[Mechanism of opioid and substance P-mediated modulation of cortical signal transduction through the striatum].
A mechanism of opioid and substance P-mediated modulation of a cortical signal transduction through the striatum is suggested. According to this mechanism, an activation of postsynaptic receptors, bound to Gi/0 proteins, should increase the magnitude of NMDA-dependent (NMDA-independent) LTD (LTP) of excitatory inputs and LTP (LTD) of inhibitory inputs to all types of striatal cells. An activation of postsynaptic receptors, bound to Gs or Gq/11 proteins, should oppositely modulate LTD and LTD in the same inputs. It follows from the model that the negative feedback loops can held the activity of a striatal output cells at the stable level due to recurrent activation by endogenous opioids of delta receptors on striatopallidal cells, mu and kappa receptors on striatonigral cells of striosomes and matrix, respectively, and subsequent suppression of the efficacy of corticostriatal inputs. Cholinergic interneurons, affected by enkephalin and substance P, are also involved in these feedback loops. We hypothesized that an activation of mu and delta receptors and/or inactivation of kappa receptors on striatal spiny cells might alleviate parkinsonian symptoms and recover locomotor activity.
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D000818:Animals; D003342:Corpus Striatum / Q000166:cytology / Q000378:metabolism*; D019204:GTP-Binding Proteins / Q000378:metabolism; D009294:Narcotics / Q000378:metabolism*; D009479:Neuropeptides / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D018040:Receptors, Neurokinin-1 / Q000502:physiology; D011957:Receptors, Opioid / Q000378:metabolism; D015398:Signal Transduction; D013373:Substance P / Q000378:metabolism*
D009294:Narcotics; D009479:Neuropeptides; D016194:Receptors, N-Methyl-D-Aspartate; D018040:Receptors, Neurokinin-1; D011957:Receptors, Opioid; D013373:Substance P; D019204:GTP-Binding Proteins