Brain dopamine

An additional benefit of COMT inhibitors can be found in positron emission tomography (PET) studies. In PET, using 6-[18F]-fluoro-L-dopa (6-FD) to visualize the brain dopamine metabolism, the peripheral formation of 3-0-methyl-6-[18F]-fluoro-L-dopa (3-OMFD) by COMT is harmful. 3-OMFD contaminates the brain radioactivity analysed since it is easily transported like 3-OMD to the... 

Opioid receptor antagonists have been found to modulate brain dopamine-mediated behavioral and cellular functions such as motor activity, drug selfadministration, and brain stimulation reward (Koob and Bloom 1988). 

Iversen, S. Brain dopamine systems and behavior. In Iversen. L. ... 

Heffner, T.G., and Seiden, L.S. The effeet of depletion of brain dopamine by 6-hydroxydopamine on toleranee to the anorexic effect of fi -amphetamine and fenfluramine in rats. J Pharmacol Exp Ther 208 134-143, 1979. 

Shafiq-ur-Rehman. 1991. Effects of lead on the behavioral complex stereotypes and regional brain dopamine levels in rats. Arch Environ Contain Toxicol 20 527-530. 

Walsh TJ, Schulz DW, Tilson HA, et al. 1996. Acute exposure to triethyl lead enhances the behavioral effects of dopaminergic agonists Involvement of brain dopamine in organolead neurotoxicity. Brain Res 363 222-229. 

Sanchez-Gonzalez M., Garcia-Cabezas M., Rico B., Cavada C. (2005). The primate thalamus is a key target for brain dopamine. J. Neurosci 25, 6076-83. 

Gariano, R.F. and Groves, P.M., Burst firing induced in mid-brain dopamine neurons by stimulation of the medial prefrontal and anterior cingulate cortices, Brain Res., 462, 194, 1988. 

Wise, R.A., Rompre, P.P. Brain dopamine and reward, in Rosenweig, M., Porter, L., Eds. Annual Review of Psychology. Annual Review, Inc., Palo Alto, CA, 1989, 191. 

Villemagne, V., Yuan, J., Wong, D.F. et al. Brain dopamine neurotoxicity in baboons treated with doses of methamphetamine comparable to those recreationally abused by humans evidence from [llC]WIN-35,428 positron emission tomography studies and direct in vitro determinations. J. Neu-rosci. 18 419, 1998. 

Sekine, Y., Iyo, M., Ouchi, Y. et al. Methamphetamine-related psychiatric symptoms and reduced brain dopamine transporters studied with PET. Am. J. Psychiatry. 58 1206, 2001. 

Little K., McLaughlin D., Zhang L. et al. Brain dopamine transporter messenger RNA and binding sites in cocaine users. Arch. Gen. Psychiatry. 55 793, 1998. 

Seeman P (1980). Brain dopamine receptors. Pharmacological Reviews, 32, 229-313. 

A drug that specifically enhances metabolically the activity of brain dopamine is... 

It blocks reuptake of catecholamine neurotransmitters and causes a depletion of brain dopamine. 

P-hydroxylase gland, brain Dopamine + ascorbate + 02 —> noradrenaline + dehydroascorbate + H2O... 

Maisonneuve IM, Rossman KL, Keiier RW Jr, Giick SD. (1992). Acute and proionged effects of ibogaine on brain dopamine metaboiism and morphine-induced iocomotor activity in rats. Brain Res. 575(1) 69-73. 

Kehoe P, Shoemaker WJ, Arons C, Triano L, Suresh G. 1998. Repeated isolation stress in the neonatal rat relation to brain dopamine systems in the 10-day-old rat. Behav Neurosci 112(6) 1466-1474. 

Third is the presence of other psychiatric or medical disorders. This can help gnide antidepressant selection in several ways. In some cases, an antidepressant may be preferred becanse it can treat both disorders. For example, the extensive evidence that flnoxetine is an effective treatment for bnlimia nervosa makes it preferable for patients with depression and bnlimia. Similarly, the depressed Parkinson s disease patient whose nenrological illness results from a lack of dopamine in a particular area of the brain may have both her depression and her Parkinson s disease improved by bnpropion, which increases brain dopamine activity. In other cases, an antidepressant shonld be avoided if it worsens the other illness or interacts adversely with a medication needed to treat the other illness. For example, TCAs and MAOIs can complicate glncose control in diabetics and shonld not rontinely be used by depressed diabetics. (See Table 3.11.)... 

L-Dopa. Dopamine itself cannot penetrate the blood-brain barrier however, its natural precursor, L-dihydroxy-phenylalanine (levodopa), is effective in replenishing striatal dopamine levels, because it is transported across the blood-brain barrier via an amino acid carrier and is subsequently decarboxy-lated by DOPA-decarboxylase, present in striatal tissue. Decarboxylation also takes place in peripheral organs where dopamine is not needed, likely causing undesirable effects (tachycardia, arrhythmias resulting from activation of Pi-adrenoceptors [p. 114], hypotension, and vomiting). Extracerebral production of dopamine can be prevented by inhibitors of DOPA-decarboxylase (car-bidopa, benserazide) that do not penetrate the blood-brain barrier, leaving intracerebral decarboxylation unaffected. Excessive elevation of brain dopamine levels may lead to undesirable reactions, such as involuntary movements (dyskinesias) and mental disturbances. 

Monoamine oxidase exists in the human body in two molecular forms, known as type A and type B. Each of these isozymes has selective substrate and inhibitor characteristics. Neurotransmitter amines, such as norepinephrine and serotonin, are preferentially metabolized by MAO-A in the brain. MAO-B is more likely to be involved in the catabolism of human brain dopamine, although dopamine is also a substrate for MAO-A. 

Baldessarini, R.J. and Tarazi, F.I. (1996) Brain dopamine receptors a primer on their current status, basic and clinical. Harv Rev Psychiatry 3 301—325. 

S., et al. (1987) Human brain dopamine receptors in children and aging adults. Synapse 1 399-404. 

All three major brain dopamine (DA) systems (nigros-triatal, mesocortical, and mesolimbic) have been implicated in aggression in animal studies (Miczek et ah, 1994). Brain DA systems appear to be involved in (1) the rewarding or reinforcing aspects of aggression, possibly via mesolimbic and mesocortical DA systems and (2) the initiation, execution, and termination of aggressive behavior patterns, possibly via the nigrostriatal and mesolimbic DA systems. 

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