Neuroscience
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The role of glutamate in quantal release at the cytoneural junction was examined by measuring mEPSPs and afferent spikes at the posterior canal in the intact frog labyrinth. Release was enhanced by exogenous glutamate, or dl-TBOA, a blocker of glutamate reuptake. Conversely, drugs acting on ionotropic glutamate receptors did not affect release; the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA-R) blocker CNQX decreased mEPSP size in a dose-dependent manner; the NMDA-R blocker d-AP5 at concentrations <200 µM did not affect mEPSP size, either in the presence or absence of Mg and glycine. ⋯ Overall, glutamate exerts both a positive feedback action on mGluR-I, through activation of the phospholipase C (PLC)/IP3 path, and the negative feedback, by interfering with substrate phosphorylation through Gi/0-coupled mGluRs-II/III. The positive feedback prevails, which may explain the increase in overall rates of release observed during mechanical stimulation (symmetrical in the excitatory and inhibitory directions). The negative feedback may protect the junction from over-activation.
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Angiotensin II (Ang II) synthesized in response to body fluid loss caused by actions such as sweating and breathing is today considered as one of the essential factors for promoting hippocampal neurogenesis. Because heat stimuli, along with exercise, increase systemic levels of Ang II, the effects of short-term heat exposure on hippocampal neurogenesis were examined in adult male rats. When rats were exposed daily to a 1-h heat treatment (36.0 ± 0.1 °C) during a 7-d experimental period, the number of doublecortin-immunoreactive newborn cells in the hippocampal dentate gyrus was increased approximately 1.4-fold compared with that in controls that were exposed to a normothermic environment (25.0 ± 0.8 °C). ⋯ Western blot and immunohistochemical analyses revealed an enhancement of vascular endothelial growth factor (VEGF) expression in hippocampal astrocytes following short-term heat exposure. These beneficial effects of short-term heat exposure were prevented when an antagonist for Ang II type 1 receptor (AT1R), candesartan, was given orally. These results indicate that short-term heat exposure enhances adult neurogenesis via activation of AT1R in the hippocampal dentate gyrus, in which VEGF may participate by promoting cell proliferation and/or newborn neuron survival.
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PACAP1-38, a ubiquitous and multifunctional regulator has been in the focus of neurotoxicity research due to its impressive neuroprotective potential. Although the literature extensively demonstrated its repressive effect on the apoptotic machinery in neurodegenerative models, there is a striking absence of analysis on its role in normal development. We performed quantitative analyses on caspase activity in developing retina upon 100, 50, 25 or 1 pmol intravitreal PACAP1-38 injection from postnatal day 1 (P1) through P7 in Wistar rats. ⋯ The fundamental novelty of these results is that PACAP1-38 induces apoptosis during early postnatal retinogenesis. The dose as well as stage-dependent response suggests that PACAP1-38 has a Janus face in apoptosis regulation. It not only inhibits development-related apoptosis, but as a long-term effect, facilitates it.
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The history of brain science is dominated by the study of neurons. However, there are as many glial cells as neurons in the human brain, their complexity increases during evolution, and glial cells play important roles in brain function, behavior, and neurological disorders. Although neurons and glial cells were first described at the same time in the early 19th century, why did the physiological study of glial cells only begin in the 1950s? What are the scientific breakthroughs and conceptual shifts that determined the history of glial cells in relation to that of neurons? What is the impact of the history of glia on the evolution of neuroscience? In order to answer these questions, we reconstructed the history of glial cells, from their first description until the mid-20th century, by examining the relative role of technical developments and scientific interpretations.
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The amygdala plays a key role in gathering social cues to context-appropriate responses that require refined motor behavior, involving either direct or indirect connections with sensorimotor-related areas. Although, several studies investigated the structural and functional limbic connectivity of the amygdala both in animals and in humans, less is known about the limbic modulation on sensorimotor-related areas. However, recent evidences suggest the amygdala as a possible cornerstone in the limbic-motor interface. ⋯ On the other hand, our connectomic analysis revealed a close interplay between the amygdala and the inferior parietal lobule, followed by the postcentral gyrus, the precentral gyrus and the paracentral lobule. The findings of the present study are in line with previous literature and reinforce the idea of the existence of a limbic-motor interface, which is likely to be involved in the emotional modulation of complex functions such as spatial perception and movement computation. Considering that these pathways may play an important role, not on in physiological conditions, but also in pathological context, further studies should be fostered in order to confirm the existence of a limbic-motor interface and its precise functional meaning.