Synaptic plasticity in the hippocampal slice: functional consequences.
Animals; Calcium Channels/physiology; Hippocampus/*physiology; Long-Term Potentiation/physiology; Models; N-Methyl-D-Aspartate/physiology; Neurological; Neuronal Plasticity/*physiology; Receptors; Synapses/*physiology
There are 3 known forms of synaptic plasticity at CNS synapses: long-term potentiation (LTP) mediated by NMDA receptor activation, LTP mediated by voltage-dependent calcium channel (VDCC) activation, and long-term depression (LTD) mediated by the NMDA receptor. All 3 forms of synaptic plasticity can be observed in hippocampal CAl cells, all are induced by afferent activation, all involve Ca2+ influx, and all activate Ca(2+)-dependent mechanisms. We consider the functional consequences of the presence of 3, sometime opposing, forms of synaptic plasticity at the same synapse. We suggest that the 2 forms of LTP have different consequences for the synapse. We postulate that the co-existence of potentiating and depressing capabilities influences the network processing capabilities of neural networks.
Teyler T J; Cavus I; Coussens C
Journal of neuroscience methods
1995
1995-06
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/0165-0270(94)00188-m" target="_blank" rel="noreferrer noopener">10.1016/0165-0270(94)00188-m</a>
Multideterminant role of calcium in hippocampal synaptic plasticity.
Animals; Calcium/*physiology; Hippocampus/drug effects/*physiology; Humans; Neuronal Plasticity/drug effects/*physiology; Synapses/drug effects/*physiology
Hippocampal CA1 cells possess several varieties of long-lasting synaptic plasticity: two different forms of long-term potentiation (LTP) and at least one form of long-term depression (LTD). All forms of synaptic plasticity are induced by afferent activation, all involve Ca2+ influx, all can be blocked by Ca2+ chelators, and all activate Ca(2+)-dependent mechanisms. The question arises as how different physiological responses can be initiated by activation of the same second messenger. We consider two hypotheses which could account for these phenomena: voltage-dependent differences in cytosolic Ca2+ concentration acting upon Ca2+ substrates of differing Ca2+ affinities and compartmentalization of the Ca2+ and its substrates.
Teyler T J; Cavus I; Coussens C; DiScenna P; Grover L; Lee Y P; Little Z
Hippocampus
1994
1994-12
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1002/hipo.450040602" target="_blank" rel="noreferrer noopener">10.1002/hipo.450040602</a>