Offsetting of aberrations associated with seizure proneness in rat hippocampus area CA1 by theta pulse stimulation-induced activity pattern.

Epileptiform activity induces long term aberrations in hippocampal network functions. This study was conducted in pentylenetetrazol (PTZ) -kindled rats to examine offsetting of aberrations associated with seizure proneness in hippocampus area CA1 by theta pulse stimulation (TPS: 5 Hz trains for 3 min) -induced activity pattern. In hippocampal slices from both control and kindled rats, the field excitatory postsynaptic potentials (fEPSP) and population spikes (PS) were simultaneously recorded through electrodes in the apical dendrites and stratum pyramidale, respectively. The following changes in kindled vs. control slices were observed. The fEPSP needed to be greater to produce the PS recorded in the cell body layer. The fEPSP was reduced by paired stimuli whereas the PS amplitude was increased. TPS selectively depressed the PS in a lasting fashion, and shifted the fEPSP slope and the PS amplitude relation toward what was observed in controls. Both the fEPSP and PS were increased by paired stimuli at 60 min after TPS application. The lasting depressive effect of TPS on the PS amplitude was converted into facilitation by adenosine A1 receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (CPX). Potentiation of the PS amplitude by TPS in the presence of CPX was blocked by an N-methyl-d-aspartate receptor antagonist AP5. We hypothesize that the extracellular adenosine spillover, acting through adenosine A1 receptors, during TPS-induced activity pattern could trigger a homeostatic process for correcting network imbalances caused by epileptiform activity.

The ability of hippocampal CA1 area for induction of long-term potentiation is persistently reduced by prior treatment with cysteamine: an in vitro study.

Using field potential recording in the CA1 region of hippocampal slices from rats injected with cysteamine (200 mg/kg, s.c.), changes in activity and plasticity of Schaffer collateral-CA1 pyramidal cell synapses were examined. Extracellular field potential recording prior to and following either theta-pattern primed bursts (PBs), perfusion with low Mg(2+) or with high Ca(2+), indicated long-term potentiation (LTP) of population spikes amplitude (PSA). The extent of LTP of PSA was significantly lower in cysteamine-treated rats. It is concluded that cysteamine can entail lasting modifications in susceptibility of hippocampal CA1 for synaptic plasticity induced by tetanus. Similarly, disability in function of CA1 synapses can be traced by other protocols of LTP induction. The relevancy of the results to the facilitatory role of endogenous somatostatin in the function of Schaffer collateral-CA1 pyramidal cell synapses is also discussed.