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Regulation and functional roles of rebound potentiation at cerebellar stellate cell-Purkinje cell synapses.

Hirano T, Kawaguchi SY - Front Cell Neurosci (2014)

Bottom Line: RP induction depends on binding of GABAAR with GABAAR associated protein (GABARAP) which is regulated by Ca(2+)/calmodulin-dependent kinase II (CaMKII).Recent studies have revealed that the subunit composition of CaMKII has significant impact on RP induction.Thus, RP is involved in a certain type of motor learning.

View Article: PubMed Central - PubMed

Affiliation: Department of Biophysics, Graduate School of Science, Kyoto University Kitashirakawa-Oiwake-cho Kyoto, Japan.

ABSTRACT
Purkinje cells receive both excitatory and inhibitory synaptic inputs and send sole output from the cerebellar cortex. Long-term depression (LTD), a type of synaptic plasticity, at excitatory parallel fiber-Purkinje cell synapses has been studied extensively as a primary cellular mechanism of motor learning. On the other hand, at inhibitory synapses on a Purkinje cell, postsynaptic depolarization induces long-lasting potentiation of GABAergic synaptic transmission. This synaptic plasticity is called rebound potentiation (RP), and its molecular regulatory mechanisms have been studied. The increase in intracellular Ca(2+) concentration caused by depolarization induces RP through enhancement of GABAA receptor (GABAAR) responsiveness. RP induction depends on binding of GABAAR with GABAAR associated protein (GABARAP) which is regulated by Ca(2+)/calmodulin-dependent kinase II (CaMKII). Whether RP is induced or not is determined by the balance between phosphorylation and de-phosphorylation activities regulated by intracellular Ca(2+) and by metabotropic GABA and glutamate receptors. Recent studies have revealed that the subunit composition of CaMKII has significant impact on RP induction. A Purkinje cell expresses both α- and β-CaMKII, and the latter has much higher affinity for Ca(2+)/calmodulin than the former. It was shown that when the relative amount of α- to β-CaMKII is large, RP induction is suppressed. The functional significance of RP has also been studied using transgenic mice in which a peptide inhibiting association of GABARAP and GABAAR is expressed selectively in Purkinje cells. The transgenic mice show abrogation of RP and subnormal adaptation of vestibulo-ocular reflex (VOR), a type of motor learning. Thus, RP is involved in a certain type of motor learning.

No MeSH data available.


Related in: MedlinePlus

Cerebellar cortical neuronal circuits. Mossy fibers from pontine nuclei etc., send excitatory synaptic outputs to granule cells. A granule cell forms one or a few excitatory glutamatergic synapses on a Purkinje cell, where LTD occurs depending on the activity of the granule cell and a climbing fiber. Molecular layer interneurons (stellate and basket cells) receive excitatory synaptic inputs from granule cells and inhibit Purkinje cells. At inhibitory GABAergic synapses between a stellate cell and a Purkinje cell, rebound potentiation (RP) is induced by climbing fiber activity.
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Figure 1: Cerebellar cortical neuronal circuits. Mossy fibers from pontine nuclei etc., send excitatory synaptic outputs to granule cells. A granule cell forms one or a few excitatory glutamatergic synapses on a Purkinje cell, where LTD occurs depending on the activity of the granule cell and a climbing fiber. Molecular layer interneurons (stellate and basket cells) receive excitatory synaptic inputs from granule cells and inhibit Purkinje cells. At inhibitory GABAergic synapses between a stellate cell and a Purkinje cell, rebound potentiation (RP) is induced by climbing fiber activity.

Mentions: The cerebellum consists of cortex and nuclei, and is involved in motor control (Figure 1; Ito, 1984, 2011; Llinás et al., 2004). There are two major inputs to the cerebellum, mossy fibers and climbing fibers. Mossy fibers coming from pons, medulla oblongata etc., innervate neurons in cerebellar nuclei and granule cells in the granular layer of cortex. Granule cells extend axons to the molecular layer, where they bifurcate. The bifurcated granule cell axons are called parallel fibers, and form excitatory glutamatergic synapses on dendrites of Purkinje cells and inhibitory GABAergic interneurons in the molecular layer, stellate and basket cells. Climbing fibers coming from inferior olivary nuclei innervate neurons in cerebellar nuclei and Purkinje cells. A single climbing fiber forms hundreds synapses on a Purkinje cell, and thus sends a powerful excitatory drive. Purkinje cells are GABAergic neuron, and send sole output from the cortex to nuclear neurons.


Regulation and functional roles of rebound potentiation at cerebellar stellate cell-Purkinje cell synapses.

Hirano T, Kawaguchi SY - Front Cell Neurosci (2014)

Cerebellar cortical neuronal circuits. Mossy fibers from pontine nuclei etc., send excitatory synaptic outputs to granule cells. A granule cell forms one or a few excitatory glutamatergic synapses on a Purkinje cell, where LTD occurs depending on the activity of the granule cell and a climbing fiber. Molecular layer interneurons (stellate and basket cells) receive excitatory synaptic inputs from granule cells and inhibit Purkinje cells. At inhibitory GABAergic synapses between a stellate cell and a Purkinje cell, rebound potentiation (RP) is induced by climbing fiber activity.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3927423&req=5

Figure 1: Cerebellar cortical neuronal circuits. Mossy fibers from pontine nuclei etc., send excitatory synaptic outputs to granule cells. A granule cell forms one or a few excitatory glutamatergic synapses on a Purkinje cell, where LTD occurs depending on the activity of the granule cell and a climbing fiber. Molecular layer interneurons (stellate and basket cells) receive excitatory synaptic inputs from granule cells and inhibit Purkinje cells. At inhibitory GABAergic synapses between a stellate cell and a Purkinje cell, rebound potentiation (RP) is induced by climbing fiber activity.
Mentions: The cerebellum consists of cortex and nuclei, and is involved in motor control (Figure 1; Ito, 1984, 2011; Llinás et al., 2004). There are two major inputs to the cerebellum, mossy fibers and climbing fibers. Mossy fibers coming from pons, medulla oblongata etc., innervate neurons in cerebellar nuclei and granule cells in the granular layer of cortex. Granule cells extend axons to the molecular layer, where they bifurcate. The bifurcated granule cell axons are called parallel fibers, and form excitatory glutamatergic synapses on dendrites of Purkinje cells and inhibitory GABAergic interneurons in the molecular layer, stellate and basket cells. Climbing fibers coming from inferior olivary nuclei innervate neurons in cerebellar nuclei and Purkinje cells. A single climbing fiber forms hundreds synapses on a Purkinje cell, and thus sends a powerful excitatory drive. Purkinje cells are GABAergic neuron, and send sole output from the cortex to nuclear neurons.

Bottom Line: RP induction depends on binding of GABAAR with GABAAR associated protein (GABARAP) which is regulated by Ca(2+)/calmodulin-dependent kinase II (CaMKII).Recent studies have revealed that the subunit composition of CaMKII has significant impact on RP induction.Thus, RP is involved in a certain type of motor learning.

View Article: PubMed Central - PubMed

Affiliation: Department of Biophysics, Graduate School of Science, Kyoto University Kitashirakawa-Oiwake-cho Kyoto, Japan.

ABSTRACT
Purkinje cells receive both excitatory and inhibitory synaptic inputs and send sole output from the cerebellar cortex. Long-term depression (LTD), a type of synaptic plasticity, at excitatory parallel fiber-Purkinje cell synapses has been studied extensively as a primary cellular mechanism of motor learning. On the other hand, at inhibitory synapses on a Purkinje cell, postsynaptic depolarization induces long-lasting potentiation of GABAergic synaptic transmission. This synaptic plasticity is called rebound potentiation (RP), and its molecular regulatory mechanisms have been studied. The increase in intracellular Ca(2+) concentration caused by depolarization induces RP through enhancement of GABAA receptor (GABAAR) responsiveness. RP induction depends on binding of GABAAR with GABAAR associated protein (GABARAP) which is regulated by Ca(2+)/calmodulin-dependent kinase II (CaMKII). Whether RP is induced or not is determined by the balance between phosphorylation and de-phosphorylation activities regulated by intracellular Ca(2+) and by metabotropic GABA and glutamate receptors. Recent studies have revealed that the subunit composition of CaMKII has significant impact on RP induction. A Purkinje cell expresses both α- and β-CaMKII, and the latter has much higher affinity for Ca(2+)/calmodulin than the former. It was shown that when the relative amount of α- to β-CaMKII is large, RP induction is suppressed. The functional significance of RP has also been studied using transgenic mice in which a peptide inhibiting association of GABARAP and GABAAR is expressed selectively in Purkinje cells. The transgenic mice show abrogation of RP and subnormal adaptation of vestibulo-ocular reflex (VOR), a type of motor learning. Thus, RP is involved in a certain type of motor learning.

No MeSH data available.


Related in: MedlinePlus