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The contribution of diffusion to the termination of penicillin-induced convulsive activity in the awake rat.

E. Horn, K. Esseling, G. Brunner, H. H. Kornhuber


1. Experiments were performed to investigate the contribution of diffusion to the termination of PCN induced convulsive (epileptiform) activity in the awake rat. The basic question was whether convulsive activity terminates at the same critical concentration Ct of PCN independently of the concentration Co of PCN injected into the superficial layer of the foreleg field of the right motor cortex. Different concentrations Co were used, the lowest being 16 IU PCN/0.5 microliters saline, the largest 1000 IU PCN/0.5 microliters saline. The convulsive activity was recorded by means of the electroencephalogram (EEG). 2. Mathematical calculations concerning the diffusion of the substances were performed by using the diffusion equation with a PCN diffusion coefficient D = 3.52 x 10(-4) mm2/s and the tortuosity factor lambda = 1.62. 3. The lowest dose of PCN used was considered as a threshold dose for acute induction of convulsive activity because only 4 out of 9 rats treated with 16 IU PCN developed epileptiform activity. For the range of doses between 16 and 32 IU, the median frequency of convulsive potentials was dose-dependent, and increased from 7.9 to 13.8 pot./min, respectively. For higher doses covering the range between 63 and 1000 IU, there was only an insignificant increase from 19.2 to 22.7 pot./min, respectively. 4. The median period of convulsive activity increased significantly (p less than 0.05 or less than 0.01) and monotonically from 19.5 min in rats treated with 16 IU PCN to 267 min after treatment with 1000 IU PCN. 5. At the end of the convulsive activity, the median critical concentration Ct within the artificial focus ranged from 1.75 to 1.31 IU/0.5 microliters saline in rats treated with 16 to 125 IU PCN, while after induction of convulsive activity with doses of 250, 500 or 1000 IU PCN, Ct gradually increased to 2.01, 2.83, and 3.75 IU/0.5 microliters, respectively. This means that the brain became less sensitive for PCN the longer the epileptiform activity lasted. 6. It is concluded that during long-lasting convulsive activity, the brain takes advantage of its plastic properties by eliciting counteracting mechanisms. These self-protective factors may utilize neuronal networks which needs some time to become effective in the control of the cortical activity.

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