Behavioral neuroscience
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Behavioral neuroscience · Apr 2012
Click-evoked otoacoustic emissions: response amplitude is associated with circulating testosterone levels in men.
In rhesus monkeys, the magnitude of the cochlear response to auditory stimuli (click-evoked otoacoustic emissions, [CEOAEs]) is correlated with seasonal changes in circulating testosterone levels. The present study investigated the association between circulating testosterone and CEOAE production in men. CEOAEs were measured in 67 men and 37 women, and saliva was analyzed to quantify bioavailable testosterone. ⋯ CEOAEs were greater in summer and fall, the seasons that showed the lowest levels of circulating testosterone. On an individual basis, men who had higher levels of testosterone at the time of assessment exhibited smaller CEOAE response amplitudes. These findings support previous data from rhesus macaques and are consistent with the prospect of an activational effect of testosterone in the human cochlea.
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Behavioral neuroscience · Apr 2012
Sustaining high acetylcholine levels in the frontal cortex, but not retrosplenial cortex, recovers spatial memory performance in a rodent model of diencephalic amnesia.
Although the thalamus and/or mammillary bodies are the primary sites of neuropathology in cases of diencephalic amnesia such as Wernicke Korsakoff Syndrome (WKS), there is also functional deactivation of certain cortical regions that contribute to the cognitive dysfunction. Acetylcholine (ACh) is a key neurotransmitter that modulates neural processing within the cortex and between the thalamus and cortex. In the pyrithiamine-induced thiamine deficiency (PTD) rat model of WKS, there are significant reductions in cholinergic innervation and behaviorally stimulated ACh efflux in the frontal (FC) and retrosplenial (RSC) cortices. ⋯ Maintaining high ACh levels in the RSC had no procognitive effects in PTD rats, but rather impaired alternation behavior in PF rats. These results demonstrate that diverse cortical regions respond differently to intensified ACh levels-and the effects are dependent on thalamic pathology. Thus, pharmacotherapeutics aimed at enhancing cognitive functions must account for the unique features of cortical ACh stimulation and the connective circuitry with the thalamus.