Neuroscience
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Widely correlated spontaneous activity in the developing nervous system is transiently expressed and is considered to play a fundamental role in neural circuit formation. The depolarization wave, which spreads over a long distance along the neuraxis, maximally extending to the lumbosacral cord and forebrain, is an example of this spontaneous activity. Although the depolarization wave is typically initiated in the spinal cord in intact preparations, spontaneous discharges have also been detected in the isolated brainstem. ⋯ The results revealed that the depolarization wave was homeostatically maintained, which was characterized by an increase in excitability and/or the number of neurons recruited to the wave. The wave was more easily maintained in younger embryos. Furthermore, we demonstrated that the ability of brainstem neurons to perform such an active compensation was not lost even at the stage when the depolarization wave was no longer observed in the intact brainstem.
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Electrical stimulation of the vagus nerve attenuates tumor necrosis factor (TNF) synthesis by macrophages and reduces the systemic inflammatory response. Current evidence suggests that the α7 nicotinic acetylcholine receptor present in the celiac/superior mesenteric ganglia is a key component in vagus nerve signaling to the spleen; however, there is currently no direct anatomical evidence that the α7 receptor is present in the murine celiac/superior mesenteric ganglia. ⋯ Double-labeling for α7 and tyrosine hydroxylase shows that α7 receptor protein is present on noradrenergic neurons within the ganglia and prejunctionally on noradrenergic nerve fibers within the spleen. The α7 receptor in the ganglia provides a possible location for the action of α7-selective agonists, while prejunctional α7 receptor expressed on splenic nerves may induce an increase in norepinephrine release in a positive feedback system enhanced by lymphocyte-derived acetylcholine.
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The pontine micturition center or Barrington's nucleus (BN) - besides regulating micturition - co-regulates the activity of other pelvic viscera such as the colon and genitals. At present, this issue is gaining particular importance due to: (i) recent findings of α-synuclein in BN, (ii) known urinary dysfunction in parkinsonian patients (part of the so-called non-motor symptoms), other patients with dementia and as in very old individuals; and (iii) its proximity to the pedunculopontine nucleus, a surgical target in deep brain stimulation for Parkinson's disease (PD). ⋯ The involvement of dopaminergic activity (physiologic inhibition of the micturition reflex mediated by dopaminergic D1 activity) that diminishes in Parkinsonism and leads to overactivity of the micturition reflex is also well known. In this review, the integrating role of the BN in the context of vesical and gastrointestinal behavior is revisited, and the principal morpho-functional findings that associate dysfunction with the urinary disorders that appear during the pre-motor stages of PD are summarized.
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Anhedonia is one of the core symptoms of depression and has been linked to blunted responses to rewarding stimuli in striatal regions. Stress, a key vulnerability factor for depression, has been shown to induce anhedonic behavior, including reduced reward responsiveness in both animals and humans, but the brain processes associated with these effects remain largely unknown in humans. Emerging evidence suggests that stress has dissociable effects on distinct components of reward processing, as it has been found to potentiate motivation/'wanting' during the anticipatory phase but reduce reward responsiveness/'liking' during the consummatory phase. ⋯ Post hoc tests revealed that stress increased striatal and amygdalar activation during anticipation but decreased striatal activation during consumption. Importantly, stress-induced striatal blunting was similar to the profile observed in clinical depression under baseline (no-stress) conditions in prior studies. Given that stress is a pivotal vulnerability factor for depression, these results offer insight to better understand the etiology of this prevalent disorder.
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Spinal cord injury (SCI) usually leads to severe sensory and motor deficits below the spinal lesion. Previous animal models have shown significant atrophic changes in the neural sensorimotor system following SCI. However, specific anatomical changes in the human brain following SCI remain poorly understood. ⋯ In addition, gray matter volume in the primary motor cortex was positively correlated with the total American Spinal Injury Association motor score in patients with SCI. In conclusion, our findings suggest that SCI causes significant anatomical changes in the human sensorimotor system, and that these anatomical changes may occur in the early phase of SCI. Future treatments that aim to restore sensorimotor functions following SCI need to attend to these anatomical changes in the brain.