Chunk #23 — Potential Biological Mechanism of Hippocampal Sensitivity to AUDs: Impact of Altered GluN and GABAR Signaling in the Hippocampus on Adult Neurogenesis
The regionally differential rates of cognitive recovery following abstinence from alcohol use are potentially consequent to the neurogenic properties (or lack thereof) of each region. To be more specific, cognitive function relying on the frontal cortical region in humans has been described as being recovered at an earlier time in abstinence than cognitive functions specific to the hippocampal formation of the limbic system as previously discussed. It is possible that this disparity is due to, at least in part, the ongoing adult neurogenesis in the hippocampus which occurs at a much lesser rate in the PFC of mammals (146); neurons which would be generated during critical periods of withdrawal would be developing into mature neurons during a time of negative affect (147, 148), potentially resulting in a pathologic phenotype and dysfunctional characteristics (149). This problematic phenomenon would be far more impactful in a region with high neurogenesis (such as the hippocampus) as compared with a region of low or absent neurogenesis, where the typical functioning of the existing circuitry may return upon complete washout of the drug.
