Neuroscience
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Abnormal brain development in a compromised prenatal and/or early postnatal environment is thought to be a risk factor for several neurobehavioural disorders. However, the mechanisms underlying these are not well understood. We have earlier reported reduced placental docosahexaenoic acid (DHA) levels in preterm deliveries. ⋯ A negative association between maternal plasma BDNF levels and placental weight (p=0.001) was observed while a positive association was seen between cord plasma BDNF levels and gestation (p=0.025). The reduction in cord BDNF levels may have implications for altered neurodevelopment in childhood and later life. Studies need to be undertaken to follow up children born preterm for risk of neurobehavioural disorders like attention deficit hyperactivity disorder (ADHD) to understand the effect of altered BDNF at birth on neurodevelopment.
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The ventral tegmental area (VTA) plays an important role in reward and motivational processes that facilitate the development of drug addiction. Glutamatergic inputs into the VTA contribute to dopamine (DA) neuronal activation related to reward and response-initiating effects in drug abuse. Previous investigations indicate that alpha1-adrenoreceptors (α1-ARs) are primarily localized at presynaptic elements in the ventral midbrain. ⋯ Chelerythrine (1μM, protein kinase C (PKC) inhibitor) but not Rp-cAMPS (11 μM, PKA inhibitor) blocked the α1-AR activation effect on AMPA EPSCs, indicating that a PKC intracellular pathway is required. These results demonstrated that presynaptic α1-AR activation modulates glutamatergic inputs that affect VTA-DA neuronal excitability. α1-AR action might be heterosynaptically localized at glutamatergic fibers terminating onto VTA-DA neurons. It is suggested that drug-induced changes in α1-AR could be part of the neuroadaptations occurring in the mesocorticolimbic circuitry during the addiction process.
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Sensory-evoked propagating waves are frequently observed in sensory cortex. However, it is largely unknown how an evoked propagating wave affects the activity evoked by subsequent sensory inputs, or how two propagating waves interact when evoked by simultaneous sensory inputs. Using voltage-sensitive dye imaging, we investigated the interactions between two evoked waves in rat visual cortex, and the spatiotemporal patterns of depolarization in the neuronal population due to wave-to-wave interactions. ⋯ Fusion significantly shortens the latency and half-width of the response, leading to changes in the spatial profile of evoked population activity. The visually-evoked propagating wave may also be suppressed by a preceding spontaneous wave. The refractory period following a propagating wave and the fusion between two waves may contribute to visual sensory processing by modifying the spatiotemporal profile of population neuronal activity evoked by sensory events.
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How can we investigate the brain mechanisms underlying self-consciousness? Recent behavioural studies on multisensory bodily perception have shown that multisensory conflicts can alter bodily self-consciousness such as in the "full body illusion" (FBI) in which changes in self-identification with a virtual body and tactile perception are induced. Here we investigated whether experimental changes in self-identification during the FBI are accompanied by activity changes in somatosensory cortex by recording somatosensory-evoked potentials (SEPs). To modulate self-identification, participants were filmed by a video camera from behind while their backs were stroked, either synchronously (illusion condition) or asynchronously (control condition) with respect to the stroking seen on their virtual body. ⋯ These data show that changes in bodily self-consciousness modulate activity in primary and higher-tier somatosensory cortex at two distinct processing steps. We argue that early modulations of primary somatosensory cortex may be a consequence of (1) multisensory integration of synchronous vs. asynchronous visuo-tactile stimuli and/or (2) differences in spatial attention (to near or far space) between the conditions. The later activation in higher-tier parietal cortex (and potentially other regions in temporo-parietal and frontal cortex) likely reflects the detection of visuo-tactile conflicts in the asynchronous condition.
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The sleep electroencephalogram (EEG) undergoes many changes during adolescence. We assessed whether sleep homeostasis is altered across adolescent development using two measures: the dissipation of slow-wave activity (SWA, 0.6-4.6Hz) across the night and the rate of build-up of SWA in the first non-rapid eye movement (NREM) sleep episode. Furthermore, we examined the association between homeostatic and circadian measures, by correlating the build-up of SWA in the first non-rapid eye movement (NREM) sleep episode with circadian phase. ⋯ Similarly, we observed no developmental changes in the rate of the build-up of SWA in the first NREM sleep episode for our within- and between-subject analyses, or a correlation between this measure and circadian phase for either cohort. With regard to parental alcohol history, we found no difference in the dissipation of sleep pressure between PH+ and PH- children and teens. These results indicate that the dissipation of sleep pressure does not change across adolescent development, is not correlated with circadian phase, and does not differ between PH+ and PH- children and teens.