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Titolo:
GABA mediates presynaptic inhibition at glycinergic synapses in a rat auditory brainstem nucleus
Autore:
Lim, R; Alvarez, FJ; Walmsley, B;
Indirizzi:
Australian Natl Univ, John Curtin Sch Med Res, Div Neurosci, Synapt Struct& Funct Grp, Canberra, ACT 0200, Australia Australian Natl Univ Canberra ACT Australia 0200 rra, ACT 0200, Australia Wright State Univ, Dept Anat, Dayton, OH 45435 USA Wright State Univ Dayton OH USA 45435 iv, Dept Anat, Dayton, OH 45435 USA
Titolo Testata:
JOURNAL OF PHYSIOLOGY-LONDON
fascicolo: 2, volume: 525, anno: 2000,
pagine: 447 - 459
SICI:
0022-3751(20000601)525:2<447:GMPIAG>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANTEROVENTRAL COCHLEAR NUCLEUS; SUPERIOR OLIVARY COMPLEX; MAMMALIAN SPINAL-CORD; GUINEA-PIG; IMMUNOCYTOCHEMICAL LOCALIZATION; BENZODIAZEPINE RECEPTOR; SYNAPTIC TRANSMISSION; TRANSMITTER RELEASE; BUSHY CELLS; NEURONS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Walmsley, B Australian Natl Univ, John Curtin Sch Med Res, Div Neurosci, Synapt Struct& Funct Grp, POB 334, Canberra, ACT 2601, Australia Australian Natl Univ POB 334 Canberra ACT Australia 2601 ralia
Citazione:
R. Lim et al., "GABA mediates presynaptic inhibition at glycinergic synapses in a rat auditory brainstem nucleus", J PHYSL LON, 525(2), 2000, pp. 447-459

Abstract

1. Many inhibitory nerve terminals in the mammalian anteroventral cochlearnucleus (AVCN) contain both glycine and GABA, but the reason for the co-localization of these two inhibitory neurotransmitters in the AVCN is unknown. We have investigated the roles of glycine and GABA at synapses on bushy cells in the rat AVCN, using receptor immunohistochemistry and electrophysiology.2. Our immunohistochemical results show prominent punctate labelling of postsynaptic clusters of glycine receptors and of the receptor clustering protein gephyrin over the surface of bushy cells. In contrast, weak diffuse membrane immunolabelling of GABA(A) receptors was observed.3. Whole-cell recordings from bushy cells in AVCN slices demonstrated thatevoked inhibitory postsynaptic currents (IPSCs) were predominantly (81%) glycinergic, based on the decrease in amplitude of the IPSCs in bicuculline (10 mu M). This observation was supported by the effect of strychnine (1 muM), which Eyas to decrease the evoked IPSC (to 10% of control IPSC amplitude) and to produce a greater than 90% block of spontaneous miniature IPSCs.4. These results suggest a minor role for postsynaptic GABA(A), receptors in bushy cells, despite a high proportion of GABA-containing terminals on these cells. Therefore, a role for metabotropic GABA(B), receptors was investigated. activation of GABA(B) receptors with baclofen revealed a significant attenuation of evoked glycinergic IPSCs. The effect of baclofen was presynaptic, as indicated by a lack of change in the mean amplitude of spontaneous IPSCs.5. Significantly, the decrease in the amplitude of evoked glycinergic IPSCs observed following repetitive nerve stimulation was reduced in the presence of the GABA(B) antagonist, CGP 35348. This indicates that synaptically released GABA can activate presynaptic GABA(B) receptors to reduce transmitter release at glycinergic synapses. Our results suggest specific pre- versus postsynaptic physiological roles for GABA and glycine in the AVCN.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 07:58:21