CTMB is an allosteric agonist of GABAA receptors, positively modulates GABAA receptors and inhibits voltage-regulated sodium channels (NaVs) to suppress neuronal membrane depolarization.
CTMB inhibits the firing activity of interneurons via GABAA receptors and NaVs.
CTMB increases the cell viability and reduces the apoptosis of mechanically scratched HT22 cells through modulation of GABAA receptors.
CTMB (30mg/kg) reduces the area of brain damage and attenuates neurobehavioral deficits at 7 days after traumatic brain injury (TBI).
CTMB (30mg/kg) improves the rats' sensory and motor functions of limbs and attenuates neuronal damage in the subacute phase of traumatic brain injury (TBI).
CTMB mitigates mitochondrial-involved neuronal apoptosis by attenuating the cascading neuro-excitotoxicity of GABAA receptors during the subacute phase of traumatic brain injury (TBI).
CTMB prolonged survival, reduced epilepsy and improved long-term motor ability during the recovery phase of traumatic brain injury (TBI) rats.