NDLI: Astrocyte-derived kynurenic acid modulates basal and evoked cortical acetylcholine release.

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Astrocyte-derived kynurenic acid modulates basal and evoked cortical acetylcholine release.

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Astrocyte-derived kynurenic acid modulates basal and evoked cortical acetylcholine release.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zmarowski, A. Wu, H-Q Brooks, J. M. Potter, M. C. Pellicciari, R. Schwarcz, R. Bruno, J. P.
Description	Country affiliation: United States Author Affiliation: Zmarowski A ( Department of Psychology and Neuroscience, The Ohio State University, Columbus, OH 43210, USA.)
Abstract	We tested the hypothesis that fluctuations in the levels of kynurenic acid (KYNA), an endogenous antagonist of the alpha7 nicotinic acetylcholine (ACh) receptor, modulate extracellular ACh levels in the medial prefrontal cortex in rats. Decreases in cortical KYNA levels were achieved by local perfusion of S-ESBA, a selective inhibitor of the astrocytic enzyme kynurenine aminotransferase II (KAT II), which catalyses the formation of KYNA from its precursor L-kynurenine. At 5 mm, S-ESBA caused a 30% reduction in extracellular KYNA levels, which was accompanied by a two-threefold increase in basal cortical ACh levels. Co-perfusion of KYNA in the endogenous range (100 nm), which by itself tended to reduce basal ACh levels, blocked the ability of S-ESBA to raise extracellular ACh levels. KYNA perfusion (100 nm) also prevented the evoked ACh release caused by d-amphetamine (2.0 mg/kg). This effect was duplicated by the systemic administration of kynurenine (50 mg/kg), which resulted in a significant increase in cortical KYNA formation. Jointly, these data indicate that astrocytes, by producing and releasing KYNA, have the ability to modulate cortical cholinergic neurotransmission under both basal and stimulated conditions. As cortical KYNA levels are elevated in individuals with schizophrenia, and in light of the established role of cortical ACh in executive functions, our findings suggest that drugs capable of attenuating the production of KYNA may be of benefit in the treatment of cognitive deficits in schizophrenia.
File Format	HTM / HTML
ISSN	0953816X
Issue Number	3
Volume Number	29
e-ISSN	14609568
Journal	European Journal of Neuroscience
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2009-02-01
Publisher Place	France
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Neuroscience Acetylcholine Metabolism Astrocytes Cerebral Cortex Kynurenic Acid Presynaptic Terminals Secretion Amphetamine Pharmacology Animals Drug Effects Central Nervous System Stimulants Enzyme Inhibitors Antagonists & Inhibitors Male Nicotinic Antagonists Prefrontal Cortex Rats Rats, Wistar Receptors, Nicotinic Schizophrenia Drug Therapy Physiopathology Synaptic Transmission Physiology Transaminases Up-regulation Alpha7 Nicotinic Acetylcholine Receptor Journal Article Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Neuroscience

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