Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Glutamate decarboxylase(65)-immunoreactive terminals in cingulate and prefrontal cortices of schizophrenic and bipolar brain
Autore:
Benes, FM; Todtenkopf, MS; Logiotatos, P; Williams, M;
Indirizzi:
McLean Hosp, Struct Neurosci Lab, Belmont, MA 02178 USA McLean Hosp Belmont MA USA 02178 ruct Neurosci Lab, Belmont, MA 02178 USA Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 Med, Dept Psychiat, Boston, MA 02115 USA Harvard Univ, Sch Med, Program Neurosci, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 , Program Neurosci, Boston, MA 02115 USA
Titolo Testata:
JOURNAL OF CHEMICAL NEUROANATOMY
fascicolo: 3-4, volume: 20, anno: 2000,
pagine: 259 - 269
SICI:
0891-0618(200012)20:3-4<259:GDTICA>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
LOCAL CIRCUIT NEURONS; GABA(A) RECEPTOR-BINDING; HIPPOCAMPAL-FORMATION; MOOD DISORDERS; AXON TERMINALS; UPTAKE SITES; CORTEX; PARVALBUMIN; ABNORMALITIES; ILLNESS;
Keywords:
anterior cingulate; GABA cells; interneurons; neuroleptics;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Benes, FM McLean Hosp, Struct Neurosci Lab, 115 Mill St, Belmont, MA 02178USA McLean Hosp 115 Mill St Belmont MA USA 02178 lmont, MA 02178 USA
Citazione:
F.M. Benes et al., "Glutamate decarboxylase(65)-immunoreactive terminals in cingulate and prefrontal cortices of schizophrenic and bipolar brain", J CHEM NEUR, 20(3-4), 2000, pp. 259-269

Abstract

Recent postmortem studies have been suggesting that a defect of GABAergic neurotransmission might occur in the corticolimbic system of subjects with schizophrenia and bipolar disorder. To explore this possibility, a method for immunolocalizing the 65 kdalton isoform of glutamate decarboxylase (GAD(65)) has been developed and applied to the anterior cingulate (ACCx) and prefrontal (PFCx) cortices of 12 normal controls (CONs), 12 schizophrenics (SZs) and 5 manic depressive (MDs) subjects. A computer-assisted technique was employed under strictly blind conditions to determine the density of GAD(65)-IR terminals in apposition with pyramidal (PNs) and nonpyramidal (NPs) neurons and in neuropil (NPL) of layers II, III, V and VI of each cortical region. For SZs, no difference in the numerical density of CAD(65)-IR terminals in contact with either PNs or NPs or in NPL of layers II-VI in ACCx orPFCx was detected. There were also no differences in the size of either PNs and NPs that could have influenced the nature of these findings. Using a pixel count analysis, the size of IR terminals was, however, found to be increased in layers II (10.3%) and III (15.8%) of SZs, but only in subjects treated with neuroleptic drugs. For MDs, the density of GAD(65)-IR terminalswas significantly reduced in all four layers of ACCx, but these differences were most significant in layers II (27.8%) and III (37.2%), whether or not the subjected were treated with neuroleptics. Tn PFCx, the MDs showed similar differences in terminal density for PNs and NPs but not neuropil in the four laminae examined. The MD group showed no differences in either the size of cell bodies or IR terminals. Age and PMI did not account for any of the differences between the CONs vs SZs and MDs. Overall, the results of this study, though preliminary, suggest that there may be complex changes in GABAergic terminals in SZ and MD, ones that may vary with respect to primary diagnosis and neuroleptic exposure. (C) 2000 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 12/07/20 alle ore 01:34:27