Dopamine cells types

Figure 4. DDC (A), serotonin (B), and tyrosine hydroxylase (C) immunore-activity in the posterior region of a wild-type Drosophila ventral ganglion. Tyrosine hydroxylase (TH) encodes the rate-limiting step in dopamine biosynthesis and is a marker for dopamine cells. B and C are the same CNS assayed for both serotonin and TH. M, medial dopamine neurons VL, ventrolateral serotonin neurons DL, dorsolateral dopamine neurons. Short unmarked arrows in C show vacuolated cells that do not contain DDC immunoreactivity. The immunoreactivity in these cells may represent a nonspecific cross-reactivity of the rat TH antibody. The length bar in A is 50 pM. The images are confocal projections generated on a Molecular Dynamics-2000 confocal laser scanning microscope.

Figure 4 shows confocal images of the staining pattern for DDC (Fig. 4A), serotonin (Fig. 4B), and TH (Fig. 4C) in the segmental ventral ganglion of the CNS from third instar larvae. Panels B and C are the same CNS double stained with serotonin and TH. The DDC-expressing cells can be categorized into a set of paired ventral lateral serotonin cells (Fig. 4A,B labeled VL in 4A), and two morphologically distinct types of dopamine cells, the medial dopamine cells (Fig. 4A,C labeled M) and the dorsal-lateral dopamine cells (Fig. 4A,C labeled DL). Figure 4 demonstrates clearly that individual DDC cells synthesize either serotonin or dopamine, but not both. One additional set of cells shows TH immunoreactivity in the ventral ganglion. These six large vacuolated cells are located more laterally than any other DDC cells (Fig. 4C, unlabeled short arrows). It is likely that the immunoreactivity in these cells results from a non-specific cross-reaction, since these cells are not...

Whereas inhibitors 1 and 2 and NIPP1 appear to be widely distributed in mammalian tissues, including brain, DARPP-32 shows a much more restricted distribution. The protein is enriched in discrete populations of neurons in the brain, most prominently those that express Dl-dopamine receptors (see Chs 12,46 and 54). Some neuronal cell types thus appear to contain unique species of phosphatase inhibitor proteins. The critical role played by these proteins in neuronal function is illustrated below. 

Other protein kinases may indirectly influence the activation of NF-kappap. For example, in contrast to the pro-inflammatory effects typically observed with activation of kinases, the elevation ofcAMP activates PKA and blocks transcription of iNOS mRNA [51,178, 229, 230]. Astrocytes contain a variety of NT receptors that are coupled to Gs-adenylate cyclase [231] and, either activation of P-adrenergic/dopamine receptors or employing agents that increase cAMP, such as forskolin (adenylate cyclase activator), PDE inhibitors [i.e. pentoxifylline], dibutyrl cAMP, or 8-bromo cAMP can attenuate lipopolysaccharide (LPS)/cytokine activated iNOS mRNA in microglia, astrocytes and a number of other cell types [51,176,177,178, 232-237]. In contrast, agents that suppress the intracellular concentration of cAM P such as H-89 and Rp-cAM P are pro-... 

Monoamine oxidase A (MAOA) oxidizes 5-HT, norepinephrine as well as dopamine, and is expressed in a cell type-specific manner. Abnormalities in... 

The first generation of antidepressants, MAO (monoamine oxidase) inhibitors, inhibited neurotransmitter degradation by inhibiting monoamine deoxidase, a flavin containing enzyme, found in the mitochondria of neurons and other cell types, that oxidatively deaminates naturally occurring sympathomimetic monoamines, such as norepinephrine, dopamine, and serotonin within the presynapse. In 1952, isoniazid and its isopropyl derivative, iproniazid (1), were developed for the treatment of tuberculosis, where it was subsequently found that these agents had a mood enhancing effect on... 

In other cell types, guanine nucleotides interact with a guanine nucleotide subunit (G- or Ng-subunit) to translate receptor stimulation into increased adenylate cyclase activity (12.) Cholera toxin inhibits a specific GTPase on this guanine nucleotide subunit and thereby increases adenylate cyclase activity (13.). In dispersed cells from the bovine parathyroid gland, cholera toxin markedly increases cAMP formation and causes a 3 to 10-fold increase in the apparent affinity cf dopamine for its receptor (as determined by cAMP accumulation or IR-PTH secretion (J y.). The effects of guanine nucleotides and cholera toxin on cAMP accumulation in parathyroid cells result from interactions with the guanine nucleotide subunit in this cell. 

There is a potentially simple reason why dysbindin-1 exerts an inhibitory effect on dopamine release by PC-12 cells, but an excitatory effect on glutamate release by cerebrocortical neurons. Knockdown of dysbindin-1 in these two cell types leads to opposite effects on SNAP-25, which is a critical t-SNARE as noted above. Knockdown of dysbindin-1 raises SNAP-25 in PC-12 cells (Kumamoto et al., 2006), but lowers SNAP-25 in cerebrocortical neurons (Numakawa et al., 2004). 

So far the discussion of firing patterns of the cells have been restricted to those seen in the most common preparations but the function of dopamine is surely best studied in conscious animals able to move and respond to external cues. In the past decade such recordings have begun to paint a very intriguing picture of the role of dopamine cells in animal behavior. Early studies of this type had been disappointing from the point of view of the involvement of dopamine cells in motor behavior. In cats (Trulson and Jacobs, 1979 Trulson, 1985) and monkeys (Schultz, 1986) it seemed that the dopamine cells were not responsive to the present behavior of the animal. Few, if any, the cells responded either to the movements in a motor task or to the sensory cues guiding the behavior. 

Lacey MG, Mercuri NB, North RA (1989) Two cell types in rat substantia nigra zona compacta distinguished by membrane properties and the actions of dopamine and opioids. J Neurosci 9 1233-1241. 

ATP has been implicated as a neurotransmitter in the peripheral chemoreceptors as a result of hypoxic (Prasad et al., 2001 Buttigieg and Nurse, 2004) and CO2/PH stimulation (Zhang and Nurse, 2004). ATP was presumed to be costored with other classical transmitters (e.g., ACh, dopamine, 5-HT, and GABA in the synaptic vesicles in the chemoreceptor cells (type 1 cells) of the carotid body) (Gonzalez et al., 1994 Zhang et al., 2000). More recently, a direct stimulus-evoked ATP release from the type-1 cells has been demonstrated (Buttigieg and Nurse, 2004), and this release was dependent on extracellular Ca via mainly L-type Ca + channels, blocked by nifedipine (50 pm) and cadmium (50 pm). 

When monkeys were exposed to MPTP they showed similar symptoms to the human victims. Furthermore, it was found that MPTP caused destruction of dopamine cell bodies in the substantia nigra of the brain. Although this example is similar to 6-hyroxydopamine, it also illustrates other important factors which determine the target organ and particular cell type which is affected by the toxicity. 

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