Somatodendritic dopamine release in midbrain
Cragg SJ., Rice ME.
© 2005 Springer Science4-Business Media, Inc. All rights reserved. Midbrain dopamine (DA) neurons of the substantia nigra (SN) and adjacent ventral tegmental area (VTA) fall into two main categories of cells, which were originally classified by their anatomical location in the SN and are consequently referred to as dorsal- and ventral-tier neurons (Fallon et al, 1978). These cells can be distinguished by their morphological characteristics, including dendritic arbor, somatic size, major efferent projections, and biochemistry (Fallon et al., 1978; Gerfen et al, 1987a,b). The primary DA cell type in the SN is the ventral-tier cell, which has a large pyramidal cell body (Fig. lA) and extends dendrites laterally along the band of cell bodies in the SN pars compacta (SNc) and ventrally into the pars reticulata (SNr) (Fig. 1B,C). Smaller DA cells are also found in the dorsal tier of the SNc; these dorsal-tier cells are the predominant cell type in the adjacent VTA. Via the median forebrain bundle, DA neurons of the SNc project primarily to the dorsal striatum, whereas those of the VTA project to the nucleus accumbens (ventral striatum), as well as to prefrontal cortex and other mesolimbic structures (Fallon and Moore, 1978; Fallon et al., 1978). The nigrostriatal DA system is essential for motor facilitation by the basal ganglia, whereas the mesolimbic DA system participates in motivation, including reward. A characteristic of DA neurons in both SN and VTA is the somatodendritic release of DA (Björkland and Lindvall, 1975; Groves et al., 1975; Geffen et al., 1976; Nieoullon et al., 1977); there is evidence for release from somata (Jaffe et al., 1998) and from dendrites (Geffen et al., 1976; Rice et al., 1994). Importantly, release in the SN is exclusively somatodendritic, but that in the VTA is not: the SN receives no identified synaptic DA input or axon coUateralization (Juraska et al., 1977; Wassef et al., 1981), whereas the VTA receives DA input from its own axon collaterals, as well as minor input from DA axons from the SNc (Deutch et al., 1988; Bayer and Pickel, 1990). This review will focus primarily on studies of somatodendritic DA release in the SNc, with comparison to release in VTA, as well as to release from nigrostriatal axons in dorsal striatum. We review the methods used to study somatodendritic DA release (Section 2), its proposed functions (Section 3), the regulation of extracellular DA concentration by uptake (Section 4), proposed mechanisms of release (Section 5), and receptor regulation of release by synaptic and non-synaptic input (Section 6).