Changes in [Ca2+]o and [K+]o during repetitive electrical stimulation and during pentetrazol induced seizure activity in the sensorimotor cortex of cats.

Changes in [Ca2+]o and [K+]o were measured in the sensorimotor cortex of cats during repetitive electrical stimulation and during pentetrazol induced epileptiform activity. Repetitive stimulation of the thalamic ventrobasal complex (VB) or of the cortical surface (CS) caused decreases in [Ca2+]o by up to 0.45 mM and increases in [K+]o by up to 7 mM. Maximum reductions of [Ca2+]o delta [Ca2+]o were found in depths of 100 to 300 micrometers below cortical surface, while rises in [K+]o were largest in depths of 600 to 1000 micrometers dependent on stimulation site. At depths below 700-900 micrometers increases in [K+]o were often accompanied by rises in [Ca2+]o of about 0.2 mM. Pentetrazol (PTZ) when injected at doses of 25 to 40 mg/kg body weight induced spontaneous seizure activity, which was in about 40% preceded by a slight fall of baseline [Ca2+]o. Repetitive stimulation and spontaneous seizures resulted in delta [Ca2+]o of up to 0.6 mM, whereas rises in [K+]o remained limited to a 'ceiling level' of about 10 mM. After PTZ application, peak delta [Ca2+]o were found at the same recording sites, but, in contrast to normal cortex, decreases in [Ca2+]o were observed in all cortical layers. The enhanced Ca2+-signals after PTZ application and the observed reduction of [Ca2+]o before seizure onset suggest that PTZ utilizes Ca2+-dependent mechanisms to initiate seizure activity.