[A possible mechanism of dopamine-induced synergistic disinhibition of thalamic cells via "direct" and "indirect" pathways in basal ganglia].
On the basis of the mechanism of synaptic plasticity that we have earlier suggested for striatal spiny neurons and with regard to the known data about the predominance of dopamine-sensitive D1/D2 receptors on the striatonigral/striatopallidal cells it is hypothesized that the induction of the long-term potentiation/depression of the efficacy of excitatory cortical inputs to these cells can underlie the excitatory/inhibitory effect of dopamine on the activity of neurons that originate the "direct"/"indirect" pathways through the basal ganglia. Both these effects will lead to an enhancement of the activity of thalamic cells and activity of the efferent neocortical neurons excited by thalamic cells. The long-term potentiation of corticostriatal inputs to striosomal neurons, where, predominantly, D1 receptors are located, can also be induced by dopamine. This effect can be responsible of a rise of inhibition of dopaminergic cells and decrease in dopamine release by these cells. Such an event sequence can provide a stable dopamine concentration in the loop neocortex-basal ganglia-thalamus-neocortex.
Sil'kis
I G
IG
Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow.
D000818:Animals; D001479:Basal Ganglia / Q000502:physiology*; D004298:Dopamine / Q000502:physiology*; D006801:Humans; D017774:Long-Term Potentiation; D019579:Neocortex / Q000502:physiology; D009415:Nerve Net / Q000502:physiology; D009473:Neuronal Plasticity; D009474:Neurons / Q000502:physiology*; D017447:Receptors, Dopamine D1 / Q000502:physiology; D017448:Receptors, Dopamine D2 / Q000502:physiology; D013788:Thalamus / Q000166:cytology / Q000502:physiology*
D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D004298:Dopamine