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J J Hablitz

Publications and source records attributed to J J Hablitz.

97 records · Page 6Linked to original sources
PubMedDate not supplied

Cerebellar nuclear stimulation in generalized penicillin epilepsy.

Comparison was made of the effectiveness of cerebellar cortical and nuclear stimulation in reducing paroxysmal activity induced in cats by parenteral penicillin administration. Vermal cortical and fastigial nuclear stimulation at high frequencies (100 Hz) were both effective in reducing the number and duration of paroxysmal events while the effects of dentate nucleus stimulation were found to be more variable. It was suggested that effective seizure inhibition appeared to be associated with increased fastigial output and resultant reticular excitation.

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PubMedDate not supplied

Neuronal firing patterns during generalized penicillin epilepsy in the awake cat.

Single unit activity was recorded in the neocortex of awake cats during spontaneous spike wave discharges. Ongoing activity was interrupted during paroxysmal events and was replaced by (1) bursts of action potentials coincident with the EEG spike and cessation of firing during the wave, or (2) cessation of firing for the duration of the paroxysm. Other units which displayed little or no background activity were recruited to fire during the EEG spike. Surface cerebellar stimulation at high frequencies led to decreased neuronal activity while single pulse shocks resulted in short latency activation. These results were compared to studies of spike wave activity elicited by electrical stimulation.

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PubMedDate not supplied

Zinc and glycine do not modify low-magnesium-induced epileptiform activity in the immature neocortex in vitro.

Exposure of neocortical slices from immature rats to saline containing no added magnesium induced spontaneous epileptiform activity that consisted of bursts of low-amplitude isolated discharges lasting 50-90 sec, recurring every 90-300 sec. Bath application of the N-methyl-D-aspartate (NMDA) receptor antagonist DL-2-amino-7-phosphonoheptanoic acid led to a rapid, reversible suppression of epileptiform activity, indicating involvement of NMDA receptors. Perfusion with zinc or glycine, putative modulators of the NMDA receptor, with suppressive and enhancing properties, respectively, had no effect on the frequency or duration of the epileptiform discharges. These results indicate that in the immature neocortex in vitro, application of zinc or glycine does not modulate NMDA receptor-mediated, low-magnesium-induced epileptiform discharges.

2-Amino-5-phosphonovalerate↗
PubMedDate not supplied

Tetraethylammonium-induced synaptic plasticity in rat neocortex.

Recordings were obtained from neurons in layer II/III of slices of rat frontal cortex maintained in vitro. We investigated whether brief application of the potassium channel blocker tetraethylammonium (TEA), which induces a novel form of synaptic plasticity in the CA1 region of the hippocampus referred to as LTPK, evokes similar responses in neocortex. Consistent with previous findings, TEA produced a persistent enhancement of excitatory transmission, which was independent of NMDA receptor activation but required the activation of nifedipine-sensitive voltage-dependent Ca2+ channels (VDCC), presumably the L-type. We also observed a persistent enhancement of presumptive CI(-)-dependent GABAA receptor-mediated transmission. Enhancement of excitatory and inhibitory synaptic transmission did not require activation of synapses with electrical stimulation during TEA application. The enhancement of excitatory, but not inhibitory synaptic transmission, was blocked when the Ca2+ chelator 1,2-bis(2-aminophenoxy)-ethane N,N,N',N'-tetraacetic acid (BAPTA) was included in the recording electrode. Under voltage clamp conditions that minimized the activation of L-type channels robust enhancement of both excitatory and inhibitory transmission was still observed. No enhancement of excitatory synaptic transmission was observed in the presence of NiCl2, a putative T-type channel blocker. The possible involvement of kinase activation was studied by including the non-specific and competitive kinase inhibitor (+/-)-1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7) in the patch pipette. H-7 retarded the time course and reduced the magnitude of the enhancement of excitatory transmission. These results suggest that TEA-induced enhancement of excitatory transmission in the neocortex requires entry of Ca2+ into the postsynaptic neuron via VDCCs and possibly the activation of a kinase.

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