The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Nerve terminal nicotinic acetylcholine receptors initiate quantal GABA release from perisomatic interneurons by activating axonal T-type (Cav3) Ca²⁺ channels and Ca²⁺ release from stores.
Ai-Hui Tang; Miranda A Karson; Daniel A Nagode; J Michael McIntosh; Victor N Uebele; John J Renger; Matthias Klugmann; Teresa A Milner; Bradley E Alger (Profiled Authors: Bradley E Alger; Miranda Karson; Ai-Hui Tang)
Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
The Journal of neuroscience : the official journal of the Society for Neuroscience 2011;31(38):13546-61.
Release of conventional neurotransmitters is mainly controlled by calcium (Ca²⁺) influx via high-voltage-activated (HVA), Ca(v)2, channels ("N-, P/Q-, or R-types") that are opened by action potentials. Regulation of transmission by subthreshold depolarizations does occur, but there is little evidence that low-voltage-activated, Ca(v)3 ("T-type"), channels take part. GABA release from cortical perisomatic-targeting interneurons affects numerous physiological processes, and yet its underlying control mechanisms are not fully understood. We investigated whether T-type Ca²⁺ channels are involved in regulating GABA transmission from these cells in rat hippocampal CA1 using a combination of whole-cell voltage-clamp, multiple-fluorescence confocal microscopy, dual-immunolabeling electron-microscopy, and optogenetic methods. We show that Ca(v)3.1, T-type Ca²⁺ channels can be activated by α3β4 nicotinic acetylcholine receptors (nAChRs) that are located on the synaptic regions of the GABAergic perisomatic-targeting interneuronal axons, including the parvalbumin-expressing cells. Asynchronous, quantal GABA release can be triggered by Ca²⁺ influx through presynaptic T-type Ca²⁺ channels, augmented by Ca²⁺ from internal stores, following focal microiontophoretic activation of the α3β4 nAChRs. The resulting GABA release can inhibit pyramidal cells. The T-type Ca²⁺ channel-dependent mechanism is not dependent on, or accompanied by, HVA channel Ca²⁺ influx, and is insensitive to agonists of cannabinoid, μ-opioid, or GABA(B) receptors. It may therefore operate in parallel with the normal HVA-dependent processes. The results reveal new aspects of the regulation of GABA transmission and contribute to a deeper understanding of ACh and nicotine actions in CNS.
2 Originating Grant
ALGER, BRADLEY E
1 April 2006 - 30 June 2013
NATIONAL INSTITUTE OF MENTAL HEALTH
ALGER, BRADLEY E
30 September 2001 - 31 March 2012
NATIONAL INSTITUTE ON DRUG ABUSE
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