1. Neurologische Klinik, Heinrich Heine Universität, Düsseldorf, Germany
2. ^*Institut für Hirnforschung, Heinrich Heine Universität, Düsseldorf, Germany

Correspondence: Otto W Witte, Neurologische Klinik, Heinrich Heine Universität, Moorenstr. 5, D-40225 Düsseldorf, Germany.

Received 31 July 1995; Revised 22 September 1995; Accepted 29 September 1995.

Abstract

Changes of neuronal excitability and -aminobutyric acid (GABA_A)-receptor expression were studied in the surround of photothrombotic infarcts, which were produced in the sensorimotor cortex of the rat by using the rose bengal technique. In a first series of experiments, multiunit recordings were performed on anesthetized animals 2–3 mm lateral from the lesion. Mean discharge frequency was considerably higher in recordings from lesioned animals (>100 Hz in the first postlesional week) compared with control animals (mean, 15 Hz). These alterations were already present after 1 day but were most pronounced 3 to 7 days after lesion induction. Thereafter the hyperexcitability declined again, although it remained visible up to 4 months. In a second series of experiments, the GABA_A-receptor expression was studied autoradiographically. This revealed a reduction of GABA_A receptors in widespread brain areas ipsilateral to the lesion. The reduction was most pronounced in the first days after lesion induction and declined with longer intervals. It is concluded that cortical infarction due to photothrombosis leads to a long-lasting and widespread reduction of GABA_A-receptor expression in the surround of the lesion, which is associated with an increased neuronal excitability. Such alterations may be responsible for epileptic seizures that can be observed in some patients after stroke and may contribute to neurologic deficits after stroke.