Micro- and Semi-Microrecordings in the Ventral Thalamus of Human Patients and Monkeys with Dyskinesias

1993 ◽  
Vol 60 (1-3) ◽  
pp. 146-146 ◽  
Author(s):  
D.M. Gao ◽  
L. Jeaugey ◽  
S. Lavallee ◽  
D. Hoffmann ◽  
P. Pollak ◽  
...  
Keyword(s):  
Ventral Thalamus

scholarly journals Dual contributions of cerebellar-thalamic networks to learning and offline consolidation of a complex motor task

2020 ◽  
Author(s):  
Andres P Varani ◽  
Romain W Sala ◽  
Caroline Mailhes-Hamon ◽  
Jimena L Frontera ◽  
Clément Léna ◽  
...  
Keyword(s):  
Motor Learning ◽  
Motor Task ◽  
Cerebellar Nuclei ◽  
Specific Inhibition ◽  
Thalamic Nuclei ◽  
Related Information ◽  
Midline Thalamus ◽  
Ventral Thalamus ◽  
Complex Motor ◽  
Offline Processing

SUMMARYThe contribution of cerebellum to motor learning is often considered to be limited to adaptation, a short-timescale tuning of reflexes and previous learned skills. Yet, the cerebellum is reciprocally connected to two main players of motor learning, the motor cortex and the basal ganglia, via the ventral and midline thalamus respectively. Here, we evaluated the contribution of cerebellar neurons projecting to these thalamic nuclei in a skilled locomotion task in mice. In the cerebellar nuclei, we found task-specific neuronal activities during the task, and lasting changes after the task suggesting an offline processing of task-related information. Using pathway-specific inhibition, we found that dentate neurons projecting to the midline thalamus contribute to learning and retrieval, while interposed neurons projecting to the ventral thalamus contribute to the offline consolidation of savings. Our results thus show that two parallel cerebello-thalamic pathways perform distinct computations operating on distinct timescales in motor learning.

scholarly journals Suprachiasmatic nucleus-dependent and independent outputs driving rhythmic activity in hypothalamic and thalamic neurons

BMC Biology ◽  
2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Court Harding ◽  
David A. Bechtold ◽  
Timothy M. Brown
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Circadian Variation ◽  
Brain Slices ◽  
Rhythmic Activity ◽  
The Body ◽  
Inhibitory Input ◽  
Thalamic Nuclei ◽  
Thalamic Neurons ◽  
Ventral Thalamus ◽  
Central Clock

Abstract Background Daily variations in mammalian physiology are under control of a central clock in the suprachiasmatic nucleus (SCN). SCN timing signals are essential for coordinating cellular clocks and associated circadian variations in cell and tissue function across the body; however, direct SCN projections primarily target a restricted set of hypothalamic and thalamic nuclei involved in physiological and behavioural control. The role of the SCN in driving rhythmic activity in these targets remains largely unclear. Here, we address this issue via multielectrode recording and manipulations of SCN output in adult mouse brain slices. Results Electrical stimulation identifies cells across the midline hypothalamus and ventral thalamus that receive inhibitory input from the SCN and/or excitatory input from the retina. Optogenetic manipulations confirm that SCN outputs arise from both VIP and, more frequently, non-VIP expressing cells and that both SCN and retinal projections almost exclusively target GABAergic downstream neurons. The majority of midline hypothalamic and ventral thalamic neurons exhibit circadian variation in firing and those receiving inhibitory SCN projections consistently exhibit peak activity during epochs when SCN output is low. Physical removal of the SCN confirms that neuronal rhythms in ~ 20% of the recorded neurons rely on central clock input but also reveals many neurons that can express circadian variation in firing independent of any SCN input. Conclusions We identify cell populations across the midline hypothalamus and ventral thalamus exhibiting SCN-dependent and independent rhythms in neural activity, providing new insight into the mechanisms by which the circadian system generates daily physiological rhythms.

Central Mechanisms of Frog Calling

Behaviour ◽  
1966 ◽  
Vol 26 (3-4) ◽  
pp. 251-285 ◽  
Author(s):  
Robert S. Schmidt
Keyword(s):  
Rana Pipiens ◽  
Hormone Receptors ◽  
Acoustic Stimulus ◽  
Control Mechanisms ◽  
Nucleus Isthmi ◽  
Hyla Cinerea ◽  
Midbrain Tegmentum ◽  
Inspiratory Phase ◽  
Ventral Thalamus ◽  
The Brain

AbstractRelease calling and warning crying in Rana pipiens are described and compared with breathing. Vokalizations consist of a vocal phase, which is merely a modification of the expiratory phase of breathing, followed by an inspiratory phase, which is identical to inspiratory phase of breathing. Electrical and mechanical stimulation of the brain and brain lesions are used to locate some of the central mechanisms controlling release calling and warning crying in Rana pipiens, and mating calling in Rana pipiens and a number of hylids (mainly Hyla cinerea). It is concluded that the main control mechanisms are in the trigeminoisthmic tegmentum (below the nucleus isthmi). Mating calling requires, in addition, input transmitted through the ventral thalamus from hormone receptors in the preoptic area. Mating calling can be evoked in hylids by presenting them with recordings of specific calls. The mechanisms for responding to an acoustic stimulus are probably located in the anterior medulla and midbrain tegmentum (below the nucleus isthmi). Mating calling was evoked in two Hyla cinerea females after replacing the ovaries with Rana testes and injecting Rana pituitaries. It is suggested that release calling evolved from breathing, and that warning crying and mating calling may then have evolved from release calling.

scholarly journals Basic Fibroblast Growth Factor Prevents Thalamic Degeneration after Cortical Infarction

1991 ◽  
Vol 11 (3) ◽  
pp. 472-478 ◽  
Author(s):  
Kazuo Yamada ◽  
Akira Kinoshita ◽  
Eiji Kohmura ◽  
Tateo Sakaguchi ◽  
Junji Taguchi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Normal Saline ◽  
Contralateral Side ◽  
Fibroblast Growth ◽  
Rat Serum ◽  
Thalamic Neurons ◽  
Retrograde Degeneration ◽  
Ventral Thalamus

In the focal infarction model of the rat middle cerebral artery (MCA), the thalamus of the occluded side becomes gradually atrophic, mainly because of retrograde degeneration. We determined whether basic fibroblast growth factor (bFGF) administered intracisternally could prevent this thalamic atrophy. We occluded the left MCA through a small cranial opening, and animals were then divided into two groups. One group received intra-cisternal injections of recombinant bFGF (1 μg dissolved in 0.1 ml of saline with 2% rat serum) starting 1 day after occlusion and repeated once a week to a total dose of 4 μg by four injections. The other group received vehicle solution by the same schedule. The animals were perfused and fixed at 28 days after occlusion, and histological examination was made at the level of the caudoputamen and thalamus. In the bFGF-treated rats, the area of the posterior ventral thalamus of the occluded side was 93% of that of the contralateral side, i.e., significantly larger than in the normal saline-treated rats (75%, p < 0.01). The infarction size was not statistically different in the two groups. Microscopic observation indicated that normal-saline-treated animals showed shrinkage and disappearance of thalamic neurons, whereas bFGF-treated groups showed preservation of thalamic neurons. Computerized analysis of the cell size substantiated this observation. To assess the effect of bFGF on astrocytes, bFGF or vehicle solution was injected into normal rats, and their histology was evaluated at 1, 2, and 4 weeks after injection. The bFGF-injected group showed a significant increase in glial fibrillary acidic protein-positive astrocytes in the brain tissue facing the ventriculocisternal system. The results suggest that bFGF prevents retrograde degeneration of thalamic neurons by working directly as a neurotrophic factor of these neurons or by activating astrocytes located in the thalamocortical pathway.

scholarly journals Brain Regional Fos Expression Elicited by the Activation of μ- but not δ-Opioid Receptors of the Ventral Tegmental Area: Evidence for an Implication of the Ventral Thalamus in Opiate Reward

2007 ◽  
Vol 33 (7) ◽  
pp. 1746-1759 ◽  
Author(s):  
Vincent David ◽  
Audrey Matifas ◽  
Stéphanie Gavello-Baudy ◽  
Laurence Decorte ◽  
Brigitte L Kieffer ◽  
...  
Keyword(s):  
Ventral Tegmental Area ◽  
Opioid Receptors ◽  
Ventral Thalamus ◽  
Fos Expression ◽  
Ventral Tegmental

Neuronal activity patterns in the ventral thalamus: Comparison between Parkinson’s disease and cervical dystonia

2017 ◽  
Vol 128 (12) ◽  
pp. 2482-2490 ◽  
Author(s):  
Dmitriy Devetiarov ◽  
Ulia Semenova ◽  
Svetlana Usova ◽  
Alexey Tomskiy ◽  
Vladimir Tyurnikov ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neuronal Activity ◽  
Cervical Dystonia ◽  
Activity Patterns ◽  
Ventral Thalamus

Reduction of Prepulse Inhibition (PPI) after Neonatal Excitotoxic Lesion of the Ventral Thalamus in Pubertal and Adult Rats

2010 ◽  
Vol 43 (03) ◽  
pp. 99-109 ◽  
Author(s):  
R. Wolf ◽  
K. Matzke ◽  
K. Paelchen ◽  
H. Dobrowolny ◽  
B. Bogerts ◽  
...  
Keyword(s):  
Prepulse Inhibition ◽  
Adult Rats ◽  
Ventral Thalamus ◽  
Excitotoxic Lesion

Cellular Mechanisms Preventing Sustained Activation of Cortex During Subcortical High-Frequency Stimulation

2006 ◽  
Vol 96 (2) ◽  
pp. 613-621 ◽  
Author(s):  
Karl J. Iremonger ◽  
Trent R. Anderson ◽  
Bin Hu ◽  
Zelma H. T. Kiss
Keyword(s):  
Motor Cortex ◽  
High Frequency ◽  
Cortical Neurons ◽  
Primary Motor Cortex ◽  
Brain Slices ◽  
Subcortical White Matter ◽  
High Frequency Stimulation ◽  
Cellular Mechanisms ◽  
Ventral Thalamus ◽  
Frequency Stimulation

Axonal excitation has been proposed as a key mechanism in therapeutic brain stimulation. In this study we examined how high-frequency stimulation (HFS) of subcortical white matter tracts projecting to motor cortex affects downstream postsynaptic responses in cortical neurons. Whole cell recordings were performed in the primary motor cortex (M1) and ventral thalamus of rat brain slices. In M1, neurons showed only an initial depolarization in response to HFS, after which the membrane potential returned to prestimulation levels. The prolonged suppression of excitation during stimulation was neither associated with GABAergic inhibition nor complete action potential failure in stimulated axons. Instead we found that HFS caused a depression of excitatory synaptic currents in postsynaptic neurons that was specific to the stimulated subcortical input. These data are consistent with the hypothesis that axonal HFS produces a functional deafferentation of postsynaptic targets likely from depletion of neurotransmitter.

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