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even after a single dose in animal models.

Mechanism and pathophysiology
Gamma-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter of the central nervous system; roughly one-quarter to one-third of synapses use GABA. GABA mediates the influx of chloride ions through ligand-gated ion channels called GABAA receptors. These receptors are bound to the post-synaptic nerve cells. When chloride enters the nerve cell, the cell membrane potential hyperpolarizes thereby inhibiting depolarization, or firing of the nerve cell. Benzodiazepine potentiates the action of GABA. When this potentiation is sustained by long-term use, neuroadaptations occur which result in decreased GABA activity and increased excitability of the glutamate system. When benzodiazepines are stopped, these neuroadaptations are "unmasked", leading to unopposed excitability of the nervous system and the appearance of withdrawal symptoms. Increased glutamate excitatory activity during withdrawal is believed to result in kindling phenomena. Those who have a prior history of withdrawing from benzodiazepines are found to be less likely to succeed the next time around. Repeated benzodiazepines withdrawals, like with alcohol withdrawal, may lead to sensitization or kindling of the CNS, possibly leading to worsening cognition and symptomatology and making each subsequent withdrawal period worse.