China
Africa
Explore chapters and articles related to this topic
Overview of Actions of Antiepileptic Drugs on Repetitive Neuronal Firing
Published in Carl L. Faingold, Gerhard H. Fromm, Drugs for Control of Epilepsy:, 2019
Several forms of short-term modulation of excitatory synaptic transmission have been described: paired pulse facilitation, frequency facilitation, and post-tetanic potentiation.45 Short-term facilitation of excitatory synapses may lead to marked enhancement of synaptic potentials, a phenomenon that may be important in seizures. Paired pulse facilitation refers to the increased synaptic response that accompanies the second of two stimuli delivered at short intervals. Frequency facilitation refers to a similar form of increased synaptic response that occurs during a train of stimuli. Post-tetanic potentiation refers to increased synaptic strength immediately following termination of synaptic stimulation. These forms of short-term facilitation are likely to involve multiple biochemical mechanisms, but each depends on accumulation of calcium in presynaptic terminals.
Mechanisms of action
Published in Fazal-I-Akbar Danish, Ahmed Ehsan Rabbani, Pharmacology in 7 Days for Medical Students, 2018
Fazal-I-Akbar Danish, Ahmed Ehsan Rabbani
It is a membrane stabiliser and acts by: Decreasing the resting fluxes of Na+ ions as well as Na+ currents during the action potential.Decreasing the influx of Ca++ ions during depolarisation.Decreasing the efflux of K+ ions during action potential.Decrease in post-tetanic potentiation.Restoration of balance between excitatory glutamate and inhibitory GABA pathways.Decrease in the duration of after-discharge.Increase in the refractory period of the neurons.Causes stimulation of cerebellum, which in turn causes stimulation of inhibitory pathways from cerebellum to cerebral cortex.
Parvalbumin expression affects synaptic development and physiology at the Drosophila larval NMJ
Published in Journal of Neurogenetics, 2018
Tao He, Michael N. Nitabach, Gregory A. Lnenicka
We found that the synaptic enhancement during 10 s of 20 Hz stimulation in PV-expressing terminals was dramatically reduced compared to controls. The synaptic enhancement seen during these brief AP trains likely result from the buildup of facilitation plus the onset of the longer lasting augmentation and post-tetanic potentiation (Zengel et al., 1980; Zengel & Magleby, 1980). During the 20 Hz train, the PV terminals showed a slower buildup of synaptic enhancement and [Ca2+]i compared to the controls. This is consistent with studies in the crayfish where the synaptic enhancement during the beginning of a train correlated with the buildup of [Ca2+]i (Delaney & Tank, 1994). We also found that the PV terminals showed much less synaptic enhancement than the controls once the EPSP amplitude had plateaued. This was apparently due to less buildup of synaptic facilitation since the synaptic enhancement measured 1–40 s after the train, when only augmentation and post-tetanic potentiation should be present, was not affected by PV expression. Studies of guinea pig hippocampal synapses found a correlation between the plateau [Ca2+]i change and synaptic enhancement for a range of stimulation frequencies (Regehr, Delaney, & Tank, 1994). Our reduction in synaptic facilitation during the plateau phase was surprising since the [Ca2+]i plateau was similar in PV and control terminals, presumably because PV was saturated and not an effective Ca2+ buffer.