Dopamine amphetamine-induced

Most animals with small lesions and many with intermediate lesions turned left or have only a modest tendency to turn toward the side of the lesion (right side). Only animals with large lesions persist in turning toward the lesioned side. Thus amphetamine induced turning provides a functional measure of the degree to which regenerated dopamine terminals can release dopamine. Amphetamine induced rotation is therefore a better measure of the degree of functional reinnervation rather than the size of a lesion. 

In experiments with mice and squirrel monkeys, we confirmed and extended the antagonism of amphetamine-induced motor hyperactivity by naltrexone at the same time, however, amphetamine s disruption of aggressive and social behavior was not reversed by naltrexone (Winslow and Miczek, in press). Specifically, in mice, the resident s attack and threat behavior toward an intruder was even further reduced by amphetamine after naltrexone pretreatment (figure 7). Squirrel monkeys that are dominant within their social group exhibit significantly lower levels of aggressive display toward other group members and initiate fewer social interactions after amphetamine treatment naltrexone did not block these effects. The interactive effects of amphetamine and naltrexone on locomotor behavior are consistent with the proposed modulation of dopamine-mediated functions by opioids however, the interaction between amphetamine and naltrexone on social behavior appears to involve a different mechanism. 

Investigation of the neurochemical substrates for the psychostimulant effects of MDMA suggests a role for the mesolimbic dopamine system. Destruction of dopamine terminal fields in the nucleus accumbens significantly attenuated the locomotor activation produced by MDMA. A similar blockade of amphetamine-induced locomotor hyperactivity is known and was observed following amphetamine injection in these same rats. Such results support the hypothesis that at least one component of MDMA-induced hyperactivity is dopamine mediated and suggest that mesolimbic dopamine specifically is the critical substrate. In this way, MDMA resembles other classical psychostimulants like amphetamine and cocaine. Interestingly, evidence for functional cross-sensitization was suggested in the study in which an injection of amphetamine followed MDMA injection. 

Olds, M.E. Amphetamine-induced increase in motor aetivity is correlated with higher firing rates of non-dopamine neurons in substantia nigra and ventral tegmental areas. Neurosci 24 477-490, 1988. 

Wagner, G.C. Ricaurte, G.A. Johanson, C.E. Schuster, C.R. and Seiden, L.S. Amphetamine induces depletion of dopamine and loss of dopamine uptake sites in caudate. Neurology 20 547-550. 1980. 

COMMENT I would favor the view that lethargy and fatigue of postamphetamine withdrawal during the withdrawal phase would be consistent with the shutting off of the dopamine neuron. Still, it is hard to imagine how that would be. First, the amphetamine-induced release is not regulated by the autoreceptor. And, as you say, if it would be impulse related, however weak, it would be regulated. But we do know that after a period of amphetamine intoxication, an individual is supersensitive behaviorally. 

This benzylisoquinoline alkaloid inhibits in vitro the specific bonding of [3H] dopamine to dopamine receptors and abrogates amphetamine-induced circling behavior in rodents with unilateral degeneration of dopaminergic neurons in the corpus striatum (109). 

Ventura R., Cabib S., Alcaro A., Orsini C., Puglisi-AUegra S. (2003). Norepinephrine in the prefrontal cortex is critical for amphetamine-induced reward and mesoaccumbens dopamine release. J. Neurosci. 23, 1879-85. 

Kahlig, K.M., Binda, F., Khoshbouei, H., Blakely, R.D., McMahon, D.G., Javitch, J.A., and Galli, A., Amphetamine induces dopamine efflux through a dopamine transporter channel, PNAS, 102, 3495, 2005. 

Laruelle, M., Abi-Dargham, A., van Dyck, C. H. etal. Single photon emission computerized tomography imaging of amphetamine-induced dopamine release in drug-free schizophrenic subjects. Proc. Natl Acad. Sci. USA 93 9235-9240,1996. 

Breier, A., Su, T. P., Saunders, R. et al. Schizophrenia is associated with elevated amphetamine-induced synaptic dopamine concentrations evidence from a novel positron emission tomography method. Proc. Natl Acad. Sci. USA 94 2569-2574,1997. 

Villemagne, V. L., Wong, D. F., Yokoi, F. et al. GBR12909 attenuates amphetamine-induced striatal dopamine release as measured by C raclopride continuous infusion PET scans. Synapse 33 268-273,1999. 

Nolen WA, Haffmans PMJ, Bouvy PF, et al Monoamine oxidase inhibitors in resistant major depression. J Affect Disord 28 189-197, 1993 Nomikos GC, Damsma G, Wenkstern D, et al Chronic desipramine enhances amphetamine-induced increases in interstitial concentrations of dopamine in the nucleus accumbens. Eur J Pharmacol 195 63-73, 1991 Nomikos GC, Damsma D, Wenkstern D, et al Effects of chronic bupropion on interstitial concentrations of dopamine in rat nucleus accumbens and striatum. Neuropsychopharmacology 7 7-14, 1992... 

Rossetti ZL, Pani L, Kuzmin A, et al Dihydropyridine calcium antagonists prevent cocaine-, but not amphetamine-, induced dopamine release and motor activity in rats. Acta Physiol Hung 75 (suppl) 249-250, 1990 Rossetti ZL, Lai M, Hmaidan Y, et al Depletion of mesohmbic dopamine during behavioural despair partial reversal by chronic imipramine. Eur J Pharmacol 242 313-315, 1993... 

Imaging studies have shown increased amphetamine-induced striatal dopamine release, increased baseline occupancy of striatal D2 receptors by extracellular dopamine, and other measures consistent with increased striatal dopamine synthesis and release. 

Paulson, Pamela E., and Terry E. Robinson. 1995. "Amphetamine-Induced Time-Dependent Sensitization of Dopamine Neurotransmission in the Dorsal and Ventral Striatum A Microdialysis Study in Behaving Rats." Synapse 19 56-65. 

This effect is not surprising Amphetamines are potent psychomotor stimulants. Whether sniffed, swallowed, snorted, or injected, they induce feelings of power, strength, exhilaration, self-assertion, focus, and enhanced motivation. Amphetamine intake causes a release of the excitatory neurotransmitters dopamine and noradrenaline (norepinephrine) in the central nervous system (CNS). The release of dopamine typically induces a sense of aroused euphoria that may last several hours unlike cocaine, amphetamine is not readily broken down by the body. After taking amphetamines, feelings are intensified, the need to sleep or eat is diminished, and the user may feel as though he or she can take on the world. ... 

Fog JU, Khoshbouei H, Holy M, Owens WA, Vaegter CB, Sen N, Nikandrova Y, Bowton E, McMahon DG, Colbran RJ, Daws LC, Sitte HH, Javitch JA, Galli A, Gether U (2006) Calmodulin kinase II interacts with the dopamine transporter C terminus to regulate amphetamine-induced reverse transport. Neuron 51 417—429. 

Khoshbouei H, Sen N, Guptaroy B, Johnson L, Lund D, Gnegy ME, Galli A, Javitch JA (2004) N-terminal phosphorylation of the dopamine transporter is required for amphetamine-induced efflux. PLoS Biol 2 E78. 

Psychostimulant amphetamines induce the release of catecholamines, such as adrenaline and dopamine [15]. 

Dawson LA, Nguyen HQ, Li P. Potentiation of amphetamine-induced changes in dopamine and 5-HT by a 5-HT6 receptor antagonist. Brain Res Bull 2003 59 513-521. 

Breier, A., Su, T. P., Saunders, R., Carson, R. E., Kolachana, B. S., de Bartolomeis, A., Weinberger, D. R., Weisenfeld, N., Malhotra, A. K., Eckelman, W. C., Pickar, D. 1997, Schizophrenia is associated with elevated amphetamine-induced synaptic dopamine concentrations evidence from a novel positron emission tomography method, Proc.Natl.Acad.Sci.U.S.A, vol. 94, no. 6, pp. 2569-2574. 

Balia A, Sershen H, Serra M, Koneru R, Javitt DC. 2003. Subchronic continuous phencyclidine administration potentiates amphetamine-induced frontal cortex dopamine release. Neuropsychopharmacology 28 34-44. 

Kegeles LS, Abi-Dargham A, Zea-Ponce Y, Rodenhiser-Hill J, Mann JJ, et al. 2000. Modulation of amphetamine-induced striatal dopamine release by ketamine in humans Implications for schizophrenia. Biol Psychiatry 48 627-640. 

There is also preliminary data that risperidone, an atypical antipsychotic that antagonizes multiple receptor types including dopamine receptors and serotonin receptors, may affect certain ERP components. A study of chronic risperidone delivery via subcutaneous implants reported increased P20 amplitude but no effects on the N40 component. Risperidone in this study was unable to block the amphetamine-induced decreases in the P20 component, but attenuated amphetamine-induced reduction of the N40 (Siegel et al., 2004). 

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