Dopamine inducement

Figure 7.7 Dopamine-induced rotation in the rat in which one (left) nigrostriatal dopamine pathway from the substantia nigra (SN) to the caudate putamen (CP) has been lesioned by a prior injection (14 days) of 6-hydroxydopamine. Amphetamine, an indirectly acting amine, releases DA and so can only act on the right side. Since the animal moves away from the dominating active side it induces ipsilateral rotation (i.e. towards the lesioned side). By contrast, the development of postS5maptic supersensitivity to DA on the lesioned side ensures that apomorphine, a directly acting agonist, is actually more active on that side and so the animal turns away from it (contralateral rotation)...

Calabresi, P, Mercuri, N, Stanzione, P, Stefani, A and Bernard, G (1987) Intracellular studies on the dopamine-induced firing inhibition of neostriatal neurons in vivo evidence for Di receptor involvement. Neurosciences 20 757-771. 

Fessler, R.G. Sturgeon, R. and Meltzer, H.Y. Phencyclidine-induced iosilateral rotation in rats with unilateral 6-hydroxy-dopamine-induced lesions of the substantia nigra. I ife Sci 24 1281-1288, 1979. 

In horizontal cells of turtle and fish retinae, a dopamine-induced increase in intracellular cAMP levels is associated with cellular uncoupling [DeVries and Schwartz, 1989 McMahon et al., 1989] (the connexin isoform involved is not identified). Inhibition of phosphodiesterase with IBMX after stimulation of adenylate cyclase using forskolin resulted in an increase in intracellular... 

GSH protects human neuronal cells from dopamine-induced apoptosis. The role of GSH and other antioxidants in dopamine-induced apoptosis in cultures of the human neuronal cell line has been studied. Apoptosis, induced by 0.1 to 0.3 mM dopamine, was blocked by GSH in a dose- and time-dependent manner. This was observed by monitoring cell morphology, cell viability, and the... 

Tubocurine In isolated rabbit ear artery, antagonized dopamine-induced inhibition of adrenergic neurotransmission 649... 

Srinivasan J, Schmidt WJ (2004b) Treatment with alpha2-adrenoceptor antagonist, 2-methoxy idazoxan, protects 6-hydroxy dopamine-induced Parkinsonian symptoms in rats neurochemical and behavioral evidence. Behav. Brain Res. 154 353-363. 

The dopamine-stimulated formation of cAMP may initiate the dopamine-induced release of IR-PTH. A linear relationship exists between the dopamine-induced release of IR-PTH and the logarithm of the dopamine-induced accumulation of cAMP (17). Similarly, other agents increasing cAMP accumulation and IR-PTH release (e.g. beta-adrenergic agonists, secretin and phosphodiesterase inhibitors, also display such a log-linear relationship. Additional support for the possibility that intracellular cAMP might initiate PTH secretion comes from the observations that cholera toxin (JJ.), phosphodiesterase inhibitors (17) and dibutyryl cAMP (18), agents known to increase intracellular cAMP or mimic the biochemical effects of cAMP, increase the release of IR-PTH. 

Dopamine induces biochemical and physiological effects in the mammalian neostriatum. The occurrence of a D-l dopamine receptor (in the classification scheme of Kebabian and Caine) accounts for the ability of dopamine to enhance cyclic AMP formation. The occurrence of a D-2 dopamine receptor accounts for the ability of dopamine to inhibit cyclic AMP formation brought about by stimulation of a D-l dopamine receptor. Dopamine receptors mediate the regulation of (1) the release or turnover of acetylcholine (postsynaptic dopamine receptor) and (2) the release or turnover of dopar mine (presynaptic autoreceptor). Both receptors can be classified as D-2 dopamine receptors. Indications for the occurrence of dopamine receptors affecting the release or turnover of GABA, glutamate, serotonin and several neuropeptides are evaluated. 

The required properties of such an agent Included (1) selectivity for peripheral vascular dopaminergic receptors versus < -and 6-adrenerglc receptors which could mediate pressor and cardiac effects, (2) absence of central dopaminergic and emetic effects, and (3) potent oral renal vasodilator effects. Dopamine has been associated with diuresis and natriuresls. Possible mechanisms include a direct tubular effect on sodium transport, indirect effects produced by changes in total or regional renal blood flow, or effects resulting from a dopamine Induced decrease in aldosterone release from the adrenal (9). Since diuretics play a key role in antihypertensive therapy, the addition of a natriuretic/diuretic component to the renal vasodilator profile would be valuable and appeared to be feasible. 

Daily, D., Vlamis-Gardikas, A., Offen, D., Mittelman, L., Melamed, E., Holmgren, A., and Barzilai, A. 2001a. Glutaredoxin protects cerebellar granule neurons from dopamine-induced apoptosis by dual activation of the ras-phosphoinositide 3-kinase and jun N-terminal kinase pathways. J. Biol. Chem. 276 21618-21626. 

Grima G, Benz B, Parpura V, Cuenod M, Do KQ. 2003. Dopamine-induced oxidative stress in neurons with glutathione deficit Implication for schizophrenia. Schizophr... 

Hoyt KR, Reynolds IJ, Hastings TG. 1997. Mechanisms of dopamine-induced cell death in cultured rat forebrain neurons Interactions with and differences from glutamate-induced cell death. Exp Neurology 143 269-281. 

It was later found that some effects of dopamine did not involve stimulation of adenylyl cyclase. Particularly, in the pituitary gland, dopamine was found to inhibit prolactin release without stimulating adenylyl cyclase activity and even by inhibiting it (Spano et al., 1978 De Camilli et al., 1979). Moreover, the antipsychotic drug sulpiride blocked the dopamine-induced release of prolactin in the pituitary gland but was unable to antagonize the dopamine response on adenylyl cyclase activity in the striatum (Trabucchi et al., 1975). These observations led to the hypothesis that the dopamine receptors exist as two... 

Brami-Cherrier K, Valjent E, Garcia M, Pages C, Hipskind RA, Caboche J (2002) Dopamine induces a PI3-kinase-independent activation of Akt in striatal neurons a new route to cAMP response element-binding protein phosphorylation. J Neurosci 22 8911-8921. 

Cole DG, Kobierski LA, Konradi C, Hyman SE (1994) 6-Hydroxydopamine lesions of rat substantia nigra up-regulate dopamine-induced phosphorylation of the cAMP-response element-binding protein in striatal neurons. Proc Natl Acad Sci USA 97 9631-9635. 

Konradi C, Leveque JC, Hyman SE (1996) Amphetamine and dopamine-induced immediate early gene expression in striatal neurons depends on postsynaptic NMDA receptors and calcium. J Neurosci 76 4231-4239. 

Rodrigues Pdos S, Dowling JE (1990) Dopamine induces neurite retraction in retinal horizontal cells via diacylglycerol and protein kinase C. Proc Natl Acad Sci USA 87 9693-9697. 

Ungerstedt U (1968) 6-Hydroxy-dopamine induced degeneration of central monoamine neurons. Eur J Pharmacol 5 107-110. 

The mechanism of action and chnical use of domperidone and its specific use in diabetic gastroparesis have been reviewed (5,6). Domperidone is generally well tolerated and has a low incidence of adverse effects. Adverse effects after oral administration include headache, dry mouth, diarrhea, itching, muscle cramps, and anxiety. Galactorrhea, breast tenderness, and pseudopregnancy can occur in women because of a dopamine-induced increase in serum prolactin concentration. 

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