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LONG-LASTING POTENTIATION OF GABAERGIC INHIBITORY SYNAPTIC TRANSMISSION IN CEREBELLAR PURKINJE CELLS: ITS PROPERTIES AND POSSIBLE MECHANISMS

Kano, Masanobu (1996) LONG-LASTING POTENTIATION OF GABAERGIC INHIBITORY SYNAPTIC TRANSMISSION IN CEREBELLAR PURKINJE CELLS: ITS PROPERTIES AND POSSIBLE MECHANISMS.

Short Abstract:

The cellular basis of motor learning in the cerebellum has been attributed mostly to long-term depression (LTD) at excitatory parallel fiber (PF)-Purkinje cell (PC) synapses. LTD is induced when PFs are activated in conjunction with a climbing fiber (CF), the other excitatory input to PCs. Recently, by using whole- cell patch-clamp recording from PCs in cerebellar slices, a new form of synaptic plasticity was discovered. Stimulation of excitatory CFs induced a long-lasting (usually longer than 30 min) 'rebound potentiation (RP)' of g-amino-butyric acid A (GABAA)-receptor mediated inhibitory postsynaptic currents (IPSCs). Similar to LTD, induction of RP requires transient elevation of intracellular calcium concentration ([Ca2+]i) due to activation of voltage-gated Ca2+ channels. Besides, activity of inhibitory synapses seems to be necessary for RP to occur. RP is mainly due to up-regulation of postsynaptic GABAA receptor function, since PC response to bath-applied exogenous GABA is also potentiated with a time course similar to RP. The difference in the time scale between the Ca2+ transients (10-30 sec) and the durations of RP (>30 min) strongly suggests that some intracellular biochemical machinery is involved. Besides the well-described LTD, RP could be a cellular mechanism that plays an important role in motor learning.

Long Abstract:

The cellular basis of motor learning in the cerebellum has been attributed mostly to long-term depression (LTD) at excitatory parallel fiber (PF)-Purkinje cell (PC) synapses. LTD is induced when PFs are activated in conjunction with a climbing fiber (CF), the other excitatory input to PCs. Recently, by using whole- cell patch-clamp recording from PCs in cerebellar slices, a new form of synaptic plasticity was discovered. Stimulation of excitatory CFs induced a long-lasting (usually longer than 30 min) 'rebound potentiation (RP)' of g-amino-butyric acid A (GABAA)-receptor mediated inhibitory postsynaptic currents (IPSCs). Similar to LTD, induction of RP requires transient elevation of intracellular calcium concentration ([Ca2+]i) due to activation of voltage-gated Ca2+ channels. Besides, activity of inhibitory synapses seems to be necessary for RP to occur. RP is mainly due to up-regulation of postsynaptic GABAA receptor function, since PC response to bath-applied exogenous GABA is also potentiated with a time course similar to RP. The difference in the time scale between the Ca2+ transients (10-30 sec) and the durations of RP (>30 min) strongly suggests that some intracellular biochemical machinery is involved. Besides the well-described LTD, RP could be a cellular mechanism that plays an important role in motor learning.

Keywords:	cerebellum, Purkinje cell, inhibitory synapse, GABAA receptor, long-lasting potentiation, Ca2+, protein kinase
Subjects:	Psychology: Cognitive Psychology Neuroscience: Neuroanatomy Neuroscience: Neurochemistry Neuroscience: Neuroendocrinology Neuroscience: Neurology Neuroscience: Neuropharmacology Neuroscience: Neurophysiology
ID code:	bbs00000534
Deposited by:	Masanobu Kano on 02 May 2001