Behavioral neuroscience
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Behavioral neuroscience · Apr 2013
Inhibition of HCN channels within the periaqueductal gray attenuates neuropathic pain in rats.
Peripheral and spinal hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channels play important roles in neuropathic pain by regulating neuronal excitability. However, the participation of HCN channels in the ventral-lateral periaqueductal gray (vlPAG) during neuropathic pain states has not been clarified. ⋯ Subsequently, the function of these upregulated channels was verified by the intravlPAG infusion of ZD7288, a specific HCN blocker, which significantly relieved mechanical allodynia and thermal hyperalgesia in CCI animals. These results suggest that the upregulation of vlPAG HCN channels plays an important role in pain maintenance and might be a target for attenuating pain.
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Behavioral neuroscience · Dec 2012
Predictors of susceptibility and resilience in an animal model of posttraumatic stress disorder.
Animal models of posttraumatic stress disorder (PTSD) are based on fear conditioning where innocuous cues elicit reactions that originally occur to traumatic events--a core feature of PTSD. Another core feature is hyperarousal--exaggerated reactions to stressful events. One limitation of animal models of PTSD is that group effects do not model the sporadic incidence of PTSD. ⋯ We found the magnitude of CRM was correlated with the onset latency and area of conditioned responding during CS-US pairings and with the peak latency of a response during US pretesting. In an animal model of PTSD that more accurately reflects clinical prevalence, we can begin to predict susceptibility not only during responding to a stressful conditioning situation but also during a screening process before the stressful situation takes place. The results suggest relatively innocuous testing may help detect PTSD after trauma and screen for it before trauma occurs.
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Behavioral neuroscience · Aug 2012
Bilateral lesions of the thalamic trigeminal orosensory area dissociate natural from drug reward in contrast paradigms.
Substance abuse and addiction are associated with an apparent devaluation of, and inattention to, natural rewards. This consequence of addiction can be modeled using a reward comparison paradigm where rats avoid intake of a palatable taste cue that comes to predict access to a drug of abuse. Evidence suggests rats avoid intake following such pairings, at least in part, because the taste cue pales in comparison to the highly rewarding drug expected in the near future. ⋯ The results show that the TOA lesion disrupts, but does not eliminate avoidance of a taste cue that predicts access to a preferred sucrose solution and leaves intact the development of a LiCl-induced conditioned taste aversion. The lesion does, however, eliminate the suppression of intake of a taste cue when paired with experimenter-administered morphine or cocaine using our standard parameters. As such, this is the first manipulation found to dissociate avoidance of a taste cue when mediated by a sweet or by a drug of abuse.
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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.