Changes in intracellular calcium transients and LTP in the surround of visual cortex lesions in rats

Abstract

Injury and loss of neurons are observed in the center of a cerebral cortical lesion. Mechanisms of early functional reorganization post-lesion involve changes in the strength of synaptic coupling as measured in long-term potentiation (LTP). Since these changes in LTP may depend on the intraneuronal calcium concentration ([Ca 2+] I), the present study analyzed the strength of synaptic LTP combined with measurements of the stimulus-induced peak calcium influx in slices from rat visual cortex in vitro. Slices were analyzed 1–7 days post-lesion by use of electrophysiological and calcium fluorescence imaging techniques. A theta-burst stimulus (TBS) was electrically applied to cortical layer IV, while changes in extracellular field potentials (FPs) and in the corresponding peak calcium influx were recorded in layers II/III. Both the strength of LTP and of the FP mediated peak calcium influx were significantly enhanced 1–6 days post-lesion at a distance of 4 mm from the lesion border. Pharmacological experiments revealed that the expression of LTP was dependent on the activation of NMDA receptors. The area of increased stimulus-evoked peak calcium influx correlated with the enhanced LTP, suggesting that changes in [Ca 2+] I mediate the strength of long-term synaptic plasticity following a cortical lesion. This mechanism may support synaptic reorganization in the surround of the deafferented region in rat visual cortex.