Stimulus-evoked and seizure-related responses of extracellular calcium activity in spinal cord compared to those in cerebral cortex

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Abstract
The extracellular activity of Ca ([Ca2+]o) was measured with ion-selective microelectrodes in the spinal cord and cerebral cortex of cats, together with the focal electric potential. Neurons in the tissue were activated by repetitive electrical stimulation of an afferent pathway or of its surface. Seizures were induced by the i.v. administration of a convulsant dose of penicillin. In the dorsal horn of the spinal cord resting [Ca2+]o was .apprx. 1.2 (SD .+-. 0.2) mM. Trains of stimuli applied to a peripheral nerve usually evoked a transient decrease of [Ca2+]o in the dorsal horn. With maximal stimulus trains of 2-4 s duration, this decrease amounted to .apprx. 2-12% of the resting level of [Ca2+]o. In a minority of cases, during very prolonged stimulation, [Ca2+]o rose after its transient decrease or instead of it; such increases had a very slow onset and decline. In the ventral gray matter [Ca2+]o was very stable and changed only slightly or not all during afferent stimulation. The i.v. administration of a convulsant dose of penicillin was usually but not invariably followed by a decline of unstimulated base line [Ca2+]o in the ventral horn. Responses to afferent stimulation then grew strikingly. Paroxysmal activity in the ventral horn was invariably accompanied by transient decreases of [Ca2+]o, of amplitude significantly greater than those associated with sustained potential shifts of the nonconvulsing cord. In the dorsal horn the behavior of [Ca2+]o was not altered by penicillin and seizure-related [Ca2+]o transients were not seen. In the cerebral cortex, responses were somewhat larger but otherwise similar to those in spinal cord. Stimulation of the ventral posterior lateral nucleus usually evoked a transient decrease of [Ca2+]o in the somatic receiving area. Direct stimulation of the cortical surface evoked a decrease or, less commonly, a slow increase of [Ca2+]o. Electrically evoked paroxysmal afterdischarges and seizures induced by penicillin were accompanied by a decrease, or an increase, or by a biphasic response, depending on the pattern of responses prevailing in a particular cortex and in a particular cytoarchitectonic locus. The possible mechanisms of Ca2+ transport resulting in the observed responses are discussed. When [Ca2+]o decreases, ions probably enter the intracellular fluid of neurons. The source supplying the excess Ca2+ for its activity to rise is not known; 3 possible sources are sequestered intracellular stores, blood plasma and a deflation of the extracellular space. A transmembrane flux of Ca2+ may have a significant role in the generation of penicillin-induced seizures.

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