| Objective: glutamic acid activated peripheral type I metabolic type glutamate receptors(mGlu Rs) to inflammatory pain, but the role of type I mGlu Rs out weeks hyperalgesia mechanism remains unclear.Study found in the dorsal root ganglion(DRG) neurons, activation of type I mGlu Rs signal is sensitive to acid ion channels(ASICs) have sensitization effect, helps to acid caused by pain.DHPG is a type I mGlu Rs selective agonist, can strengthen the function of ASICs.Finally, peripheral DHPG dose dependence to aggravate the digit injection pain caused by acetic acid in rats.Methods: the separation of dorsal root ganglion neurons, first clear the connective tissue around the dorsal root ganglion, using fine spring scissors to cut up it again,then enzyme digestion, clamp pliers record by switching to the current model,stability of whole-cell voltage clamp structure formation model.Results: type I mGlu Rs agonist DHPG on primary sensory neurons have to strengthen the role of the function of ASICs activities.In acute separation of DRG neurons, DHPG strengthening ASIC current amplitude and the membrane excitability of neurons.We found that mGlu Rs especially mGlu R5 and intracellular signal mediated DHPG ASIC current to strengthen.In addition, DHPG dose dependence to aggravate the rat toes caused by injection of acetic acid pain behavioral response.Conclusion: the activation of type I mGlu Rs signals to enhance the function of ASICs activities, to reveal the role of type I mGlu Rs in hyperalgesia provides a new peripheral mechanism. |