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In pyramidal cells, somatic action potentials can propagate actively back into the apical dendrites and potentiate calcium influx at simultaneously activated glutamatergic synapses, presumably by relieving the voltage-dependent block of NMDA channels. We have used computer simulations to investigate the conditions under which this potentiation will be optimal. We find that a spike with a long duration and limited amplitude (peak of ∼−10 mV) will be most effective. A back-propagating action potential will achieve this form if the dendritic membrane has a low Kchannel density and a modest Nachannel density (30–70 pS/μm2, similar to experimentally observed densities). The relative increase in calcium due to the backpropagating spike will be small, however, unless the accumulated calcium is rapidly removed.

AN essential feature of episodic memory, the type of memory dependent on hippocampus, is that individual memories belong to particular moments in time. Recent PET studies suggest that memory encoding and recall occur at different locations in human hippocampus. Coupled with other attributes of hippocampus, this suggested to us that the septo-temporal hippocampal axis may play an important role in time perception. We propose a temporo-septal engram shift model of hippocampal memory. The model posits that memories gradually move along the hippocampus from a temporal encoding site to ever more septal sites from which they are recalled. We propose that the sense of time is encoded by the location of the engram along the temporo-septal axis.

RESULTS from a computer model of a thalamic network predict that agents augmenting GABAA-mediated inhibition in the reticular thalamic (RE) nucleus will be antiepileptic or desynchronizing. This provides support for the hypothesis that antiepileptics like benzodiazepines may exert their effects through an isolated increase of inhibition in the RE nucleus. When desynchronized, the model thalamocortical neurons showed a decreased probability of firing a low threshold spike, a decreased secondary inhibitory postsynaptic potential and a higher frequency of oscillations. The transition to desynchrony was also accompanied by an increased frequency in the firing of the model RE neurons.