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Titolo:
Differential changes of synaptic transmission in spiny neurons of rat neostriatum following transient forebrain ischemia
Autore:
Gajendiran, M; Ling, GY; Pang, Z; Xu, ZC;
Indirizzi:
Indiana Univ, Sch Med, Dept Anat & Cell Biol, Indianapolis, IN 46202 USA Indiana Univ Indianapolis IN USA 46202 l Biol, Indianapolis, IN 46202 USA
Titolo Testata:
NEUROSCIENCE
fascicolo: 1, volume: 105, anno: 2001,
pagine: 139 - 152
SICI:
0306-4522(2001)105:1<139:DCOSTI>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
UNILATERAL DOPAMINE DEPLETION; GAMMA-AMINOBUTYRIC ACID; CEREBRAL-ISCHEMIA; STRIATAL DOPAMINE; PROJECTION NEURONS; TYROSINE-HYDROXYLASE; DAMAGE; BRAIN; HIPPOCAMPUS; INHIBITION;
Keywords:
excitation; inhibition; cell death; lateralization; intracellular recording; in vivo;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
67
Recensione:
Indirizzi per estratti:
Indirizzo: Xu, ZC Indiana Univ, Sch Med, Dept Anat & Cell Biol, 635 Barnhill Dr,MS 507, Indianapolis, IN 46202 USA Indiana Univ 635 Barnhill Dr,MS 507 Indianapolis IN USA 46202 2 USA
Citazione:
M. Gajendiran et al., "Differential changes of synaptic transmission in spiny neurons of rat neostriatum following transient forebrain ischemia", NEUROSCIENC, 105(1), 2001, pp. 139-152

Abstract

Spiny neurons in neostriatum are vulnerable to cerebral ischemia. To reveal the mechanisms underlying the postischemic neuronal damage, the spontaneous activities, evoked postsynaptic potentials and membrane properties of spiny neurons in rat neostriatum. were compared before and after transient forebrain ischemia using intracellular recording and staining techniques in vivo. In control animals the membrane properties of spiny neurons were aboutthe same between the left and right neostriatum but the inhibitory synaptic transmission was stronger in the left striatum. After severe ischemia, the spontaneous firing and membrane potential fluctuation of spiny neurons dramatically reduced. The cortically evoked initial excitatory postsynaptic potentials were suppressed after ischemia indicated by the increase of stimulus threshold and the rise time of these components. The paired-pulse facilitation test indicated that such suppression might involve presynaptic, mechanisms. The inhibitory postsynaptic potentials in spiny neurons were completely abolished after ischemia and never returned to the control levels. A late depolarizing postsynaptic potential that was elicited from similar to5% of the control neurons by cortical stimulation could be evoked from similar to 30% of the neurons in the left striatum and similar to 50% in the right striatum after ischemia. The late depolarizing postsynaptic potential could not be induced after acute thalamic transection. The intrinsic excitability of spiny neurons was suppressed after ischemia evidenced by the significant increase of spike threshold and rheobase as well as the decrease of repetitive firing rate following ischemia. The membrane input resistance andtime constant increased within 6 h following ischemia and the amplitude offast afterhyperpolarization significantly increased after ischemia. These results indicate the depression of excitatory monosynaptic transmission, inhibitory synaptic transmission and excitability of spiny neurons after transient forebrain ischemia whereas the excitatory polysynaptic transmission in neostriatum was potentiated. The facilitation of excitatory polysynaptic transmission is stronger in the right neostriatum than in the left neostriatum after ischemia. The suppression of inhibitory component and the facilitation of excitatory polysynaptic transmission may contribute to the pathogenesis of neuronal injury in neostriatum after transient cerebral ischemia. (C) 2001 IBRO. Published by Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/02/20 alle ore 07:55:56