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Modulating excitation through plasticity at inhibitory synapses.

Chevaleyre V, Piskorowski R - Front Cell Neurosci (2014)

Bottom Line: As a result, a profusion of studies has tried to elucidate the mechanisms underlying these forms of plasticity.Traditionally, experience-dependent changes at excitatory synapses were assumed to underlie learning and memory formation.We will focus on the hippocampus because this region has a relatively well-understood circuitry, numerous forms of activity-dependent plasticity and a multitude of identified interneuron subclasses.

View Article: PubMed Central - PubMed

Affiliation: Centre National de la Recherche Scientifique, UMR8118, Université Paris Descartes Paris, France.

ABSTRACT
Learning is believed to depend on lasting changes in synaptic efficacy such as long-term potentiation and long-term depression. As a result, a profusion of studies has tried to elucidate the mechanisms underlying these forms of plasticity. Traditionally, experience-dependent changes at excitatory synapses were assumed to underlie learning and memory formation. However, with the relatively more recent investigation of inhibitory transmission, it had become evident that inhibitory synapses are not only plastic, but also provide an additional way to modulate excitatory transmission and the induction of plasticity at excitatory synapses. Thanks to recent technological advances, progress has been made in understanding synaptic transmission and plasticity from particular interneuron subtypes. In this review article, we will describe various forms of synaptic plasticity that have been ascribed to two fairly well characterized populations of interneurons in the hippocampus, those expressing cholecystokinin (CCK) and parvalbumin (PV). We will discuss the resulting changes in the strength and plasticity of excitatory transmission that occur in the local circuit as a result of the modulation of inhibitory transmission. We will focus on the hippocampus because this region has a relatively well-understood circuitry, numerous forms of activity-dependent plasticity and a multitude of identified interneuron subclasses.

No MeSH data available.


Related in: MedlinePlus

Modulation and roles of GABA release from PV+ interneurons. PV+ interneurons target either the soma (basket cell, BS), the axon (axo-axonic cell, AA) or the dendrites (bistratified cell, BS and oriens-lacunosum moleculare cell, OLM) of pyramidal cells (see Somogyi and Klausberger, 2005). The release of GABA from PV+ cell terminals is mediated by P/Q-type calcium channels. The tight coupling between calcium influx and exocytosis machinery results in precisely timed vesicle release. The release of GABA at PV+ cell synapses is negatively controlled by diverse receptors including mu- and delta-opioid receptors (MOR and DOR) and muscarinic M2 receptors. Conversely, GABA release from PV cells is increased by activation of the Neuregulin 1 receptor ErbB4. LTP induction at SC-CA1 synapses is impaired following ErB4 activation in PV+ cells due to increased pre-synaptic GABA release by PV+ cells.
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Figure 2: Modulation and roles of GABA release from PV+ interneurons. PV+ interneurons target either the soma (basket cell, BS), the axon (axo-axonic cell, AA) or the dendrites (bistratified cell, BS and oriens-lacunosum moleculare cell, OLM) of pyramidal cells (see Somogyi and Klausberger, 2005). The release of GABA from PV+ cell terminals is mediated by P/Q-type calcium channels. The tight coupling between calcium influx and exocytosis machinery results in precisely timed vesicle release. The release of GABA at PV+ cell synapses is negatively controlled by diverse receptors including mu- and delta-opioid receptors (MOR and DOR) and muscarinic M2 receptors. Conversely, GABA release from PV cells is increased by activation of the Neuregulin 1 receptor ErbB4. LTP induction at SC-CA1 synapses is impaired following ErB4 activation in PV+ cells due to increased pre-synaptic GABA release by PV+ cells.


Modulating excitation through plasticity at inhibitory synapses.

Chevaleyre V, Piskorowski R - Front Cell Neurosci (2014)

Modulation and roles of GABA release from PV+ interneurons. PV+ interneurons target either the soma (basket cell, BS), the axon (axo-axonic cell, AA) or the dendrites (bistratified cell, BS and oriens-lacunosum moleculare cell, OLM) of pyramidal cells (see Somogyi and Klausberger, 2005). The release of GABA from PV+ cell terminals is mediated by P/Q-type calcium channels. The tight coupling between calcium influx and exocytosis machinery results in precisely timed vesicle release. The release of GABA at PV+ cell synapses is negatively controlled by diverse receptors including mu- and delta-opioid receptors (MOR and DOR) and muscarinic M2 receptors. Conversely, GABA release from PV cells is increased by activation of the Neuregulin 1 receptor ErbB4. LTP induction at SC-CA1 synapses is impaired following ErB4 activation in PV+ cells due to increased pre-synaptic GABA release by PV+ cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3975092&req=5

Figure 2: Modulation and roles of GABA release from PV+ interneurons. PV+ interneurons target either the soma (basket cell, BS), the axon (axo-axonic cell, AA) or the dendrites (bistratified cell, BS and oriens-lacunosum moleculare cell, OLM) of pyramidal cells (see Somogyi and Klausberger, 2005). The release of GABA from PV+ cell terminals is mediated by P/Q-type calcium channels. The tight coupling between calcium influx and exocytosis machinery results in precisely timed vesicle release. The release of GABA at PV+ cell synapses is negatively controlled by diverse receptors including mu- and delta-opioid receptors (MOR and DOR) and muscarinic M2 receptors. Conversely, GABA release from PV cells is increased by activation of the Neuregulin 1 receptor ErbB4. LTP induction at SC-CA1 synapses is impaired following ErB4 activation in PV+ cells due to increased pre-synaptic GABA release by PV+ cells.
Bottom Line: As a result, a profusion of studies has tried to elucidate the mechanisms underlying these forms of plasticity.Traditionally, experience-dependent changes at excitatory synapses were assumed to underlie learning and memory formation.We will focus on the hippocampus because this region has a relatively well-understood circuitry, numerous forms of activity-dependent plasticity and a multitude of identified interneuron subclasses.

View Article: PubMed Central - PubMed

Affiliation: Centre National de la Recherche Scientifique, UMR8118, Université Paris Descartes Paris, France.

ABSTRACT
Learning is believed to depend on lasting changes in synaptic efficacy such as long-term potentiation and long-term depression. As a result, a profusion of studies has tried to elucidate the mechanisms underlying these forms of plasticity. Traditionally, experience-dependent changes at excitatory synapses were assumed to underlie learning and memory formation. However, with the relatively more recent investigation of inhibitory transmission, it had become evident that inhibitory synapses are not only plastic, but also provide an additional way to modulate excitatory transmission and the induction of plasticity at excitatory synapses. Thanks to recent technological advances, progress has been made in understanding synaptic transmission and plasticity from particular interneuron subtypes. In this review article, we will describe various forms of synaptic plasticity that have been ascribed to two fairly well characterized populations of interneurons in the hippocampus, those expressing cholecystokinin (CCK) and parvalbumin (PV). We will discuss the resulting changes in the strength and plasticity of excitatory transmission that occur in the local circuit as a result of the modulation of inhibitory transmission. We will focus on the hippocampus because this region has a relatively well-understood circuitry, numerous forms of activity-dependent plasticity and a multitude of identified interneuron subclasses.

No MeSH data available.


Related in: MedlinePlus