A transient increase in the activity of CA3 neurons induces a long-lasting reduction in the excitability of Schaffer collateral terminals in rat hippocampus.
Following high frequency discharges of CA3 neurons, a long-lasting potentiation (LLP) of the CA1 neuronal population spike results. Subsequent to a transient increase in the firing rate of CA3 neurons produced by the application of DL-homocysteate on the soma in the presence of normal medium but not in the presence of Ca2+ -free (Mn2+ -containing) medium, the threshold for antidromic activation in the CA1 area of the neuron was increased for a prolonged period of time. Since the induction of the presynaptic terminal excitability reduction as well as LLP of the CA1 population spike are Ca2+ -dependent, a cause-and-effect relationship may exist between these two processes.
Sastry
B R
BR
Murali Mohan
P
P
Goh
J W
JW
D000818:Animals; D002118:Calcium / Q000502:physiology; D005071:Evoked Potentials; D006624:Hippocampus / Q000187:drug effects / Q000502:physiology*; D006710:Homocysteine / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D008345:Manganese / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D009435:Synaptic Transmission / Q000187:drug effects
D006710:Homocysteine; D008345:Manganese; D002118:Calcium