The effect of denervation of the locus coeruleus projections with N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) on cocaine-induced locomotion and place preference in rats.

The potential contribution of locus coeruleus (LC)-derived noradrenaline (NA) in the motor activating and rewarding effects of cocaine (15 mg/kg) were assessed following administration of the neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4). In Experiment 1, administration of 10 mg/kg of DSP-4 similarly to substantial denervation with 50 mg/kg of DSP-4 significantly attenuated the activating effects of cocaine during the first cocaine-paired training session (30 min) in the conditioned place preference (CPP) apparatus. Only administration of the higher dose (50 mg/kg) of DSP-4 attenuated line crossings during the last training, while both doses reduced rearings.

Denervation of the locus coeruleus projections by treatment with the selective neurotoxin DSP-4 [N (2-chloroethyl)-N-ethyl-2-bromobenzylamine] reduces dopamine release potential in the nucleus accumbens shell in conscious rats.

Pretreatment with DSP-4, a neurotoxin highly selective for the locus coeruleus (LC) noradrenergic projections, 2 weeks before in vivo microdialysis in conscious rats had no effect on baseline extracellular dopamine (DA) levels in the nucleus accumbens shell, but reduced dose-dependently the dopamine response to depolarisation induced by 50 mM KCl. DA metabolism in the frontal cortex, as measured ex vivo, was increased in animals treated with a low (10 mg/kg) but not with a high dose (50 mg/kg) of DSP-4, possibly indicating an increased sensitivity to stress in these animals and thus suggesting differential regulation of DA in the forebrain by the LC lesions. The reduced DA release potential in the nucleus accumbens after DSP-4 treatment suggests that weakening of the LC input to DA nerve cells contributes to motivational deficits.

Neuropeptide Y Y1 receptor antagonist BIBP3226 produces conditioned place aversion in rats.

1. Previous studies have shown that the blockade of the neuropeptide Y (NPY) Y1 receptors with N2-(diphenylacetyl)-N-[(4-hydroxy-phenyl)methyl]-D-arginine amide (BIBP3226) induces anxiogenic-like reaction in rats tested in elevated plus-maze test. 2.

Involvement of opioid mu1-receptors in opioid-induced acceleration of striatal and limbic dopaminergic transmission.

The role of mu1-opioid receptors in the acceleration of cerebral dopaminergic transmission induced by morphine and the putative mu1-opioid agonist, etonitazene, was studied in rats by measuring the tissue levels of dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in the dorsal striatum and nucleus accumbens. The striatal extracellular concentrations of DA and its metabolites in freely moving rats were estimated as well. Morphine (3 mg/kg) and etonitazene (2.

Effects of morphine in rats withdrawn from repeated nifedipine administration.

The effects of withdrawal from repeated nifedipine treatment on morphine-induced analgesia, hyperthermia and catalepsy as well as on cerebral [3H]nitrendipine binding and on morphine-induced changes in striatal and limbic dopamine and 5-hydroxytryptamine metabolism were studied in rats. Repeated administration of nifedipine (5 mg/kg i.p.