Copiracetam can be used as a nootropic drug to treat memory and intellectual impairments caused by senile dementia, mild to moderate vascular dementia, trauma and other diseases, and to promote children's intellectual development; it also has antidepressant effects.
Copiracetam has the ability to improve cognition by participating in the HACU process, increasing the rate-limiting step of synaptic intake of choline to synthesize the neurotransmitter acetylcholine, and increasing the activity of cholinergic neurons.
Coluracetam (10(-10)-10(-6) moll), also known as MKC-231, significantly increased high affinity choline uptake (HACU) when it was incubated with the hippocampal synaptosomes of ethylcholine mustard aziridinium ion (AF64A) treated rats, but not of normal rats. MKC-231 did not affect the AChE activity, [3H]- quinuclidinyl benzilate binding, and [3H]-pirenzepine binding.
Oral administration of MKC-231 (Coluracetam; 1-10 mg/kg) significantly improved the learning deficits in the Morris' water maze of AF64A-treated rats, but it did not produce any significant side effects, like tremor, salivation or hypothermia, which were observed in rats treated with high doses of tacrine [1]. In acute behavioral experiments, MKC-231 and THA had no significant effect on AF64A-induced memory deficits at any doses tested (0.3, 1.0 and 3.0 mg/kg), whereas Dup 996, at a dose of 1.0 mg/kg, significantly improved memory deficits. In chronic experiments, MKC-231 improved memory deficit at all doses tested (0.3, 1.0, or 3.0 mg/kg p.o., once daily for 11 days) and Dup 996 did so only at a dose of 3.0 mg/kg, whereas THA did not improve memory deficit at any doses tested.
