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Titolo:
Synaptic reliability correlates with reduced susceptibility to synaptic potentiation by brain-derived neurotrophic factor
Autore:
Berninger, B; Schinder, AF; Poo, MM;
Indirizzi:
Univ Calif San Diego, Dept Biol, La Jolla, CA 92093 USA Univ Calif San Diego La Jolla CA USA 92093 t Biol, La Jolla, CA 92093 USA
Titolo Testata:
LEARNING & MEMORY
fascicolo: 3, volume: 6, anno: 1999,
pagine: 232 - 242
SICI:
1072-0502(199905/06)6:3<232:SRCWRS>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
NERVE GROWTH-FACTOR; CULTURED HIPPOCAMPAL-NEURONS; LONG-TERM POTENTIATION; TRUNCATED TRKB RECEPTORS; NT-3 MESSENGER-RNA; FACTOR NGF; RAT HIPPOCAMPUS; MONOCULAR DEPRIVATION; TRANSMITTER RELEASE; FACTOR BDNF;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Poo, MM Univ Calif San Diego, Dept Biol, La Jolla, CA 92093 USA Univ CalifSan Diego La Jolla CA USA 92093 La Jolla, CA 92093 USA
Citazione:
B. Berninger et al., "Synaptic reliability correlates with reduced susceptibility to synaptic potentiation by brain-derived neurotrophic factor", LEARN MEM, 6(3), 1999, pp. 232-242

Abstract

Recent studies have implicated brain-derived neurotrophic factor (BDNF) inuse-dependent modification of hippocampal synapses. BDNF can rapidly potentiate synaptic transmission at glutamatergic synapses by enhancing transmitter release. Using simultaneous perforated patch recording from pairs and triplets of glutamatergic hippocampal neurons, we have examined how the initial state of the glutamatergic synapse determines its susceptibility to synaptic modification by BDNF. We found that the degree of synaptic potentiation by BDNF depends on the initial reliability and strength of the synapse: Relatively weak connections were strongly potentiated, whereas the effect was markedly reduced at stronger synapses. The degree of BDNF-induced potentiation strongly correlated with the initial coefficient of variation (CV) of the amplitude of excitatory postsynaptic currents (EPSCs) and inversely correlated with the initial paired-pulse facilitation, suggesting that synapses with lower release probability (P-r) are more susceptible to the actionof BDNF. To determine whether saturation of P-r could have masked the potentiation effect of BDNF in the stronger synapses, we lowered the initial P-r either by reducing the extracellular Ca2+ concentration ([Ca2+](o)) or bybath application of adenosine. Synapses that were initially strong remained unaffected by BDNF under these conditions of reduced P-r. Thus, the lack of BDNF effect on synaptic efficacy cannot simply be accounted for by saturation of P-r, but rather may be due to intrinsic changes associated with synaptic maturation that might covary with P-r. Finally, the dependence on initial synaptic strength was also found for divergent outputs of the same presynaptic neuron, suggesting that synaptic terminals with different degreesof responsiveness to BDNF can coexist within in the same neuron.

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Documento generato il 03/04/20 alle ore 06:36:49