Co-localization of GABA with other neuroactive substances in the basal ganglia
Section snippets
Location of neuropeptides and receptors in MSNs
Figure 1 illustrates the circuitry and cellular location of some of the major peptides and receptors that will be discussed in this review. MSNs in both patch and matrix compartments contribute to two distinct projection pathways: striatonigral and striatopallidal (Gerfen and Young, 1988). The striatonigral pathway projects from the striatum to the internal segment of the globus pallidus (rodent entopeduncular nucleus) and the substantia nigra; these neurons are distinguished by the expression
Dopamine agonists increase neuropeptide expression in MSNs
Direct and indirect dopamine agonists induce behavioral activity in rodents that is positively correlated with neuropeptide gene expression in the striatum. Induction of striatal neuropeptides, preprodynorphin (PPD), preproenkephalin (PPE), neurotensin/neuromedin N (NT), and the SP precursor, preprotachykinin (PPT) in MSNs occurs after acute or repeated administration of the psychostimulants, cocaine, amphetamine, or methamphetamine (Castel et al., 1994; Merchant et al., 1994; Smith and
Neuropeptide regulation of local striatal circuitry
It often goes unrecognized that local regulation within the striatum has a major impact on MSN output and that endogenous inhibitory or homeostatic systems also are activated by dopamine agonists. Two of the inhibitory substrates that are critical to controlling excessive dopamine and glutamate neurotransmission in the striatum are the muscarinic cholinergic (Wang and McGinty, 1996b, Wang and McGinty, 1996d, Wang and McGinty, 1997a, Wang and McGinty, 1997b, Wang and McGinty, 1998) and
Conclusion
The studies described above suggest a model for local striatal interactions when peptides are released from MSNs (Fig. 5). When dopamine stimulates D1 receptors on striatonigral MSNs, for example, SP and dynorphin are released from local collaterals. SP stimulates NK-1 receptors, predominantly expressed by cholinergic interneurons, and stimulates ACh release. Dynorphin stimulates KORs that presynaptically inhibit dopamine and glutamate release. The net effect is a local regulation of striatal
Acknowledgment
The studies from the author's laboratory were supported by NIH DA03982.
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