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Locomotor stimulant

Nation JR, Liver,ore CL, Burkey RT. 1996. Chronic lead exposure attenuates sensitization to the locomotor-stimulating effects of cocaine. Drug Alcohol Dependence 41 143-149. [Pg.554]

A2aRs, or both in combination. Locomotor stimulation might also contribute to increased waking and the combination of an AjR and A R antagonist stimulates locomotion in mice, as does caffeine, and much more effectively than either antagonist alone (Kuzmin et al., 2005). [Pg.341]

Kuzmin, A., Johansson, B., Gimenez, L., Ogren, S. O. Fredholm, B. B. (2005). Combination of adenosine A(l) and A(2A) receptor blocking agents induces caffeine-like locomotor stimulation in mice. Eur. Neuropsychopharmacol. 00, 000-000. [Pg.357]

Sellings, L.H. and Clarke, P.B., Segregation of amphetamine reward and locomotor stimulation between nucleus accumbens medial shell and core, J. Neurosci., 23, 6295, 2003. [Pg.15]

Strombom, U.H. and Liedman, B., Role of dopaminergic neurotransmission in locomotor stimulation by dexamphetamine and ethanol, Psychopharmacology, 78, 271, 1982. [Pg.18]

Chiamulera, C., Epping-Jordan, M.R, Zocchi, A. et al. Reinforcing and locomotor stimulant effects of cocaine are absent in mGluR5 null mutant mice. Nat. Neurosci. 4 873, 2001. [Pg.72]

Witkin, J.M. Blockade of the locomotor stimulant effects of cocaine and methamphetamine by glutamate antagonists. Eife Sci. 53 PL405, 1993. [Pg.72]

Pudiak C., Bozarth M. L-NAME and MK-801 attenuate sensitization to the locomotor-stimulating effect of cocaine. life Sci. 53 1517, 1993. [Pg.105]

Sershen H, Harsing LG Jr, Hashim A, Lajtha A. (1992b). Ibogaine reduces amphetamine-induced locomotor stimulation in C57BL/6By mice, but stimulates locomotor activity in rats. Life Sci. 51(13) 1003-11. [Pg.550]

Sershen H, Hashim A, Harsing L, Lajtha A. (1992a). Ibogaine antagonizes cocaine-induced locomotor stimulation in mice. Life Sci. 50(15) 1079-86. [Pg.550]

Clarke PBS (1990) Dopaminergic mechanisms in the locomotor stimulant effects of nicotine, Biochem Pharmacol 40 1427-1432... [Pg.230]

As mentioned in the previous section, we have observed greater impact of nicotine on locomotor activity in female than in male rats (Kanyt et al. 1999). The psychostimulant theory of addiction also proposes that the locomotor stimulant and rewarding effects of addictive drugs have a common neuronal substrate, although there are some studies that do not support this hypothesis (Carr et al. 1988 Villegier et al. 2006). Species differences or methodological differences in the studies may underlie the discrepancies. [Pg.268]

Carr GD, PhtUips AG, et al (1988) Independence of amphetamine reward from locomotor stimulation demonstrated by conditioned place preference. Psychopharmacology 94(2) 221-226 Chaudhri N, Caggiula AR, et al (2005) Sex differences in the contribution of nicotine and non-pharmacological stimuh to nicotine setf-administration in rats. Psychopharmacology 180(2) 258-266... [Pg.285]

Nisell M, Nomikos GG, et al (1996) Condition-independent sensitization of locomotor stimulation and mesocortical dopamine release following chronic nicotine treatment in the rat. Synapse 22(4) 369-381... [Pg.288]

Experiments and data presented in this chapter demonstrate that delta opioid agonists have antidepressant-like effects in animal models used to measure antidepressant activity. The antidepressant-like effects can be separated from other behavioral effects produced by these compounds, such as locomotor stimulation, convulsions, and learning impairments. This separation lends validity to this potential target for depression by eliminating effects or sources that may produce false positives. These compounds should be tested in other models of antidepressant activity to confirm these findings in the forced swim test. [Pg.366]

In conclusion, these data may provide information about the possibility of developing classes of delta opioid agonists that demonstrate potential therapeutic effects of delta opioid agonists, but do not demonstrate convulsions and locomotor-stimulating effects. [Pg.369]

In addition to foot-licking latency, another parameter frequently measured is the latency to jumping attempts to escape from the apparatus. Jumping is less selective as analgesic parameter because it can be influenced by substances without known analgesic activity, but which cause either locomotor stimulation or sedation, for example neuroleptics. In our own procedure, with a 30 second cut-off, jumping is not reliably observed during the observation period under control conditions, and is therefore not a useful parameter. [Pg.30]

Boye SM, Grant RJ, Clarke PB (2001) Disruption of dopaminergic neurotransmission in nucleus accumbens core inhibits the locomotor stimulant effects of nicotine and D-amphetamine in rats. Neuropharmacology 40(6) 792-8O5. [Pg.376]


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See also in sourсe #XX -- [ Pg.211 , Pg.216 ]




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