scholarly journals Heterogeneity of intrinsic plasticity in cerebellar Purkinje cells linked with cortical molecular zones

iScience ◽  
2021 ◽  
pp. 103705
Author(s):  
Nguyen-Minh Viet ◽  
Tianzhuo Wang ◽  
Khoa Tran-Anh ◽  
Izumi Sugihara
Keyword(s):  
Purkinje Cells ◽  
Intrinsic Plasticity ◽  
Cerebellar Purkinje Cells

scholarly journals mGlu1 receptor mediates homeostatic control of intrinsic excitability through Ih in cerebellar Purkinje cells

2016 ◽  
Vol 115 (5) ◽  
pp. 2446-2455 ◽  
Author(s):  
Hyun Geun Shim ◽  
Sung-Soo Jang ◽  
Dong Cheol Jang ◽  
Yunju Jin ◽  
Wonseok Chang ◽  
...  
Keyword(s):  
Purkinje Cells ◽  
Neuronal Activity ◽  
Metabotropic Glutamate Receptor ◽  
Activity Level ◽  
Network Activity ◽  
Firing Rates ◽  
Metabotropic Glutamate ◽  
Gated Channel ◽  
Intrinsic Plasticity ◽  
Cerebellar Purkinje Cells

Homeostatic intrinsic plasticity is a cellular mechanism for maintaining a stable neuronal activity level in response to developmental or activity-dependent changes. Type 1 metabotropic glutamate receptor (mGlu1 receptor) has been widely known to monitor neuronal activity, which plays a role as a modulator of intrinsic and synaptic plasticity of neurons. Whether mGlu1 receptor contributes to the compensatory adjustment of Purkinje cells (PCs), the sole output of the cerebellar cortex, in response to chronic changes in excitability remains unclear. Here, we demonstrate that the mGlu1 receptor is involved in homeostatic intrinsic plasticity through the upregulation of the hyperpolarization-activated current ( Ih) in cerebellar PCs. This plasticity was prevented by inhibiting the mGlu1 receptor with Bay 36–7620, an mGlu1 receptor inverse agonist, but not with CPCCOEt, a neutral antagonist. Chronic inactivation with tetrodotoxin (TTX) increased the components of Ih in the PCs, and ZD 7288, a hyperpolarization-activated cyclic nucleotide-gated channel selective inhibitor, fully restored reduction of firing rates in the deprived neurons. The homeostatic elevation of Ih was also prevented by BAY 36–7620, but not CPCCOEt. Furthermore, KT 5720, a blocker of protein kinase A (PKA), prevented the effect of TTX reducing the evoked firing rates, indicating the reduction in excitability of PCs due to PKA activation. Our study shows that both the mGlu1 receptor and the PKA pathway are involved in the homeostatic intrinsic plasticity of PCs after chronic blockade of the network activity, which provides a novel understanding on how cerebellar PCs can preserve the homeostatic state under activity-deprived conditions.

scholarly journals Intrinsic Excitability Increase in Cerebellar Purkinje Cells Following Delay Eyeblink Conditioning in Mice

2018 ◽  
Author(s):  
Heather K. Titley ◽  
Gabrielle V. Watkins ◽  
Carmen Lin ◽  
Craig Weiss ◽  
Michael McCarthy ◽  
...  
Keyword(s):  
Purkinje Cells ◽  
Neuronal Excitability ◽  
Eyeblink Conditioning ◽  
Underlying Mechanism ◽  
Learning Task ◽  
Sk Channels ◽  
Calcium Dependent ◽  
Cerebellar Learning ◽  
Intrinsic Plasticity ◽  
Cerebellar Purkinje Cells

AbstractCerebellar learning is canonically thought to rely on synaptic plasticity, particularly at synaptic inputs to Purkinje cells. Recently, however, other complementary mechanisms have been identified. Intrinsic plasticity is one such mechanism, and depends in part on the down-regulation of calcium-dependent SK-type K channels, which is associated with an increase in neuronal excitability. In the hippocampus, SK-mediated intrinsic plasticity has been shown to play a role in trace eyeblink conditioning; however, it is not yet known how intrinsic plasticity contributes to a cerebellar learning task such as delay eyeblink conditioning. Whole cell recordings were obtained from acute cerebellar slices from mice ~48 hours after learning a delay eyeblink conditioning task. Over a period of repeated training sessions mice received either distinctly paired trials of a tone co-terminating with a periorbital shock (conditioned mice) or trials in which these stimuli were presented in an unpaired manner (pseudoconditioned mice). Conditioned mice show a significantly reduced afterhyperpolarization (AHP) following trains of parallel fiber stimuli. Moreover, we find that SK-dependent intrinsic plasticity is occluded in conditioned, but not pseudoconditioned mice. These findings show that excitability is enhanced in Purkinje cells after delay eyeblink conditioning and point toward a downregulation of SK channels as a potential underlying mechanism.

scholarly journals Intrinsic plasticity of cerebellar Purkinje cells in motor learning circuits

2019 ◽  
Author(s):  
Dong Cheol Jang ◽  
Hyun Geun Shim ◽  
Sang Jeong Kim
Keyword(s):  
Purkinje Cells ◽  
Neural Plasticity ◽  
Memory Consolidation ◽  
Vestibular Nucleus ◽  
Motor Memory ◽  
Long Term Storage ◽  
Vestibulo Ocular Reflex ◽  
Intrinsic Plasticity ◽  
Cerebellar Purkinje Cells ◽  
Local Circuits

AbstractIntrinsic plasticity of cerebellar Purkinje cells (PCs) is recently highlighted in the cerebellar local circuits, however, its physiological impact on the cerebellar learning and memory remains elusive. Using a mouse model of memory consolidation deficiency, we found that the intrinsic plasticity of PCs may be involved in motor memory consolidation. Gain-up training of the vestibulo-ocular reflex produced a decrease in the synaptic weight of PCs in both the wild-type and knockout groups. However, intrinsic plasticity was impaired only in the knockout mice. Furthermore, the observed defects in the intrinsic plasticity of PCs led to the formation of improper neural plasticity in the vestibular nucleus (VN) neurons. Our results suggest that the synergistic modulation of intrinsic and synaptic plasticity in PCs is required for the changes in following plasticity in the VN, thereby contributes to the long-term storage of motor memory.

scholarly journals Intrinsic Plasticity Complements Long-Term Potentiation in Parallel Fiber Input Gain Control in Cerebellar Purkinje Cells

2010 ◽  
Vol 30 (41) ◽  
pp. 13630-13643 ◽  
Author(s):  
A. Belmeguenai ◽  
E. Hosy ◽  
F. Bengtsson ◽  
C. M. Pedroarena ◽  
C. Piochon ◽  
...  
Keyword(s):  
Purkinje Cells ◽  
Gain Control ◽  
Long Term Potentiation ◽  
Parallel Fiber ◽  
Term Potentiation ◽  
Input Gain ◽  
Intrinsic Plasticity ◽  
Cerebellar Purkinje Cells

Ultrastorcture of Cerebellar Purkinje Cells in Rats Subjected To Partial Global Cerebral Ischemia

1985 ◽  
Vol 43 ◽  
pp. 674-675
Author(s):  
R.V.W. Dimlich ◽  
M.H. Biros
Keyword(s):  
Cerebral Ischemia ◽  
Purkinje Cells ◽  
Cell Types ◽  
Microscopic Level ◽  
Global Cerebral Ischemia ◽  
Light Microscopic Level ◽  
Cerebellar Damage ◽  
Cerebellar Injury ◽  
Cerebellar Purkinje Cells ◽  
Cell Changes

In severe cerebral ischemia, Purkinje cells of the cerebellum are one of the cell types most vulnerable to anoxic damage. In the partial (forebrain) global ischemic (PGI) model of the rat, Paljärvi noted at the light microscopic level that cerebellar damage is inconsistant and when present, milder than in the telencephalon, diencephalon and rostral brain stem. Cerebellar injury was observed in 3 of 4 PGI rats following 5 minutes of reperfusion but in none of the rats after 90 min of reperfusion. To evaluate a time between these two extremes (5 and 90 min), the present investigation used the PGI model to study the effects of ischemia on the ultrastructure of cerebellar Purkinje cells in rats that were sacrificed after 30 min of reperfusion. This time also was chosen because lactic acid that is thought to contribute to ischemic cell changes in PGI is at a maximum after 30 min of reperfusion.

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