Brain research
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It is well known that prior experience to the elevated plus-maze increases the avoidance of rodents to the open arms and impairs the anxiolytic-like effect of benzodiazepines evaluated during a subsequent exposure to the maze, a phenomenon known as "one-trial tolerance". Centrally injected benzodiazepine drugs attenuate anxiety in some limbic structures, such as hypothalamus, amygdala and the midbrain periaqueductal gray (PAG). This study investigated the effects of intra-PAG infusions of midazolam (MDZ) in maze-naïve and maze-experienced mice. ⋯ The antiaversive effects of MDZ were completely blocked by prior injection of flumazenil which in turn did not alter any other behavioral measure. In maze-experienced mice, intra-PAG infusion of MDZ did not modify any behavioral measure. Taken together, present results corroborate previous studies demonstrating that GABA/benzodiazepine receptor complex located within the PAG plays a role on anxiety modulation in maze-naïve mice as well as indicate its involvement in the OTT phenomenon.
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Changes in the partial pressure of arterial CO2 (PaCO2) regulates cerebrovascular tone and dynamic cerebral autoregulation (CA). Elevations in PaCO2 also increases autonomic neural activity and may alter the arterial baroreflex. We hypothesized that hypercapnia would impair, and hypocapnia would improve, dynamic CA and that these changes would occur independently of any change in baroreflex sensitivity (BRS). ⋯ Hypercapnia caused a progressive increase in PaCO2 and MCAv whereas hypocapnia caused the opposite effect. Despite marked changes in CPP, there were no evident change in transfer-function gain, coherence, MAP variability or BRS; however, both MCAv variability and phase in the very-low frequency range was reduced during the most severe level of hyper- and hypocapnia (P < 0.05), and were related to elevations in ventilation (R2 = 0.42-0.52, respectively; P < 0.001). It seems that hyperventilation, rather than PaCO2, has an important influence on dynamic CA.
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Neurite (axon and dendrite) degeneration requires self-destructive programs independent of cell death programs to segregate neurite degeneration from cell soma demise. We have here addressed the question of whether neuritic degeneration is delayed or occurs normally under conditions in which sympathetic neurons acquire resistance to somal apoptosis upon maturation. For this purpose, we have examined both beading formation and fragmentation, two hall-marks of neurite degeneration, caused by three experimental paradigms including NGF deprivation, treatment with microtubule-disrupting agents, and in vitro Wallerian degeneration. ⋯ Neuritic ATP levels of young ganglia decreased rapidly, while those of mature ganglia did so slowly during degeneration, although the basal levels of neuritic ATP of both ganglia were similar. Notably, mature neurites were resistant to fragmentation caused by NGF deprivation and capable of growing again after replenishment of NGF. This development of resistance to neurite degeneration in mature neurons may be thought as an important protective mechanism for the maintenance of the adult nervous system.
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The behavioral manifestations of autism, including reduced sociability (reduced tendency to seek social interaction), may be related to underdevelopment of the corpus callosum (CC). The BALB/cJ inbred mouse strain is a useful model system for testing the relationship between reduced sociability and CC underdevelopment. BALB/cJ mice show low levels of sociability, on average, but substantial intrastrain variability in sociability, as well as striking variability in CC development. ⋯ C57BL/6J mice showed consistently high levels of sociability and normal corpus callosum development. These results suggest that abnormal white matter structure is associated with deficits in sociability in BALB/cJ mice. Additional studies are warranted to elucidate the relationship between brain connectivity and sociability in this model system.
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Comparative Study
An experimental model to measure excitatory and inhibitory pain mechanisms in humans.
Numerous approaches have been used to induce and measure experimental pain perception with the goal of better understanding excitatory and inhibitory pain mechanisms. In this study, the objective was to develop a simple experimental design which would enable us to elicit and measure multiple nociceptive mechanisms that have been reported to play a role in the development and persistency of chronic pain, such as temporal summation (TS) and diffuse noxious inhibitory control (DNIC). Eighty-three healthy subjects (42 men, 41 women) participated in this study where we examined pain perception of two tonic heat pain stimulation (thermode) separated by a 2 minute cold pressor test (CPT) (7 degrees C, 10 degrees C or 12 degrees C) which allowed us to activate DNIC. ⋯ Our experimental pain design allowed us to measure several excitatory and inhibitory pain mechanisms in one experimental session. We were able to separate the effect of DNIC on the peak pain and on TS. This method is simple, sensitive and can easily be used in different population of either healthy subjects or chronic pain patients.