular Nuclei ◽  
Neural Substrates ◽  
Parabrachial Nucleus ◽  
Novel Food ◽  
Novel Foods ◽  
Insight Into

ABSTRACTPassive motion can induce kinetosis (motion sickness, MS) in susceptible individuals. MS is an evolutionary conserved mechanism caused by mismatches between motion-related sensory information and past visual and motion memory, triggering a malaise accompanied by hypolocomotion, hypothermia, hypophagia and aversion to novel foods presented coincidentally. Vestibular nuclei (VN) are critical for the processing of movement input, and motion-induced activation of VN neurons recapitulates MS-related signs. However, the genetic identity of VN neurons mediating MS-related autonomic and aversive responses remains unknown. Here, we identify a glutamatergic vestibular circuitry necessary to elicit MS-related behavioral responses, defining a central role of cholecystokinin (CCK)- expressing glutamatergic VN neurons in vestibular-induced malaise. Moreover, we show that CCK VN inputs onto the parabrachial nucleus activate Calca-expressing neurons and are sufficient to establish hypothermia and aversion to novel food. Together, we provide novel insight into the neurobiological regulation of MS, unravelling key genetically defined neural substrates for kinetosis.

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