Neuroscience
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Review Historical Article
Endogenous morphine and its metabolites in mammals: history, synthesis, localization and perspectives.
Morphine derived from Papaver somniferum is commonly used as an analgesic compound for pain relief. It is now accepted that endogenous morphine, structurally identical to vegetal morphine-alkaloid, is synthesized by mammalian cells from dopamine. ⋯ However, the exact role of these compounds is a matter of debate although different links with infection, sepsis, inflammation, as well as major neurological pathologies (Parkinson's disease, schizophrenia) have been proposed. The present review describes endogenous morphine and morphine derivative discovery, synthesis, localization and potential implications in physiological and pathological processes.
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Comparative Study
Basolateral amygdala activity during the retrieval of associative learning under anesthesia.
Associative learning can occur under anesthesia and its neural correlates have begun to be elucidated. During discrimination learning under anesthesia in rats, lateral amygdala excitability increases in response to a conditioned stimulus (CS+) previously paired with electrical stimulation of the paw but not to another stimulus presented alone (CS-). Similarly, medial prefrontal cortex activity increases selectively during CS+ presentation after discrimination learning but this occurs only in neurons receiving input from the basolateral amygdala (BLA), the main source of amygdaloid projections to this region. ⋯ LFP power also showed a modest increase during CS+, compared to CS-, presentation. These findings suggest that discrimination learning under anesthesia can occur at the neural level in BLA. The potential relevance of these results is discussed in relation to previous studies examining neural activity during fear learning and memory processing in conscious animals.
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Comparative Study
Updating process of internal models of action as assessed from motor and postural strategies in children.
The objective of this study was to investigate the updating process of internal models of action in children and young adults, through the postural and motor strategies adopted in simple tasks, namely sit-to-stand (STS) and back-to-sit (BTS). To this end, 11 healthy children from 7 to 10years (latest stage of childhood) and 12 healthy adults participated in the experiment. The STS and BTS tasks were performed with horizontal support surface and support surface tilted 10° to the right or forward in order to investigate the immediate adaptation of the internal representations of the movement. ⋯ Despite certain similarities with adults, especially in terms of the asymmetry of the performance times for the two tasks (STS vs. BTS) and the partial movement adaptations, the children were less able than adults to adapt both postural and movement controls to the new support conditions. Thus, it appears that the updating of internal models of action is a process that matures slowly throughout ontogenesis.
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Hydrogen sulfide (H₂S) is involved in central regulation of respiratory rhythm at the level of the medulla oblongata. The present study was carried out to test our hypothesis that H₂S exerts site-specific regulatory action on respiratory rhythm in the medulla oblongata of neonatal rats. The rhythmic discharge of hypoglossal rootlets in medullary slices of neonatal rats was recorded. 200 μM NaHS (an H₂S donor) increased burst frequency (BF) in 900-μm slices containing the pre-Bötzinger complex (preBötC), whereas it caused diphasic responses in 1200-, 1400- and 1800-μm slices containing both the preBötC and part or all of the parafacial respiratory group (pFRG): an initial decrease in BF followed by an increase. ⋯ In addition, BF was increased by a unilateral micro-injection of NaHS into the preBötC region, but was decreased by an injection into the pFRG region. These data support our hypothesis that the regulatory action of H₂S on respiratory rhythm in the medulla oblongata is site-specific. The excitatory effect is caused by the preBötC, while the inhibitory effect is from the pFRG.
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Microglial phagocytosis plays a key role in neuroprotective and neurodegenerative responses of the innate immune system in the brain. Here we investigated the regulatory function of phosphoinositide 3-kinase γ (PI3Kγ) in phagocytosis of bacteria and Zymosan particles by mouse brain microglia in vitro and in vivo. ⋯ These data suggest kinase-independent stimulation of cAMP phosphodiesterase activity by PI3Kγ as a crucial mediator of phagocytosis. In sum our findings indicate PI3Kγ-dependent suppression of cAMP signaling as a critical regulatory element of microglial phagocytosis.