Results 231 to 240 of about 72,066 (264)
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Estradiol Modulates Long-Term Synaptic Depression in Female Rat Hippocampus
Journal of Neurophysiology, 2000Fluctuating estradiol levels in the adult, female rat modify the anatomical and functional organization of the hippocampal CA1 region. When systemic levels of estradiol are low, e.g., on estrus or in ovariectomized (OVX) rats, long-term synaptic potentiation is difficult to induce in vivo.
M R, Zamani, N L, Desmond, W B, Levy
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Long‐term synaptic depression in the adult entorhinal cortex in vivo
Hippocampus, 2003AbstractThe piriform cortex provides a major input to the entorhinal cortex. Mechanisms of long‐term depression (LTD) of synaptic transmission in this pathway may affect olfactory and mnemonic processing. We have investigated stimulation parameters for the induction of homosynaptic LTD and depotentiation in this pathway using evoked synaptic field ...
Raby, Bouras, C Andrew, Chapman
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Transmitter Release Associated with Long‐term Synaptic Depression in Rat Corticostriatal Slices
European Journal of Neuroscience, 1995AbstractUsing a corticostriatal slice preparation, we have recently shown that tetanic stimulation of the corticostriatal pathway produces long‐term depression (LTD) of striatal excitatory synaptic transmission. In the present study we have analysed the relationship between LTD and the striatal release of different endogenous transmitters.
CALABRESI, PAOLO +6 more
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Long-Term Depression Mimicked in an IGZO-Based Synaptic Transistor
IEEE Electron Device Letters, 2017Amorphous indium-gallium-zinc oxide-based synaptic transistors with hafnium oxide (HfOx) insulating layer were fabricated to mimic synaptic long-term depression (LTD) characteristics. The fabrication temperature was less than 120°. Interval time of presynaptic spikes-dependent synaptic depression was first demonstrated in these IGZO-based synaptic ...
Jiabin Wang +4 more
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Priming of homosynaptic long-term depression in hippocampus by previous synaptic activity
NeuroReport, 1993Mechanisms regulating long-lasting, activity-dependent decreases in synaptic strength are poorly understood. Theoretical studies have suggested that the critical level (threshold) of synaptic activity needed to induce long-term depression (LTD) versus potentiation (LTP) of synaptic transmission should vary as a function of previous synaptic activity ...
E M, Wexler, P K, Stanton
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Flip side of synaptic plasticity: Long‐term depression mechanisms in the hippocampus
Hippocampus, 1994AbstractThere is growing interest in the phenomenon of long‐term depression (LTD) of synaptic efficacy that, together with long‐term potentiation (LTP), is a putative information storage mechanism in mammalian brain. In neural network models, multiple learning rules have been used for LTD induction.
B R, Christie, D S, Kerr, W C, Abraham
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Phospholipase A2 activation is not required for long-term synaptic depression
European Journal of Pharmacology, 1995Low-frequency synaptic stimulation evokes long-term depression of synaptic strength. One hypothesis is that modification of AMPA receptors by phospholipase A2 causes long-term depression. A previous study reported bromophenacylbromide, a completely nonselective phospholipase A2 inhibitor, blocked long-term depression at Schaffer collateral-CA1 synapses
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Modulation of gene expression following long-term synaptic depression in the striatum
Molecular Brain Research, 1999A number of behavioural and cellular studies have suggested that activity-dependent synaptic plasticity associated with learning and memory may lead to the expression of various genes whose protein products can play a critical role in memory acquisition and consolidation.
NAPOLITANO, Maddalena +9 more
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[Mechanisms of long-term synaptic depression in the hippocampus].
Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova, 2001Long-term depression (LTD) was studied in hippocampal slices obtained from neonatal rats at the synapses between CA3 and CA1 pyramidal neurons. The induction of the LTD required pairing of Ca2+ influx into the postsynaptic CA1 neuron through voltage-gated Ca2+ channels with activation of metabotropic glutamate receptors.
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