PubMed · 10422164
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P Carli, O Gisserot, S Marlier, J F Paris. 1999. [Exasperating hematomas].. https://doi.org/10.1016/s0248-8663(99)80459-7
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Using real-time voltammetry, we compared the effects of cocaine (1.0, 3.0, or 10 microM), WIN 35428 (0.1, 0.5, or 2.0 microM), and nomifensine (0.2, 1.0, or 5.0 microM) on electrically evoked dopamine release and uptake in the rat accumbens slice. The time course for onset and offset of the drug effects were determined by perfusing single drug concentration for 30 min, followed by a 60-min washout. Cocaine elicited a rapid, concentration-independent increase in dopamine release and a more gradual, concentration-dependent inhibition of uptake. During washout, uptake inhibition rapidly abated to near baseline values. During the same period, the potentiation of dopamine release exhibited a slower offset for all concentrations and, for 10 microM cocaine, was even greater than that observed during drug perfusion ("rebound" increase). The release rebound was not observed during continuous 90-min perfusion, verifying that cocaine washout per se was a sufficient condition. Selective D1 or D2 antagonists (0.5 microM SCH 39166 or 2 microM sulpiride, respectively) were without effect on cocaine-induced release alterations. WIN 35428 and nomifensine induced similar changes in dopamine kinetics during perfusion. However, in contrast to cocaine, no consistent release rebound was observed during their washout. For 2 microM WIN 38425, washout and continuous perfusion groups exhibited similar changes in dopamine release and uptake. The time-course mismatch between uptake inhibition and DA release potentiation as well as release rebound during washout suggests that altered dopamine release might play a role in behavioral effects of cocaine.
The noradrenergic system is involved in the regulation of many physiological and psychological processes, including the modulation of mood. The alpha(2)-adrenergic receptors (alpha(2)-ARs) modulate norepinephrine release, as well as the release of serotonin and other neurotransmitters, and are therefore potential targets for antidepressant and anxiolytic drug development. The current studies were undertaken to examine the role of the alpha(2A) subtype of alpha(2)-AR in mouse behavioral models of depression and anxiety. We have observed that the genetic knock-out of the alpha(2A)-AR makes mice less active in a modified version of Porsolt's forced swim test and insensitive to the antidepressant effects of the tricyclic drug imipramine in this paradigm. Furthermore, alpha(2A)-AR knock-out mice appear more anxious than wild-type C57 Bl/6 mice in the rearing and light-dark models of anxiety after injection stress. These findings suggest that the alpha(2A)-AR may play a protective role in some forms of depression and anxiety and that the antidepressant effects of imipramine may be mediated by the alpha(2A)-AR.
A single administration of a low (0.5 mg/kg) or high (10 mg/kg) dose of methamphetamine (METH) significantly altered the met-enkephalin (M-Enk) systems associated with some, but not all, limbic structures examined. Neither treatment influenced M-Enk levels 3 h after drug exposure in any limbic region studied; however, 12 h after drug administration, 0.5 mg/kg of METH reduced the tissue content of this peptide in both the nucleus accumbens shell (NAs) and the frontal cortex (FrCx). This was similar to the effect of this treatment on the anterior striatal region. In contrast, the high dose of METH increased M-Enk content in the frontal cortex and anterior striatum (AS), but had no effect in the nucleus accumbens shell. By 24 h, the effects of METH in the anterior striatum subsided, but decreases in M-Enk levels were still observed after both the low- and the high-dose METH treatments in the nucleus accumbens shell. The levels of M-Enk were not changed at any of the time points examined in the core of the nucleus accumbens (NAc). In general, treatment with a low or high dose of METH causes distinct and regional selective changes in the tissue levels of M-Enk in the limbic system. These changes appear to be mediated by dopamine (DA) D(2) and D(1) receptor activation.