Behavioural brain research
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Hydrocodone (HYD) is one of the most widely prescribed opioid analgesic drugs. Several neurotransmitters are involved in opioids relapse. Among these neurotransmitters, glutamate is suggested to be involved in opioid dependence and relapse. ⋯ HYD exposure downregulated xCT expression in the nucleus accumbens and hippocampus, but no effects were observed in the dorsomedial prefrontal cortex and amygdala. Importantly, CEF treatment attenuated the reinstatement effect of HYD and normalized xCT expression in the affected brain regions. These findings demonstrate that the attenuating effect of HYD reinstatement with CEF might be mediated through xCT.
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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.
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Cortical electrical stimulation (CES) has shown to be an effective therapeutic alternative for neuropathic pain refractory to pharmacological treatment. The primary motor cortex(M1) was the main cortical target used in the vast majority of both invasive and non-invasive studies. Despite positive results M1-based approaches still fail to relieve pain in a significant proportion of individuals. ⋯ Pharmacological blockade of μ-opioid (MOR) or type 1-cannabinoid receptors (CB1R) abolished ESI-induced antinociceptive effects. Evaluation of CB1R and MOR spatial expression demonstrated differential modulation of CB1R and MOR in the periaqueductal gray matter (PAG) of ESI-treated rats in sub-areas involved in pain processing/modulation. These results indicate that ESI induces antinociception by functionally modulating opioid and cannabinoid systems in the PAG pain circuitry in rats with experimentally induced neuropathic pain.
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Stressful events during gestation can have sex-specific effects on brain and behaviour, and may contribute to some of the differences observed in adult stress responding and psychopathology. We investigated the impact of a novel repeated prenatal psychological stress (prenatal predator exposure - PPS) during the last week of gestation in rats on offspring behaviours related to social interaction (play behaviour), open field test (OFT), forced swim test (FST) and sucrose preference test (SP) during the juvenile period and in adulthood. We further examined the role of postnatal environmental, using an enhanced housing condition (EHC), to prevent/rescue any changes. ⋯ Contrary to this, EHC had few independent effects; most were apparent only when combined with PPS. In keeping with age-group differences, juvenile behaviours did not necessarily predict the same adult behaviours although juvenile OFT rearing and freezing, and juvenile FST immobility did predict adult FST immobility and sucrose preference, suggesting that some aspects of depressive behaviours may emerge early and predict adult vulnerability or coping behaviours. Together, these results suggest an important, though complex, role for early life psychological stressors and early life behaviours in creating an adult vulnerability to anxiety or depressive disorders and that environmental factors further modulate the effects of the prenatal stressors.
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Comparative Study
Intermittent intense exercise protects against cognitive decline in a similar manner to moderate exercise in chronically stressed mice.
It is well known that regular low or mild exercise helps to improve and maintain cognition. On the other hand, ever thought many people prefer high-intensity exercise (e.g., running, swimming, biking, soccer, basketball, etc.) to get rid of stress or improve their health, the previous studies reported that intense exercise either impairs cognition or has no effect on cognitive function. However, we previously showed that intermittent intense exercise prevents stress-induced depressive behavior in mice in a similar manner to moderate exercise. ⋯ Chronic stress decreased cognition, and newborn cell survival and blood vessel density in the hippocampus. However, both regular intense and moderate exercise prevented decrease of cognition, improved newborn cell survival and blood vessel density. These findings suggest that intermittent intense exercise may protect against decrease of cognition in a similar manner to moderate exercise and that both exercise-induced protection of decrease of cognition is closely related to newborn cell survival and angiogenesis in the hippocampus.