Neuroscience
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Schedule-induced polydipsia (SIP) is an adjunctive behavior in which rats exhibit excessive drinking as a consequence of intermittent feeding, and it has been proposed as a candidate model to study the development of compulsive and repetitive behavior. Although several brain structures are involved in compulsive behavior, it has been suggested that alterations in fronto-striatal circuits may underlie compulsive spectrum disorders. In the present work, we examined whether SIP would induce modifications in dorsolateral striatum (DLS) and anterior prefrontal cortex (aPFC) neurons. ⋯ By contrast, we observed no differences either in dendritic spine density or in the morphological structure of the dendrites of the aPFC in SIP rats compared to their control counterparts. We hypothesize that SIP-induced structural plasticity in DLS neurons could be related to inflexible response in compulsive behavior. The findings of this study could provide new insights into the involvement of particular cell populations of the dorsolateral striatum and anterior prefrontal cortex regions in compulsive spectrum disorders.
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The aim of the present study was to investigate the possible role of basolateral amygdala (BLA) 5-HT1A receptors in memory formation under stress. We also examined whether the blockade of these receptors is involved in stress-induced state-dependent memory. Adult male Wistar rats received cannula implants that bilaterally targeted the BLA. ⋯ Moreover, pre-test injection of (S)-WAY-100135 (2μg/rat) that targeted the BLA inhibited the stress-induced state-dependent memory retrieval. Taken together, our findings suggest that post-training or pre-test exposure to acute stress induced the impairment of memory consolidation, retrieval and state-dependent learning. The BLA 5-HT1A receptors have a critical role in learning and memory under stress.
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Recently, the fascia innervation has become an important issue, particularly the existence of nociceptive fibers. Fascia can be a source of pain in several disorders such as fasciitis and non-specific low back pain. However, nothing is known about possible changes of the fascia innervation under pathological circumstances. ⋯ In conclusion, the inflamed TLF showed an increase of presumably nociceptive fibers, which may explain the pain from a pathologically altered fascia. The meaning of the decreased innervation by sympathetic fibers is obscure at present. The lack of proprioceptive corpuscular receptors within the TLF does not preclude its role as a proprioceptive structure, because some of the free nerve endings may function as proprioceptors.
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Whereas activation of α1-adrenoceptors (α1-ARs) modulates glutamatergic transmission, the roles of α1-ARs in GABAergic transmission in the medial prefrontal cortex (mPFC) are elusive. Here, we examined the effects of the α1-AR agonist phenylephrine (Phe) on GABAergic transmission onto pyramidal neurons in the deep layers of the mPFC. We found that bath application of Phe dose-dependently increased the amplitude of evoked IPSCs (eIPSCs). ⋯ Phe-induced depolarization is independent of extracellular Na(+), Ca(2+) and T-type calcium channels, but requires inward rectifier K(+) channels (Kirs). The present study demonstrates that Phe enhances GABAergic transmission onto mPFC pyramidal neurons through inhibiting interneurons Kirs, which further depolarizes interneurons leading to increase in Ca(2+) influx via T-type calcium channels. Our results may provide a cellular and molecular mechanism that helps explain α1-AR-induced PFC dysfunction.