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Titolo:
GABAERGIC INHIBITION OF GRANULE CELLS AND HILAR NEURONAL SYNCHRONY FOLLOWING ISCHEMIA-INDUCED HILAR NEURONAL LOSS
Autore:
MODY I; OTIS TS; BRAGIN A; HSU M; BUZSAKI G;
Indirizzi:
UNIV TEXAS,SW MED CTR,DEPT ANESTHESIOL & PAIN MANAGEMENT DALLAS TX 75235 UNIV WISCONSIN,DEPT NEUROPHYSIOL MADISON WI 53706 RUTGERS STATE UNIV,CTR MOLEC & BEHAV NEUROSCI NEWARK NJ 07102
Titolo Testata:
Neuroscience
fascicolo: 1, volume: 69, anno: 1995,
pagine: 139 - 150
SICI:
0306-4522(1995)69:1<139:GIOGCA>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSIENT FOREBRAIN ISCHEMIA; PIG HIPPOCAMPAL SLICE; RAT HIPPOCAMPUS; DENTATE GYRUS; MONGOLIAN GERBIL; DARK NEURONS; SOMATOSTATIN; GOLGI; GABA; AREA;
Keywords:
DENTATE GYRUS; EPILEPSY; GABA; HIPPOCAMPUS; PATCH-CLAMP;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
43
Recensione:
Indirizzi per estratti:
Citazione:
I. Mody et al., "GABAERGIC INHIBITION OF GRANULE CELLS AND HILAR NEURONAL SYNCHRONY FOLLOWING ISCHEMIA-INDUCED HILAR NEURONAL LOSS", Neuroscience, 69(1), 1995, pp. 139-150

Abstract

In the dentate gyrus, granule cells are ischemia-resistant, but at least five types of predominantly spiny hilar neurons are extremely vulnerable to ischemia. Many of the ischemia-sensitive subtypes of hilar neurons appear to be involved in: (i) the regulation of GABAergic inhibition in the dentate gyrus, and (ii) the generation of hilar neuronal synchrony. The present study examined functional consequences of ischemia-induced hilar neuronal loss on GABAergic inhibition of granule cells and hilar neuronal synchrony. Transient (15 min) forebrain ischemiawas induced by a modification of the four-vessel-occlusion method producing a substantial hilar neuronal loss as demonstrated by the Gallyas silver stain method. Three months later, we have examined spontaneous and stimulus-evoked inhibitory postsynaptic currents mediated by both GABA(A) and GABA(B) receptors, and inhibitory bursts induced by 4-aminopyridine (50 mu M) using whole-cell recordings in coronal brain slices maintained at 34-36 degrees C in the presence of excitatory amino acid receptor blockers. Spontaneous dentate spikes reflecting hilar neuronal synchrony and synaptic responses evoked by perforant path stimulation were also recorded in vivo to assess synchrony and inhibition in the dentate gyrus. In spite of significant damage to several types of hilar neurons, there were no marked differences in the conductance, kinetics, and 4-aminopyridine-induced burst frequencies of synaptic GABA(A) and GABA(B) responses in granule cells. Furthermore, both paired-pulse inhibition and dentate spikes appeared to be normal in vivo. Weconclude that there appears to be little impairment of GABAergic inhibition of granule cells or of hilar neuronal synchrony three months following a massive ischemic damage to spiny hilar neurons.

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Documento generato il 22/09/20 alle ore 10:28:25