Cellular and molecular neurobiology
-
Cell. Mol. Neurobiol. · Aug 2010
Early changes of beta-Catenins and Menins in spinal cord dorsal horn after peripheral nerve injury.
Injury to the peripheral nervous system can lead to spontaneous pain, hyperalgesia and allodynia. Previous studies have shown sprouting of Abeta-fibres into lamina II of the spinal cord dorsal horn after nerve injury and the formation of new synapses by these sprouts. beta-Catenin and menin as synaptogenic factors are critically involved in synapse formation. However, the roles of beta-catenin and menin in neuropathic pain are still unclear. ⋯ However, the injury-associated increases in beta-catenins and menins levels returned to control levels at day 14. In conclusion, these results indicate that peripheral nerve injury induces upregulation of beta-catenins and menins in the dorsal horn of the spinal cord, which may contribute to the development of chronic neuropathic pain. Antagonists of these molecules may serve as new therapeutic agents.
-
Cell. Mol. Neurobiol. · Aug 2010
The roles of striatal serotonin and L -amino-acid decarboxylase on L-DOPA-induced Dyskinesia in a Hemiparkinsonian rat model.
The administration of L: -DOPA is the standard treatment for Parkinson's disease (PD). However, the symptomatic relief provided by long-term administration may be compromised by L: -DOPA-induced dyskinesia (LID) that presents as adverse fluctuations in motor responsiveness and progressive loss of motor control. In the later stages of PD, raphestriatal serotonin neurons compensate for the loss of nigrostriatal dopamine (DA) neurons by converting and releasing DA derived from exogenous L: -DOPA. ⋯ These results of this study reveal that 5-HT contributes to LID. Striatal DA positively influences LID, while 5-HT is negatively associated with LID. Finally, we suggest that by strategic modification of the serotonin system it may be possible to attenuate the adverse effects of chronic L: -DOPA therapy in PD patients.