Help


from Wikipedia
« »  
Alcohol is implicated as a therapeutic agent for GABA < sub > A </ sub > receptor α1 -/- mice because of its interaction with Purkinje cells which mediate their actions via GABA transmission.
GABA < sub > A </ sub > receptor α1 -/- mice respond positively to ethanol treatment.
Ethanol reduces tremor activity in GABA < sub > A </ sub > receptor α1 -/- mice in a dose dependent manner.
An optimum dose of 2. 5 g / kg of ethanol completely suppresses tremors in GABA < sub > A </ sub > receptor α1 -/- mice.
Purkinje cells in these knockout mice also exhibit a lack of GABAergic inhibitory postsynaptic potentials in response to both exogenous and endogenous GABA.
The loss of GABAergic inhibition in purkinje cells likely underlies the pathological tremors observed.
These ameliorative effects are thought to involve inhibition of glutamatergic transmission, though the numerous targets of ethanol make it difficult to determine the exact underlying mechanism.

2.384 seconds.