Neuroscience
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Brain glucose metabolism is altered in sporadic Alzheimer's disease (sAD), whose pathologies are reproduced in rodents by intracerebroventricular (icv) infusion of streptozotocin (STZ) in subdiabetogenic doses. The icv-STZ model also culminates in central cholinergic dysfunctions, which in turn are known to underlie both the sAD cognitive decline, and synaptic plasticity impairments. Considering the cognitive-enhancing potential of chronic nicotine (Nic), we investigated whether it attenuates icv-STZ-induced impairments in recognition memory and synaptic plasticity in a cognition-relevant substrate: the hippocampal CA1-medial prefrontal cortex (mPFC) pathway. ⋯ We found that Nic treatment prevents icv-STZ-induced disruptions in recognition memory and LTP. STZ did not precipitate neuronal death, while Nic alone was associated with higher neuronal density in CA1 when compared to vehicle-injected animals. Through combining behavioral, neurophysiological, and neuropathological observations into the Nic-STZ interplay, our study reinforces that cholinergic treatments are of clinical importance against early-stage Alzheimer's disease and mild cognitive impairments.
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As maternal treatment with magnesium sulfate (MG) may protect the fetal brain, we sought to assess the inflammation associated neuroprotective potential of MG and its association to interleukin 1β (IL-1β). ⋯ Intrauterine fetal exposure to maternal inflammation and pro-inflammatory cytokines is associated with adverse offspring neurological outcomes. Although its precise mechanism is not elucidated, magnesium sulfate (MG) is commonly used as neuroprotection for white matter brain injuries in preterm fetuses. A proposed mechanism involves the ability of MG to reduce pro-inflammatory cytokine levels. In the current study, we used a rat model of LPS-induced maternal inflammation to investigate the short-term effect of MG on fetal brain IL-1β levels, and its long-term neuroprotective effect on the offspring brain by using MRI. We demonstrated that maternal administration of MG can prevent long-term neonatal brain injury but, since no decrease was observed in fetal brain IL-1β levels, the neuro-protective mechanism of MG is not mediated by inhibition of IL-1β production.
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Even when performing invariant behavioral task repeatedly on invariant physical stimuli, our behavioral performance always changes as manifested in varying response times (RTs), which is associated with fluctuations in attentional control and thus the underlying self-organization states of the human brain. In a visuospatial task of the present fMRI study, physical stimuli differed across six levels of spatial scope, but were kept invariant within each level. The slower RTs with larger spatial area attended suggested higher demands on visuospatial attention. ⋯ These findings thus for the first time suggested that the within-level variance of attentional control corresponded to dynamic changes in the frontoparietal network and the DMN, in terms of not only the height but also the latency of neural activity. Moreover, although the two networks are anti-correlated in terms of the height of neural activity, they are tightly coupled in terms of the temporal dynamics. Based on the current results, we proposed a tentative hypothesis on the optimal working mode of the frontoparietal attentional control system in the human brain: even a lower height of neural activity in frontoparietal network can significantly improve behavioral performance as long as it starts relatively early.
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In the present study, we investigated the possible participation of the endocannabinoid system in the basolateral amygdala and N-methyl-d-aspartate (NMDA) or GABA-A receptor neurotransmission in the ventral tegmental area in the memory consolidation impairment induced by morphine administration. To measure memory formation, step-through type passive avoidance apparatus was used with adult male Wistar rats. The results showed that intraperitoneal (i.p.) administration of morphine (3 and 6mg/kg) after the successful training phase had an amnestic effect and induced memory consolidation impairment. ⋯ Also, the results showed that the injection of bicuculline, a GABA-A receptor antagonist (0.3-0.5µg/rat) or NMDA (0.005-0.02µg/rat) into the ventral tegmental area reversed ACPA-induced potentiation of morphine response and improved memory consolidation. It should be considered that the injection of ACPA into the basolateral amygdala and the injection of bicuculline or NMDA into the ventral tegmental area alone could not affect memory consolidation. Taken together, it seems that there is a functional interaction between the basolateral amygdala endocannabinoid system and the ventral tegmental area GABAergic- or glutamatergic neurotransmission in the modulation of morphine-induced memory consolidation impairment.
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Neuroscientific research has made a concerted effort to determine cortical localization using various functional imaging techniques. This approach has undoubtedly yielded important novel anatomical knowledge, albeit at times contradictory, regarding the structural organization of the vestibular cortex. Unfortunately however, this knowledge has not translated to our understanding regarding how neural mechanisms control vestibular function. ⋯ Contrastingly, in the second half of this review, I present previous findings that show how disrupting interhemispheric interactions can modulate the brainstem-mediated vestibular-ocular reflex (VOR). I conclude by speculating why interhemispheric competition induces correlated biases at the cortical and brainstem level respectively. Specifically, I propose that brainstem-mediated vestibulo-spatial and vestibulo-temporal transformations, in addition to coding for head displacement, underpin a generalized cortical magnitude estimation system which the CNS uses to construct dynamic spatio-temporal maps of the physical world, in-turn ensuring spatial orientation.