Brain research
-
Higher-order processing of nociceptive input is distributed in corticolimbic regions of the brain, including the anterior cingulate, parieto-insular and prefrontal cortices, as well as subcortical structures such as the bed nucleus of stria terminalis and amygdala. In addition to their role in pain processing, these regions encode or modulate emotional, motivational and sensory responses to stress. Thus, pain and stress pathways in the brain intersect at cortical and subcortical forebrain structures. ⋯ Defeated rats exhibited a significant increase in cold preference after social defeat compared to the baseline. In the escape task, the rats exhibited increased escape from warm and nociceptive cold and heat temperatures. Thus, chronic social stress produces hyperalgesia for both hot and cold stimuli in male rats, suggesting a mutually facilitatory cross-regulation between central pathways regulating stress and pain.
-
In this study, we evaluated the expression of MCP-1 in the rat dorsal root ganglion (DRG) and spinal cord following axotomy and chronic constriction injury (CCI) of the sciatic nerve and L5 spinal nerve ligation (L5 SNL) using an immunohistochemical approach. MCP-1 expression in the DRG peaked and declined before the full onset of pain hypersensitivity following nerve injury. Spinal expression of MCP-1 peaked when mechanical allodynia was maximal, but then declined rapidly despite the remarkable persistence of mechanical allodynia. ⋯ Despite increased MCP-1 in small and large DRG neurons, a remarkable increase in MCP-1-IR terminals was observed in the spinal superficial laminae following CCI and L5SNL, but not following axotomy; however, in the deeper laminae, a considerable increase in MCP-1-IR terminals, which may originate from the large and injured L5 DRG neurons, was found after L5 SNL. Our results demonstrate that MCP-1 synthesized in DRG neurons may or may not be transported to the spinal cord depending on the type of peripheral nerve injury. Additionally, increased MCP-1 in both intact L4 and injured L5 DRG neurons may contribute to neuropathic pain hypersensitivity following L5 SNL.
-
Rehabilitation improves recovery after intracerebral hemorrhage (ICH) in rats. In some cases, brain damage is attenuated. In this study, we tested whether environmental enrichment (EE) combined with skilled reach training improves recovery and lessens brain injury after ICH in rats. ⋯ Unexpectedly, REHAB treatment lessened spontaneous use of the contralateral-to-ICH limb at 4 (p=0.045) and 6 weeks (p=0.041). In summary, the combination of EE and reach training significantly attenuates lesion volume (striatal injury) while improving skilled reaching and walking ability. These findings encourage the use of early rehabilitation therapies in patients suffering from basal ganglia hemorrhaging.
-
A subset of German function verbs can be used either in a full, concrete, 'heavy' ("take a computer") or in a more metaphorical, abstract or 'light' meaning ("take a shower", no actual 'taking' involved). The present magnetoencephalographic (MEG) study explored whether this subset of 'light' verbs is represented in distinct cortical processes. A random sequence of German 'heavy', 'light', and pseudo verbs was visually presented in three runs to 22 native German speakers, who performed lexical decision task on real versus pseudo verbs. ⋯ Thus, 'heavy' versus 'light readings' of verbs already modulate early posterior visual evoked response even when verbs are presented in isolation. This response becomes clearer in the disambiguating contextual condition. This type of study shows for the first time that language processing is sensitive to representational differences between two readings of one and the same verb stem.
-
Transient receptor potential vanilloid 1 (TRPV1) receptors are critical to nociceptive processing. Understanding how these receptors are modulated gives insight to potential therapies for pain. We demonstrate using double labeling immunohistochemistry that Group II metabotropic glutamate receptors (mGluRs) are co-expressed with TRPV1 on rat dorsal root ganglion (DRG) cells. ⋯ The data indicate that group II mGluRs and TRPV1 receptors are co-expressed on peripheral nociceptors and activation of mGluRs can inhibit painful sensory transmission following TRPV1 activation. The data are consistent with group II and TRPV1 receptors being linked intracellularly by the cAMP/PKA pathway. Peripheral group II mGluRs are important targets for drug discovery in controlling TRPV1-induced nociception.