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Titolo:
The role of brain-derived neurotrophic factor receptors in the mature hippocampus: Modulation of long-term potentiation through a presynaptic mechanism involving TrkB
Autore:
Xu, BJ; Gottschalk, W; Chow, A; Wilson, RI; Schnell, E; Zang, KL; Wang, DA; Nicoll, RA; Lu, B; Reichardt, LF;
Indirizzi:
Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Calif San Francisco, Howard Hughes Med Inst, Program Neurosci, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Calif San Francisco, Dept Mol & Cellular Pharmacol, San Francisco, CA94143 USA Univ Calif San Francisco San Francisco CA USA 94143 rancisco, CA94143 USA NICHHD, Unit Synapse Dev & Plast, NIH, Bethesda, MD 20892 USA NICHHD Bethesda MD USA 20892 pse Dev & Plast, NIH, Bethesda, MD 20892 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 18, volume: 20, anno: 2000,
pagine: 6888 - 6897
SICI:
0270-6474(20000915)20:18<6888:TROBNF>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL-NERVOUS-SYSTEM; BDNF KNOCKOUT MICE; SYNAPTIC TRANSMISSION; PROTEIN-KINASE; CA1 REGION; ADULT-RAT; NEURONS; SYNAPSES; PLASTICITY; NT-3;
Keywords:
TrkB; conditional mutant; CA1; long-term potentiation; presynaptic; neuronal survival;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Reichardt, LF Univ Calif San Francisco, Dept Physiol, 533 Parnassu Ave, San Francisco, CA 94143 USA Univ Calif San Francisco 533 Parnassu Ave San Francisco CA USA 94143
Citazione:
B.J. Xu et al., "The role of brain-derived neurotrophic factor receptors in the mature hippocampus: Modulation of long-term potentiation through a presynaptic mechanism involving TrkB", J NEUROSC, 20(18), 2000, pp. 6888-6897

Abstract

The neurotrophin BDNF has been shown to modulate long-term potentiation (LTP) at Schaffer collateral-CA1 hippocampal synapses. Mutants in the BDNF receptor gene trkB and antibodies to its second receptor p75NTR have been used to determine the receptors and cells involved in this response. Inhibition of p75NTR does not detectably reduce LTP or affect presynaptic function, but analyses of newly generated trkB mutants implicate TrkB. One mutant hasreduced expression in a normal pattern of TrkB throughout the brain. The second mutant was created by cre-loxP-mediated removal of TrkB in CA1 pyramidal neurons of this mouse. Neither mutant detectably impacts survival or morphology of hippocampal neurons. TrkB reduction, however, affects presynaptic function and reduces the ability of tetanic stimulation to induce LTP. Postsynaptic glutamate receptors are not affected by TrkB reduction, indicating that BDNF does not modulate plasticity through postsynaptic TrkB. Consistent with this, elimination of TrkB in postsynaptic neurons does not affect LTP. Moreover, normal LTP is generated in the mutant with reduced TrkB bya depolarization-low-frequency stimulation pairing protocol that puts minimal demands on presynaptic terminal function. Thus, BDNF appears to act through TrkB presynaptically, but not postsynaptically, to modulate LTP.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 08:19:22