Neuroscience
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Glutamate and norepinephrine (NE) are believed to mediate the long-lasting synaptic plasticity in the accessory olfactory bulb (AOB) that underlies pheromone recognition memory. The mechanisms by which these neurotransmitters bring about the synaptic changes are not clearly understood. In order to study signals that mediate synaptic plasticity in the AOB, we used AOB neurons in primary culture as a model system. ⋯ We found that the glutamatergic and noradrenergic stimulation caused significant induction of c-Fos mRNA and protein. Induction of c-Fos was significantly reduced in the presence of inhibitors of protein kinase C, mitogen-activated protein kinase (MAPK) and phospholipase C. These results suggest that glutamate and NE induce gene expression in the AOB through a signaling pathway mediated by protein kinase C and MAPK.
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To improve behavior, one must detect errors and initiate subsequent corrective adaptations. This action monitoring process has been widely studied, but little is known about how one may improve this aspect of cognition. To examine the relationship between cardiorespiratory fitness and action monitoring, we recorded the error-related negativity (ERN), an event-related brain potential believed to index action monitoring, as well as post-error behavioral indices of action monitoring from healthy young adults (18-25 years) who varied in cardiorespiratory fitness. ⋯ Higher fitness was associated with greater post-error accuracy and ERN amplitude during task conditions emphasizing accuracy, as well as greater modulation of these indices across task instruction conditions. These findings suggest that higher fitness is associated with increased cognitive flexibility, evidenced through greater change in action monitoring indices as a function of task parameters. Thus, fitness may benefit action monitoring by selectively increasing cognitive control under conditions where error detection and performance adjustments are more salient.
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Opiate addiction is a chronic medical disorder characterized by drug tolerance and dependence, behavioral sensitization, vulnerability to compulsive relapse, and high mortality. In laboratory animals, the potential effect of opiate drugs to induce cell death by apoptosis is a controversial topic. This postmortem human brain study examined the status of the extrinsic and intrinsic apoptotic pathways in the prefrontal cortex of a large group of well-characterized heroin or methadone abusers. ⋯ Taken together, the data revealed that the extrinsic and intrinsic canonical apoptotic pathways are not abnormally activated in the prefrontal cortex of opiate abusers. Instead, the chronic modulation of some of their components (downregulation of FADD and cytochrome c; upregulation of FLIP(L) and Bcl-2) suggests the induction of non-apoptotic actions by opiate drugs related to phenomena of synaptic plasticity in the brain. These neurochemical adaptations could play a major role in the development of opiate tolerance, sensitization and relapse in human addicts.
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A topic of high current interest and controversy is the basis of the homeostatic sleep response, the increase in non-rapid-eye-movement (NREM) sleep and NREM-delta activity following sleep deprivation (SD). Adenosine, which accumulates in the cholinergic basal forebrain (BF) during SD, has been proposed as one of the important homeostatic sleep factors. It is suggested that sleep-inducing effects of adenosine are mediated by inhibiting the wake-active neurons of the BF, including cholinergic neurons. ⋯ Two weeks after i.c.v. saporin injection there was a 59% cholinergic cell loss, correlated with significant increase in SD-induced adenosine level in the BF and an intact sleep response. Three weeks after i.c.v. saporin injection there was an 87% cholinergic cell loss, nearly complete abolition of the SD-induced adenosine increase in the BF and the homeostatic response, implying that the time course of i.c.v. saporin lesions is a key variable in interpreting experimental results. Taken together, these results strongly suggest that cholinergic neurons in the BF are important for the SD-induced increase in adenosine as well as for its sleep-inducing effects and play a major, although not exclusive, role in sleep homeostasis.
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Mole-rat species within the family Bathyergidae exhibit a wide range of reproductive strategies and social systems. Various forms of reproductive suppression are displayed within this family: in the solitary species, breeding is suspended for part of the year and in the social species, reproduction is suppressed in subordinate animals. This study investigated the gonadotrophin-releasing hormone 1 (GnHR-1) systems of breeding and non-breeding solitary Cape mole-rats and social Natal mole-rats for possible inter- and/or intra-species differences. ⋯ In female and male Natal mole-rats, GnRH-1-immunoreactivity in the median eminence is less dense in the reproductive animals; no such difference was found in Cape mole-rats between the breeding and non-breeding seasons. These immunohistochemical results are discussed in the light of earlier studies which identified no functional neuroendocrine impediments underlying regulated reproduction in either Cape or Natal mole-rats. The cumulative findings suggest that the principal factors determining seasonal or socially induced suppression of reproduction in these species are behavioral rather than neuroendocrine.