The Striatum and Pain Modulation

Abstract

The aim of this review was to give a general aspect of the sensorial function of the striatum related to pain modulation, which was intensively studied in our laboratory. We analyse the effect of electrical and chemical stimulation of the striatum on the orofacial pain, especially that produced by tooth pulp stimulation of the lower incisors. We demonstrated specific sites within the nucleus which electrical or chemical stimulation produced inhibition of the nociceptive jaw opening reflex. This analgesic action of the striatum was mediated by activation of its dopamine D(2) receptors and transmitted through the indirect pathways of the basal ganglia and the medullary dorsal reticular nucleus (RVM) to the sensorial nuclei of the trigeminal nerve. Its mechanism of action was by inhibition of the nociceptive response of the second order neurons of the nucleus caudalis of the V par.

Novel endogenous N-acyl amides activate TRPV1-4 receptors, BV-2 microglia, and are regulated in brain in an acute model of inflammation

“…Both the striatum and hippocampus have been heavily implicated as CNS regions involved in pain processing and perception (Malow and Olson, 1981; Mcewen, 2001; Ploghaus et al, 2001; Ferre et al, 2009; Barcelo et al, 2012), and our study confirms that there are changes in the production of these putative N -acyl amide signaling molecules in the striatum and hippocampus due to inflammatory pain. However, one of the major limitations of this study is the heterogeneity of these brain areas.…”

Dorsal striatum metabotropic glutamate receptor 8 affects nocifensive responses and rostral ventromedial medulla cell activity in neuropathic pain conditions

“…Thus the DRt is strategically positioned among the extrapyramidal and pain descending systems, indicating a possible involvement in the motor reaction to pain. It has been also recently reported that RVM mediates the analgesic action of the striatum: lesion of RVM blocked the inhibition control of striatum on orofacial pain (Barceló et al 2012). Evidence that stimulation of striatum leads to pain reflex inhibition (Belforte et al 2001) through RVM, however, has been scarcely investigated so far (Barceló et al 2012).…”

“…It has been also recently reported that RVM mediates the analgesic action of the striatum: lesion of RVM blocked the inhibition control of striatum on orofacial pain (Barceló et al 2012). Evidence that stimulation of striatum leads to pain reflex inhibition (Belforte et al 2001) through RVM, however, has been scarcely investigated so far (Barceló et al 2012). Within the RVM, ON cells are activated by nociceptive stimuli and have a pain facilitatory effect (Fields et al 1983), whereas OFF cells are inactivated and have an inhibitory effect on nociception (Fields et al 1983(Fields et al , 2006Heinricher and Tortorici 1994;Kincaid et al 2006;Neubert et al 2004).…”

“…In particular, group III mGluRs have been reported to be expressed in the striatum at the presynaptic level on excitatory corticostriatal terminals and GABAergic output fibers (Corti et al 2002;Kosinski et al 1999;Testa et al 1994Testa et al , 1998. Moreover, previous studies demonstrated that RVM could mediate the action of the striatum; indeed, electrolytic or kainic acid lesion of RVM blocked the inhibition of the nocifensive reflex produced by striatal activation in a model of orofacial pain (Barceló et al 2012).…”

“…There is accumulating evidence indicating that the dorsal striatum (DS), the main input of the basal ganglia, might play a role in pain processing (Barceló et al 2012). In situ hybridization and immunohistochemistry studies have demonstrated the expression of mGluRs at different levels of the DS (Ferraguti and Shigemoto 2006; Testa et al 1994;Wang et al 1997).…”