Substantia nigra input

D2 Mostly in striatum, nucleus accumbens and olfactory tubercle but also on neuron cell bodies in substantia nigra and ventral tegmentum where they are the autoreceptors for locally (dendritic) released DA. The loss of specific D2 antagonist binding in the striatum after lesions of the afferent nigro-striatal tract indicates their presynaptic autoreceptor role on terminals there. Other lesion studies have also established D2 receptors on other inputs such as the cortico striatal tract. 

As competitive inhibitors of postsynaptic D2 receptors, neuroleptics decrease dopaminergic input from the substantia nigra and ventral tegmental area into the basal ganglia. 

SSRIs reduce dopamine cell firing in the substantia nigra through their effects on serotonin input to this nucleus. The net result is that they can cause generally mild extrapyramidal side effects (EPS) (500). The most common are restlessness and tremors. The same mechanism is probably responsible for their interaction with other agents that affect central motor systems. Thus, the SSRIs can potentiate the tremor seen with lithium, as well as EPS caused by antipsychotics, bupropion, and psychostimulants (376, 500). 

Stanford IM, Lacey MG. Differential actions of serotonin, mediated by 5-HT1B and 5-HT2C receptors, on GABA-mediated synaptic input to rat substantia nigra pars reticulata neurons in vitro. J Neurosci 1996 16 7566-7573. 

Bolam JP, Francis CM, Henderson Z. 1991. Cholinergic input to dopaminergic neurons in the substantia nigra A double immunocytochemical study. Neuroscience 41 483-494. 

The pedunculopomtine nucleus (PPN) is reciprocally connected to the BG. It input is from the globus pallidus interna, substantia nigra pars reticulata, and STN. Its output is glutamatergic to STN, GPOi, and SNC. It has been reported that in PD about 50% of its intrinsic cholinergic neurons are lost. Combined deep brain... 

Adrenergic variability may be a neurochemical cause of blepharospasm. Decreased norepinephrine levels have been identified in the hypothalamus, mamillary bodies, and locus ceruleus, whereas increased norepinephrine levels have been identified in the dorsal raphe nucleus, red nucleus, substantia nigra, and thalamus. A neurochemical abnormality, if it exists, appears to result from a loss of inhibitory adrenergic input to the locus ceruleus, which supplies information to the cortex, brainstem, and spinal cord, resulting in adrenergic excess at the distal sites. This neurochemical abnormality may be genetically identifiable in 33% of patients. 

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