Concurrent activation of the somatosensory forebrain and deactivation of periaqueductal gray associated with diabetes-induced neuropathic pain
| Autor: | John W. Wiley, Pamela E. Paulson, Thomas J. Morrow |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Male
medicine.medical_specialty Habenular nuclei Diabetic neuropathy endocrine system diseases Somatosensory system Amygdala Periaqueductal gray Article Diabetes Mellitus Experimental Rats Sprague-Dawley Prosencephalon Technetium Tc 99m Exametazime Diabetic Neuropathies Developmental Neuroscience Internal medicine Reaction Time medicine Animals Periaqueductal Gray Habenula Behavior Animal Secondary somatosensory cortex business.industry Brain nutritional and metabolic diseases Somatosensory Cortex medicine.disease Rats medicine.anatomical_structure Endocrinology Neurology Cerebrovascular Circulation Hyperglycemia Thalamic Nuclei Anesthesia Neuropathic pain Neuralgia Radiopharmaceuticals business Basolateral amygdala |
| Zdroj: | Experimental Neurology. 208:305-313 |
| ISSN: | 0014-4886 |
| DOI: | 10.1016/j.expneurol.2007.09.001 |
| Popis: | We combined behavioral testing with brain imaging using 99mTc-HMPAO (Amersham Health), to identify CNS structures reflecting alterations in pain perception in the streptozotocin (STZ) model of Type 1 diabetes. We induced diabetic hyperglycemia (blood glucose >300 mg/dl) by injecting male Sprague-Dawley rats with STZ (45 mg/kg i.p.). Four weeks after STZ, diabetic rats exhibited behaviors indicative of neuropathic pain (hypersensitivity thermal stimuli) and this hypersensitivity persisted for up to six weeks. Imaging data in STZ-diabetic rats revealed significant increases in the activation of brain regions involved in pain processing after six weeks duration of diabetes. These regions included secondary somatosensory cortex, ventrobasal thalamic nuclei and the basolateral amygdala. In contrast, the activation in habenular nuclei and the midbrain periaqueductal gray were markedly decreased in STZ rats. These data suggest that pain in diabetic neuropathy may be due in part to hyperactivity in somatosensory structures coupled with a concurrent deactivation of structures mediating antinociception. |
| Databáze: | OpenAIRE |
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