Gabapentin is neuroprotective through glutamate receptor-independent mechanisms in staurosporine-induced apoptosis of cultured rat cerebellar neurons

摘要: The anticonvulsants that are currently available modulate the activity of neuronal receptors and ion channels, which equally involved in apoptotic pathways. We investigated hypothesis gabapentin (GP), an anticonvulsant without effect on glutamate acting as GABA analog, has neuroprotective properties. For comparison, we chose topiramate (TPM), been reported to be via AMPA blockade. this purpose, used rat cerebellar granule neuron (CGN) cultures triggered apoptosis independent with staurosporine, a broad-spectrum protein kinase inhibitor. GP at therapeutic range concentration significantly increased cell viability CGN maintained physiological KCl reversed induced by staurosporine. Blockade NMDA or MK801 NBQX, respectively, did not alter neuroprotection, was instead GABA. In contrast, protective TPM STS-treated annihilated altered Treatments concentrations modify expression adhesion molecule synaptophysin morphological aspect endings. summary, report is through glutamate-receptor mechanisms alteration plasticity markers, makes it possible candidate for clinical neuroprotection trials.