Neuroscience letters
-
Neuroscience letters · Sep 2015
Relationship between cerebral sodium-glucose transporter and hyperglycemia in cerebral ischemia.
Post-ischemic hyperglycemia exacerbates the development of cerebral ischemia. To elucidate this exacerbation mechanism, we focused on sodium-glucose transporter (SGLT) as a mediator that lead hyperglycemia to cerebral ischemia. SGLT transport glucose into the cell, together with sodium ion, using the sodium concentration gradient. ⋯ Our in vitro study indicates that SGLT is not involved in neuronal cell death in non-hyperglycemic condition. We have already reported that post-ischemic hyperglycemia begins to develop at 6h after MCAO. Therefore, current our in vivo study show post-ischemic hyperglycemic condition may be necessary for the SGLT-mediated exacerbation of cerebral ischemic neuronal damage.
-
Neuroscience letters · Aug 2015
Neuropathic pain depends upon D-serine co-activation of spinal NMDA receptors in rats.
Activation of N-methyl-d-aspartate (NMDA) receptors is critical for hypersensitivity in chronic neuropathic pain. Since astroglia can regulate NMDA receptor activation by releasing the NMDA receptor co-agonist d-serine, we investigated the role of NMDA receptor and d-serine in neuropathic chronic pain. Male Wistar rats underwent right L5-L6 spinal nerve ligation or sham surgery and were tested for mechanical allodynia and hyperalgesia after 14 days. ⋯ Immunocytochemistry showed that about 70% of serine racemase, the synthesizing enzyme of d-serine, was expressed in astrocyte processes in the superficial laminae of L5 dorsal horn. Serine racemase expression was upregulated in astrocyte processes in neuropathic rats compared to sham rats. These results show that neuropathic pain depends upon glial d-serine that co-activates spinal NMDA receptors.
-
Neuroscience letters · Aug 2015
Activation of satellite glial cells in the trigeminal ganglion contributes to masseter mechanical allodynia induced by restraint stress in rats.
It is commonly accepted that psychological stress contributes to the development of chronic orofacial pain. However, the neural mechanism underlying this process has remained unclear. The present study was performed to determine the involvement of satellite glia cells (SGCs) in the trigeminal ganglion (TG) in stress-induced increases in masseter muscle allodynia in rats. ⋯ In addition, LAA or interleukin-1 receptor antagonist (IL-1ra) administration into the TG could significantly attenuate the mechanical masseter allodynia and overexpression of SP in the TG induced by restraint stress. These results suggest that SGC activation in the TG may play a role in masseter allodynia induced by restraint stress. The over-release of IL-1β and excessive IL1-RI expressions have close relationship with the stress induced masseter allodynia.
-
Neuroscience letters · Aug 2015
Leptin dependent changes in the expression of tropomyosin receptor kinase B protein in nucleus of the solitary tract to acute intermittent hypoxia.
To investigate the possibility that leptin exerts an effect in NTS by inducing changes in the expression of pre- and/or post-synaptic proteins, experiments were done in Sprague-Dawley wild-type rats (WT) rats and leptin-deficient rats (Lep(Δ151/Δ151); KILO rat) exposed to 8h of continuous intermittent hypoxia (IH) or normoxia. Protein was extracted from the caudal medial NTS and analyzed by western blot for the expression of brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB), synaptophysin, synaptopodin and growth-associated protein-43 (GAP-43). In WT rats, BDNF and GAP 43 protein expression levels were not altered after IH or normoxia, although there was a trend towards an increase in BDNF expression. ⋯ However, synaptophysin was lower in the IH exposed KILO rat compared to normoxic controls, as found in the WT rat. Expression of synaptopodin was not detected in NTS in either IH or normoxic animals of all groups. These results suggest that leptin released during IH may contribute to neurotrophic changes occurring within NTS and that these changes may be associated with altered chemoreceptor reflex function.
-
Neuroscience letters · Aug 2015
Antihyperalgesic effect of duloxetine and amitriptyline in rats after peripheral nerve injury: Influence of descending noradrenergic plasticity.
Antidepressants such as serotonin-noradrenaline reuptake inhibitors (SNRIs) and tricyclic antidepressants (TCAs) are frequently used for the management of neuropathic pain. Noradrenaline (NA) and serotonin (5-HT) increase in the spinal cord by reuptake inhibition is considered to be main mechanism of the therapeutic effect of antidepressants in neuropathic pain. In the present study, we examined the analgesic effects of duloxetine (SNRI) and amitriptyline (TCA) in a rat model of neuropathic pain induced by spinal nerve ligation (SNL). ⋯ Although the NA content in SNL rats 2 weeks after ligation was higher than that in SNL rats 4 weeks after ligation, the analgesic efficacy of duloxetine and amitriptyline was similar between two groups. The present study suggests that NA/5-HT increase in the spinal cord is crucial in the antihyperalgesic effect of duloxetine and amitriptyline. The plastic change of the descending noradrenergic system does not obviously affect the analgesic efficacy of duloxetine and amitriptyline.