Book contents
- Frontmatter
- Contents
- Preface
- 1 Cerebellar long-term depression as investigated in a cell culture preparation
- 2 Cellular mechanisms of long-term depression in the cerebellum
- 3 Long-lasting potentiation of GABAergic inhibitory synaptic transmission in cerebellar Purkinje cells: Its properties and possible mechanisms
- 4 Nitric oxide and synaptic plasticity: NO news from the cerebellum
- 5 Models of the cerebellum and motor learning
- 6 On climbing fiber signals and their consequence(s)
- 7 Does the cerebellum learn strategies for the optimal time-varying control of joint stiffness?
- 8 On the specific role of the cerebellum in motor learning and cognition: Clues from PET activation and lesion studies in man
- Open Peer Commentary and Authors' Responses
- References
- Index
1 - Cerebellar long-term depression as investigated in a cell culture preparation
Published online by Cambridge University Press: 04 August 2010
- Frontmatter
- Contents
- Preface
- 1 Cerebellar long-term depression as investigated in a cell culture preparation
- 2 Cellular mechanisms of long-term depression in the cerebellum
- 3 Long-lasting potentiation of GABAergic inhibitory synaptic transmission in cerebellar Purkinje cells: Its properties and possible mechanisms
- 4 Nitric oxide and synaptic plasticity: NO news from the cerebellum
- 5 Models of the cerebellum and motor learning
- 6 On climbing fiber signals and their consequence(s)
- 7 Does the cerebellum learn strategies for the optimal time-varying control of joint stiffness?
- 8 On the specific role of the cerebellum in motor learning and cognition: Clues from PET activation and lesion studies in man
- Open Peer Commentary and Authors' Responses
- References
- Index
Summary
Abstract: Cerebellar long-term depression (LTD) is a form of synaptic plasticity, first described by Ito and co-workers, in which simultaneous activation of two excitatory inputs to a Purkinje neuron, parallel fibers (PFs) and climbing fibers (CFs), results in a sustained depression of PF synaptic drive. The purpose of this target article is not to assess the possible role of this synaptic alteration in motor learning, an issue which is addressed by other authors in this volume, nor is it to provide a detailed summary of the work on cerebellar LTD to this point (see Linden & Connor 1993; Crépel et al. 1993 for review) or to place cerebellar LTD within the context of other forms of persistent synaptic depression that occur within the mammalian brain (see Linden 1994b). Rather, it is to discuss results obtained using a very reduced preparation for the study of LTD, embryonic Purkinje neurons grown in culture and stimulated with exogenous excitatory amino acids, and to consider some advantages and limitations of this approach. Recent work using this preparation has suggested that three processes are necessary for the induction of cerebellar LTD: Ca influx through voltage-gated channels, Na influx through AMPA receptor-associated channels or voltage-gated Na channels, and protein kinase C activation – which is dependent upon activation of the metabotropic glutamate receptor mGluR1. In addition, input-specific induction of LTD has been demonstrated in this preparation under conditions where both spontaneous and evoked neurotransmitter release are reduced or eliminated, indicating that postsynaptic alterations are sufficient to confer this important computational property.
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- Publisher: Cambridge University PressPrint publication year: 1997
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