In intracellular recordings from three neocortical pyramidal cells in vitro, intracellular dye injection identified the impalement site as the primary trunk of the apical dendrite. Dendritic recordings displayed two types of regenerative events: relatively fast, low-threshold spikes with amplitudes of 12-69 mV, and slower, higher-threshold spikes up to 80 mV in amplitude. This distinctive dendritic firing pattern was also encountered in six recordings without dye-filled electrodes. Fast spike frequency was extremely sensitive to small changes in membrane potential at the recording site. In one recording, the fast spikes were blocked by 1 microM TTX, while slow events were spared. A computational model of a pyramidal cell was constructed to assist in interpreting the recordings. Simulations suggested that the fast spikes were generated primarily by active Na+ conductance concentrated at a distance from the impalement site, probably in the region of the soma. The low threshold of the fast spikes suggested that Na+ channels also exist in the apical dendrites, where they have a relatively low density. The data strongly imply that there are Ca2+ channels in the apical dendrites.

Action Potentials↗

PubMedDate not supplied

Hyperexcitability in a model of cortical maldevelopment.

The presence of developmental cortical malformations has been associated with the occurrence of epilepsy, and correlative anatomic-clinical electrophysiological studies suggest that microdysgenic lesions may actually initiate epileptiform activity. We have investigated the electrophysiological properties of an animal model of polymicrogyria created by making cortical freeze lesions in rat pups at P0 or P1. Such lesions create microgyri with histological features similar to those of human polymicrogyria. We have determined that there is a focal region of hyperexcitability around the lesion in this rat microgyrus. Field potentials evoked by stimulation within a few millimeters of the microgyrus have characteristics typical of epileptiform activity. This aberrant activity is seen as early as 12 d after the lesion, as well as in animals as old as 118 d. Immunochemical staining for the calcium binding protein, parvalbumin, shows a decrease in neuronal and neuropil staining within the microgyrus. These findings suggest that inhibition might be decreased within the lesion, which may contribute to generation of the adjacent hyperexcitable region. These results demonstrate that this animal model is appropriate for examining the mechanisms contributing to epileptogenesis associated with a cortical malformation.

Animals↗

PubMedDate not supplied

Local anesthetic drug-induced seizures in rhesus monkeys.

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Acid-Base Equilibrium↗