Search

The link between decrease in levels of attention and total sleep deprivation is well known but the respective contributions of slow wave sleep (SWS) and rapid eye movement sleep (REM) is still largely unknown. The aim of this study was to characterize the effects of sleep deprivation during the SWS phase (i.e., early night sleep) and the REM phase (i.e., late night sleep) on tasks that tap automatic and selective attention; these two forms of attention were indexed respectively by "mismatch negativity" (MMN) and "negative difference" (Nd) event-related potential (ERP) difference waves. Ten young adult participants were subjected to a three-night sleep protocol. They were each received one night of full sleep (F), one night of sleep deprivation during the first half of the night (H1), and one night of sleep deprivation during the second half of the night (H2). MMN and Nd were recorded the following morning of each night during two auditory oddball tasks that tapped automatic and selective attention. The effect of sleep deprivation condition was assessed using ERP amplitude measures and standardized low-resolution electromagnetic tomography method (sLORETA). ERP results revealed significant MMN amplitude reduction over frontal and temporal recording areas following the H2 night compared to F and H1, indicating reductions in levels of automatic attention. In addition, Nd amplitude over the parietal recording area was significantly increased following the H2 night compared to F and H1. sLORETA findings show significant changes from F to H2 night in frontal cortex activity, decreasing during the automatic attention task but increasing during the selective attention task. No significant change in brain activity is observed after H1 night. The restoration of attention processes is mainly achieved during REM sleep, which confirms results from previous studies in rat models. The anterior cortex seems to be more sensitive to sleep loss, while the parietal cortex acts as a compensatory resource to restore cognitive performance in a task context.

Physical restraint applied during gestation is a commonly employed animal model of human pregnancy stress. The consequences of such a paradigm have been extensively investigated in adult male rats using a variety of physiological and behavioral measures. The behavioral repertoire of female offspring, however, has been largely ignored. The current study examines adult offspring-male and female Long Evans rats (55-90 days of age) and is a follow-up report to the consequences of maternal restraint (gestation days 10 through 19) in mother rats and their juvenile offspring. Physiological measures included weight and estrous cycle regularity. Elevated plus maze and emergence tests were used to measure anxiety, and the T-maze test, cognition. Data were analyzed via hierarchical linear modeling to account for the nesting of offspring within litters. Compared to same-sex controls, males from stressed mothers displayed a progressive attenuated weight gain over experimental weeks while females from stressed mothers maintained a stable, lower weight throughout. Twenty-five percent of females in the stressed group and none in the control group displayed irregular cycles in the first week of testing; on subsequent weeks, this group discrepancy ranged from 1% to 11%. Subtle effects were observed in anxiety measures: an interaction between sex and stress group in the analysis of head dip behavior in the elevated plus maze and decreased emergence latencies in stress groups. Results demonstrate the importance of examining the effects of maternal stress in offspring of both sexes at various developmental stages.

In both humans and animals, stress experienced during gestation is associated with physiological changes and disruptions in emotional function and cognitive ability in offspring; however, much less is known about the effects of such stress in mothers. In animal models, physical restraint is commonly employed to induce stress during gestation and results in elevated postpartum maternal anxiety and changes in maternal care. The purpose of the current study was to evaluate the consequences of restraint stress applied on gestation days 10 through 19 in mother rats and their juvenile offspring. Progeny were reared by birth mothers. Preterm anxiety was assessed in the elevated plus maze and maternal behavior in the retrieval test. Cognitive (T-maze) and anxiety measures (elevated plus maze and emergence) were applied to a subset of male and female offspring at 30-31 days of age. Weight and litter characteristics were also recorded. Mother rats exposed to stress during gestation had attenuated weight gain, elevated anxiety-like behavior, and reduced maternal care. Stressed mothers also had fewer pups and an elevated offspring mortality rate. The consequences of gestational stress in offspring were subtle and gender-dependent. Only juvenile females displayed marginal effects of gestational stress in the form of elevated anxiety-like behavior and attenuated weight gain. In the current study, although gestational stress had robust effects in the mother rat, these did not translate to similar changes in offspring behavior. The importance of focusing research on maternal responses to gestational stress is highlighted by these findings.

Apoptosis is known to occur in the limbic system after myocardial infarction (MI) in the rat. Our study was designed to evaluate the time course dynamics of this phenomenon in limbic areas. Apoptosis, i.e., caspase-3 activity and the number of terminal dUTP nick-end labelling-positive cells, as well as brain-derived neurotrophic factor (BDNF) were quantitated in sham-operated controls and MI rats 1, 2 and 7 days after surgery. Both apoptosis parameters were increased throughout, although in different structures: the CA1 region of the hippocampus and the medial amygdala at day 1, the CA1 region of the hippocampus and the lateral amygdala at day 2, and the frontal cortex at day 7. At day 2, BDNF was decreased in the prefrontal cortex and medial amygdala, whereas it was elevated in the dentate gyrus of the hippocampus; at day 7, BDNF was reduced in the frontal cortex and posterior hypothalamus but was augmented in the medial amygdala. These data indicate that post-MI apoptosis in the limbic system is a dynamic process occurring mainly in the hippocampus and amygdala during the first days after MI. The fact that BDNF was increased as early as 2 days after MI suggests that neurogenesis can occur rapidly in selected limbic regions after MI.

Gamma-hydroxybutyrate (GHB) at low doses (5–10 mg/kg i.p.) increased and at high doses (160–320 mg/kg i.p.) decreased the spontaneous firing rate of prefrontal cortex (PFC) neurons recorded in urethane-anesthetized rats. Only excitations were blocked by NCS-382, a specific GHB receptor antagonist; this suggests that the excitatory effect of low doses of GHB is mediated by a GHB receptor whereas the inhibitory effect of high doses of GHB involves a more complex mechanism.