Neuroscience letters
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Neuroscience letters · Jul 2015
Progesterone alleviates acute brain injury via reducing apoptosis and oxidative stress in a rat experimental subarachnoid hemorrhage model.
This study aimed to investigate the therapeutic effect of progesterone on acute brain injury after subarachnoid hemorrhage (SAH). Subarachnoid hemorrhage was induced in male Sprague-Dawley rats (n=72) by endovascular perforation. Progesterone (8 mg/kg or 16 mg/kg) was administered to rats at 1, 6, and 12h after SAH. ⋯ Progesterone treatment could alleviate acute brain injury after SAH by inhibiting cell apoptosis and decreasing damage due to oxidative stress. The mechanism involved in the anti-apoptotic effect was related to the mitochondrial pathway. These results indicate that progesterone possesses the potential to be a novel therapeutic agent for the treatment of acute brain injury after SAH.
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Neuroscience letters · Jul 2015
Spinal 5-HT1A, not the 5-HT1B or 5-HT3 receptors, mediates descending serotonergic inhibition for late-phase mechanical allodynia of carrageenan-induced peripheral inflammation.
Previous electrophysiological studies demonstrated a limited role of 5-hydroxytryptamine 3 receptor (5-HT3R), but facilitatory role of 5-HT1AR and 5-HT1BR in spinal nociceptive processing of carrageenan-induced inflammatory pain. The release of spinal 5-HT was shown to peak in early-phase and return to baseline in late-phase of carrageenan inflammation. We examined the role of the descending serotonergic projections involving 5-HT1AR, 5-HT1BR, and 5-HT3R in mechanical allodynia of early- (first 4h) and late-phase (24h after) carrageenan-induced inflammation. ⋯ Similarly, intrathecal 5-HT1AR agonist (8-OH-DPAT) attenuated the intensity of late-phase allodynia in a dose dependent fashion which was antagonized by 5-HT1AR antagonist (WAY-100635), but produced no effect on the early-phase allodynia. However, other agonists or antagonists of 5-HT1BR (CP-93129, SB-224289) and 5-HT3R (m-CPBG, ondansetron) did not produce any anti- or pro-allodynic effect in both early- and late- phase allodynia. These results suggest that spinal 5-HT1A, but not 5-HT1B or 5-HT3 receptors mediate descending serotonergic inhibition on nociceptive processing of late-phase mechanical allodynia in carrageenan-induced inflammation.
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Neuroscience letters · Jul 2015
Glycine transporter GlyT1, but not GlyT2, is expressed in rat dorsal root ganglion--Possible implications for neuropathic pain.
Glycinergic inhibitory neurotransmission plays a pivotal role in the development of neuropathic pain. The glycine concentration in the synaptic cleft is controlled by the glycine transporters GlyT1 and GlyT2. GlyT1 is expressed throughout the central nervous system, while GlyT2 is exclusively located in glycinergic neurons. ⋯ GlyT1, but not GlyT2, is expressed in the peripheral sensory nervous system. The co-expression of GlyT1 and NMDA receptors in DRG suggests that GlyT1 regulates glycine concentration at the glycine binding site of the NMDA receptor. Differential regulation of GlyT1 expression in the spinal cord or DRG, however, does not seem to be associated with the development of neuropathic pain.
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Neuroscience letters · Jul 2015
Neuroanatomical deficits correlate with executive dysfunction in boys with attention deficit hyperactivity disorder.
Previous structural imaging studies have revealed gray matter volume abnormalities to reflect the etiology of attention deficit hyperactivity disorder (ADHD), however, which are confounded by age, medication and comorbidity and also ignore the core feature of brain structure in the executive impairments of ADHD. In the present study, we explored gray matter volume abnormalities in male children and adolescents with ADHD who were drug-naive and without comorbidities, and tried to connect structural data and behavioral executive dysfunction to provide more information regarding the brain-behavior relationships in ADHD. Seventy-two male subjects (37 patients and 35 controls) underwent three-dimensional high-resolution structural magnetic resonance imaging and executive function assessments, including the Stroop Color-Word Test and Wisconsin Card Sorting Test (WCST). ⋯ In patients group, the gray matter volumes of the right orbitofrontal cortex and left posterior midcingulate cortex were positively correlated with the completed categories on the WCST, and the gray matter volume of the left posterior midcingulate cortex was negatively correlated with the total and non-perseverative errors on the WCST (P<0.05). The present findings show gray matter volume reductions in motor regions as well as the orbitofrontal and cingulate cortex; this evidence supports theories that suggest frontal abnormalities in children and adolescents with ADHD at early illness stage. The correlations between structural abnormalities and executive dysfunction suggest that neuroanatomical substrate deficits are implicated in the pathophysiology of ADHD.
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Neuroscience letters · Jul 2015
Increased autophagic activity in dorsal root ganglion attenuates neuropathic pain following peripheral nerve injury.
Autophagy is a process of cellular self-cannibalization, and provides an adaptive mechanism to protect cells against diverse pathological settings. Following peripheral nerve injury, autophagic process was changed in Schwann cells and spinal neurons and glial cells, implicating a vital role of autophagy in chronic pain. However, little is known about the role of autophagy in dorsal root ganglion (DRG) in neuropathic pain. ⋯ Injection of autophagy inducer rapamycin into L5 DRG before or after SNL dose-dependently attenuated neuropathic pain. The expression of LC3 was enhanced in L5 DRG by rapamycin. These data suggest that the autophagy in L5 DRG neurons is a defensive reaction to L5 spinal nerve injury, and pharmacological enhancement of autophagy may be a potential treatment to prevent the onset and chronification of neuropathic pain.