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Titolo:
BDNF reduces miniature inhibitory postsynaptic currents by rapid downregulation of GABA(A) receptor surface expression
Autore:
Brunig, I; Penschuck, S; Berninger, B; Benson, J; Fritschy, JM;
Indirizzi:
Univ Zurich, Inst Pharmacol & Toxicol, CH-8057 Zurich, Switzerland Univ Zurich Zurich Switzerland CH-8057 icol, CH-8057 Zurich, Switzerland Max Planck Inst Neurobiol, Dept Neurochem, D-82152 Martinsried, Germany Max Planck Inst Neurobiol Martinsried Germany D-82152 rtinsried, Germany
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 7, volume: 13, anno: 2001,
pagine: 1320 - 1328
SICI:
0953-816X(200104)13:7<1320:BRMIPC>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVITY-DEPENDENT REGULATION; CULTURED HIPPOCAMPAL-NEURONS; NMDA GLUTAMATE RECEPTORS; NEUROTROPHIC FACTOR BDNF; SYNAPTIC TRANSMISSION; SIGNAL-TRANSDUCTION; RAT HIPPOCAMPUS; PROTEIN-KINASE; MESSENGER-RNAS; TRKB RECEPTORS;
Keywords:
hippocampus; inhibitory synapse; neurotrophins; primary cultures; rat;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Fritschy, JM Univ Zurich, Inst Pharmacol & Toxicol, Winterthurerstr 190, CH-8057 Zurich, Switzerland Univ Zurich Winterthurerstr 190 Zurich Switzerland CH-8057 d
Citazione:
I. Brunig et al., "BDNF reduces miniature inhibitory postsynaptic currents by rapid downregulation of GABA(A) receptor surface expression", EUR J NEURO, 13(7), 2001, pp. 1320-1328

Abstract

Changes in neurotransmitter receptor density at the synapse have been proposed as a mechanism underlying synaptic plasticity. Neurotrophic factors are known to influence synaptic strength rapidly. In the present study, we found that brain-derived neurotrophic factor (BDNF) acts pastsynaptically to reduce gamma -aminobutyric acid (GABA)-ergic function. Using primary cultures of rat hippocampal neurons, we investigated the effects of BDNF on GABAergic miniature inhibitory postsynaptic currents (mIPSCs) and on the localization of GABAA receptors. Application of BDNF (100 ng/ml) led within minutes to a marked reduction (33.5%) of mIPSC amplitudes in 50% of neurons, recorded in the whole-cell patch-clamp mode, leaving frequency and decay kinetics unaffected. This effect was blocked by the protein kinase inhibitor K252a, which binds with high affinity to trkB receptors. Immunofluorescence staining with an antibody against trkB revealed that about 70% of cultured hippocampal pyramidal cells express trkB. In dual labelling experiments, use of neurobiotin injections to label the recorded cells revealed that all cells responsive to BDNF were immunopositive for trkB. Treatment of cultures with BDNF reduced the immunoreactivity for the GABAA receptor subunits-alpha2, -beta2,3 and gamma2 in the majority of neurons. This effect was detectable after 15 min and lasted at least 12 h. Neurotrophin-4 (NT-4), but not neurotrophin-3 (NT-3), also reduced GABA(A) receptor immunoreactivity, supporting the proposal that this effect is mediated by trkB. Altogether the results suggest that exposure to BDNF induces a rapid reduction in postsynaptic GABA(A) receptor number that is responsible for the decline in GABAergic mIPSC amplitudes.

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Documento generato il 22/01/20 alle ore 09:58:56