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When asked when she first hypothesized that LAC may play a pivotal role in depression, Nasca responds that results from several rodent studies generated [a] hypothesis for a deficiency in LAC in major depression. She adds that rodents with behavioral abnormalities have a LAC deficiency that signals impaired neural and systemic functions such as hippocampal glutamatergic dysfunction, abnormal structural plasticity, as well as systemic insulin resistance. These traits were improved in the rodents by supplementation with LAC, suggesting a possible role for LAC as a treatment for depression in humans
Dihexa or its analogs were administered 5 minutes after scopolamine, either intracerebroventricularly at doses of 0.1 or 1 nmol), intraperitoneally at doses of 0.05, 0.25, or 0.50 mg/kg, or orally at doses of 1.25 or 2.0 mg/kg
