Behavioural brain research
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The relationship between the piriform cortex and flavor recognition memory was investigated in adult and aged rats. By using c-Fos immunohistochemistry, we assessed the piriform cortex activity induced by flavor familiarity. ⋯ Aged rats exhibited overall increased activity in the posterior, but not the anterior piriform cortex, which was not related to flavor familiarity. This suggests that the posterior piriform cortex is related to flavor recognition memory and that aging modifies its activity pattern which might underlie their slower attenuation of flavor neophobia.
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Activation of 5-HT1B receptors in the Lateral Habenula attenuates the anxiogenic effects of cocaine.
Recent work has implicated the Lateral Habenula (LHb) in the production of anxiogenic and aversive states. It is innervated by all the major monoamine neurotransmitter systems and has projections that have been shown to modulate the activity of both dopaminergic and serotonergic brain regions. Cocaine is a stimulant drug of abuse that potentiates neurotransmission in these monoamine systems and recent research suggests that the drug's behavioral effects may be related in part to its actions within the LHb. ⋯ Intra-LHb pretreatment with the 5-HT1B agonist CP 94,253 (0, 0.1, or 0.25 μg/side) attenuated the development of approach/avoidance "retreat" behaviors known to be a consequence of cocaine's dual rewarding (approach) and anxiogenic (avoidance) properties. This effect was reversed by co-administration of a selective 5-HT1B antagonist, NAS-181 (0.1 μg/side), demonstrating drug specificity at the 5-HT1B receptor. These data suggest that 5-HT1B signaling within the LHb contributes to the anxiogenic effects of cocaine.
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Total hippocampal volume has previously been shown to correlate with performance on tests for verbal episodic memory. However, there are sparse evidence on how hippocampal subfield volumes are related to verbal episodic memory in healthy adults. The present study investigated the association between volumes of separate hippocampal subfields and verbal episodic memory performance in healthy volunteers. ⋯ There were no significant correlations between right hippocampal subfields and CVLT II performance, and no significant correlation between WASI results and hippocampal subfields. The present results suggest that better verbal episodic memory measured by the CVLT II is associated with relative larger volumes of specific left CA hippocampal subfields in healthy adults. Due to the small sample size and large age-span of the participants, the present findings are preliminary and should be confirmed in larger samples.
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TBI is a significant risk factor for the development of dementia, with the interaction between structural damage from TBI and neuroinflammation potentially driving this relationship. This study investigated the early chronic post-TBI neuroinflammatory response and its relationship to both neurodegenerative pathology and functional impairment up to 3 months post-injury. Sprague-Dawley rats underwent either sham surgery or the Marmarou model of diffuse moderate-severe TBI. ⋯ In contrast, minimal pathology was evident within the hippocampus at 1 month, with only a decrease in neurofilament-light seen at 3 months post-injury. Thus, following a moderate-severe diffuse injury, the pre-frontal cortex is most vulnerable to early neuro-structural changes. While these changes are resolved at 3 months post-injury, future studies should investigate whether they re-emerge or progress to other areas, such as the hippocampus, at later time points, which could predispose individuals to the development of dementia.
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L-DOPA-induced dyskinesia (LID) is a frequent complication of chronic L-DOPA therapy in the clinical treatment of Parkinson's disease (PD). The pathogenesis of LID involves complex molecular mechanisms in the striatum. Metabolomics can shed light on striatal metabolic alterations in LID. ⋯ The results showed that the metabolic pathways of "Retrograde endocannabinoid signaling", "Phospholipase D signaling pathway", "Glycerophospholipid metabolism" and "Sphingolipid signaling", etc. were dysregulated in LID rats compared to non-LID controls. Moreover, integrated pathway analysis based on results from the present metabolomics and our previous gene expression data in LID rats further demonstrates that aberrant "Retrograde endocannabinoid signaling" pathway might be involved in the development of LID. The present results provide a new profile for the understanding of the pathological mechanism of LID.