Neuroscience
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Developmental alcohol exposure causes a host of cognitive and neuroanatomical abnormalities, one of which is impaired executive functioning resulting from medial prefrontal cortex (mPFC) damage. This study determined whether third-trimester equivalent alcohol exposure reduced the number of mPFC GABAergic parvalbumin-positive (PV+) interneurons, hypothesized to play an important role in local inhibition of the mPFC. The impact on passive avoidance learning and the therapeutic role of aerobic exercise in adulthood was also explored. ⋯ Alcohol impaired acquisition, but not retrieval of passive avoidance, and had no effect on motor performance on the rotarod. Exercise had no impact on PV+ cell number, mPFC volume, or acquisition of passive avoidance, but enhanced retrieval in both control and alcohol-exposed groups, and enhanced rotarod performance in the control mice. Results support the hypothesis that part of the behavioral deficits associated with developmental alcohol exposure are due to reduced PV+ interneurons in the ACC, but unfortunately exercise does not appear to be able to reverse any of these deficits.
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Since Ebbinghaus' classical work on oblivion and saving effects, we know that declarative memories may become at first spontaneously irretrievable and only subsequently completely extinguished. Recently, this time-dependent path toward memory-trace loss has been shown to correlate with different patterns of brain activation. Environmental enrichment (EE) enhances learning and memory and affects system memory consolidation. ⋯ At day 21 SC mice do not show preferential exploration of novel object, irrespective of the retraining, while EE mice are still capable to benefit from retraining, even if they were not able to spontaneously recover the trace. Analysis of c-fos expression 20days after learning shows a different pattern of active brain areas in response to the retraining session in EE and SC mice, with SC mice recruiting the same brain network as naïve SC or EE mice following de novo learning. This suggests that EE promotes formation of longer lasting object recognition memory, allowing a longer time window during which saving is present.
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The μ-opioid receptor (MOR) and dopamine D1 receptor are co-expressed in the medium spiny neurons of striatal areas and the signaling pathways activated by these two receptors are in functional competition. However, in certain conditions an integrated response mediated by the dopamine D1 receptor transduction system is observed. In mice, morphine administration induces hypermotility and this response has been described in terms of a β-arrestin2-dependent mechanism that favors prevalent dopamine D1 receptor activation. ⋯ We then examined MOR-dopamine D1 receptor interactions after sucrose consumption. Sucrose increased NAcS dopamine D1 receptor signaling in NFD and FD rats, and a reduction in β-arrestin2 expression prevented this effect selectively in FD rats. These results show the β-arrestin2-dependent prevalence of dopamine D1 receptor signaling in response to acute morphine or sucrose consumption elicited by food deprivation in rats.
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Few minutes of focal vibration (FV) on limb muscles can improve motor control in neurological (stroke, Parkinson) patients for unknown underlying neurophysiological mechanisms. Here we hypothesized that in healthy volunteers this FV would increase excitability in the primary sensorimotor cortex (S1-M1) during an isometric contraction of the stimulated muscle. The design included an initial control condition with no FV stimulation (Baseline) as well as three short experimental sessions of FV and a Sham (fake) session in a pseudo-random order. ⋯ Results showed that, compared to the Baseline (no FV) or Sham stimulation, the first two FV sessions showed a cumulative increase in alpha (but not beta) MRPD at C3 electrode, suggesting a specific effect of vibration on the excitability of contralateral S1-M1 generating EEG "mu" rhythms. FV over limb muscles modulates neurophysiological oscillations enhancing excitability of contralateral S1-M1 in healthy volunteers. The proposed mechanism may explain the clinical effects of vibratory rehabilitation in neurological patients with motor deficits.
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Premature or ill full-term infants are subject to a number of noxious procedures as part of their necessary medical care. Although we know that human infants show neural changes in response to such procedures, we know little of the sensory or affective brain circuitry activated by pain. In rodent models, the focus has been on spinal cord and, more recently, midbrain and medulla. ⋯ Formalin induced the oft-reported biphasic response at this age and induced a conditioned aversion to cues associated with its injection, thus demonstrating the aversiveness of the stimulation. Morphometric analyses, structural equation modeling and co-expression analysis showed that limbic and sensory paths were activated, the most prominent of which were the prefrontal and anterior cingulate cortices, nucleus accumbens, amygdala, hypothalamus, several brainstem structures, and the cerebellum. Therefore, both sensory and affective circuits, which are activated by pain in the adult, can also be activated by noxious stimulation in 12-day-old rat pups.