Expressions For Jumps Research Articles

Effects of imipramine on the expression and development of morphine dependence in mice

In the present study, the effects of imipramine and/or α-adrenoceptor agents on naloxone-induced jumping in morphine-dependent mice were examined. In the first set of experiments, the drugs were used before naloxone injection, to test their effects on the expression of jumping. Administration of imipramine (10–60 mg/kg) 15 min before naloxone increased the number of jumping in mice. Injection of the α 2-adrenoceptor agonist, clonidine (0.1 mg/kg), or α 1-adrenoceptor agonist, phenylephrine (4 mg/kg), themselves neither altered naloxone-induced jumping nor influenced the imipramine response. The α 2-adrenoceptor antagonist, yohimbine (4 mg/kg), itself but not the α 1-adrenoceptor antagonist, prazosin (1 mg/kg), increased jumping and decreased the imipramine effect. In the second set of experiments, imipramine and/or the α-adrenoceptor drugs were injected during the development of morphine dependence. Imipramine (10–40 mg/kg) increased the development of dependence and increased jumping was seen. Clonidine did not influence the imipramine effect. Phenylephrine was lethal in combination with imipramine. Both yohimbine and prazosin decreased the effect of imipramine. Imipramine and phenylephrine but not clonidine, yohimbine or prazosin decreased locomotion. It is concluded an α 2-adrenoceptor mechanism may be involved in the influence of imipramine on the expression and development of naloxone-induced withdrawal signs in mice.

Influence of histamine, cimetidine and pyrilamine on naloxone-induced jumping in morphine-dependent mice

In the present study, the effects of histamine on naloxone-induced jumping in the presence or absence of adrenoceptor or acetylcholine receptor antagonists in morphine-dependent mice were examined. In these experiments, the drugs were used before s.c. injection of naloxone (2 mg/kg), to test their effects on the expression of jumping. The i.c.v. administration of histamine (5–20 μg/mouse) 15 min before naloxone injection decreased the number of jumps in mice. When the histamine H 2 receptor antagonist, cimetidine (5–20 mg/kg), and the histamine H 1 receptor antagonist, pyrilamine (5–20 mg/kg), were administered i.p. to morphine-dependent mice, only cimetidine enhanced the jumping behaviour. Administration of cimetidine (20 mg/kg, i.p.), 30 min, of the β-adrenoceptor antagonist, propranolol (2.5–10 mg/kg, i.p.), 15 min but not of pyrilamine (20 mg/kg, i.p.), 30 min before naloxone injection, decreased the histamine effect. The i.p. administration of an acetylcholine receptor antagonist, atropine (5 and 10 mg/kg, i.p.), the α 1-adrenoceptor antagonist, prazosin (0.5, 1 and 2 mg/kg, i.p.), and α 2-adrenoceptor antagonist, yohimbine (0.5, 1 and 2 mg/kg, i.p.), 15 min before naloxone injection, had no effect on the histamine response. Single administration of propranolol, atropine or prazosin decreased, while yohimbine increased the naloxone-induced jumping. It is concluded that the histamine H 2 receptor mechanism may be involved in the influence of histamine on the expression of naloxone-induced jumping in morphine-dependent mice.

The effects of dopamine receptor agents on naloxone-induced jumping behaviour in morphine-dependent mice

In the present study, the effects of dopamine receptor agonists and antagonists on naloxone-induced jumping in morphine-dependent mice were examined. Mice were rendered dependent as described in the methods section. Naloxone was injected to elicit jumping (as withdrawal sign). The first group received dopamine receptor drugs before naloxone injection to test the effects of the drugs on the expression of jumping. Administration of the dopamine D1/D2 receptor agonist, apomorphine (0.25, 0.5 and 1 mg/kg), decreased jumping, but not diarrhoea, induced by naloxone. The effect of apomorphine on jumping was reduced by the dopamine D2 receptor antagonist, sulpiride. The dopamine D2 receptor agonist, quinpirole (0.1, 0.3 and 0.5 mg/kg), increased jumping, while it decreased diarrhoea in mice. Different doses of sulpiride did not alter jumping, but one dose of the drug (12.5 mg/kg) decreased jumping. Neither the dopamine D1 receptor agonist, SKF38393 (1-phenyl-7,8-dihydroxy-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride; 8 and 16 mg/kg), nor the dopamine D1 receptor antagonist, SCH23390 (R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-benzazepine-7-ol maleate; 5, 10 and 25 mg/kg), altered jumping, but they decreased diarrhoea. The second group of animals received the drugs during the development of dependence. Administration of quinpirole (0.1, 0.3 and 0.5 mg/kg), but not bromocriptine (4, 8 and 16 mg/kg), apomorphine (0.25, 0.5, 1 and 2 mg/kg) or sulpiride (12.5, 25 and 50 mg/kg) decreased naloxone-induced jumping and diarrhoea. A dose of SKF38393 (8 mg/kg) decreased jumping, while both SKF38393 (4 and 16 mg/kg) and SCH23390 (5 and 10 μg/kg) increased diarrhoea. It is concluded that activation of both dopamine D1 and D2 receptors may suppress naloxone-induced jumping in morphine-dependent mice, and that stimulation of dopamine D1 receptors during development of morphine dependence may increase diarrhoea through peripheral mechanism.

The global structure of the pulsar magnetospheres

The model of the pulsar magnetosphere filled with massless charged particles (rest massm=0) is considered. The gas of charged massless particles can be found in two different phases: (1) dynamical phase (DP), when the particles move with nonvanishing energy e along some base line, determined by the electromagnetic field only, (2) statical phase (SP), when the particles have vanishing energy e=0. The pulsar magnetosphere occurs to be divided into regions of different types: (a) the accelerating regions (DP-regions) containing only DP, (b) the capture regions, containing only SP, (3) leaky capture regions, where DP moves through SP. The leaky capture regions are the active regions, which are responsible for the pulsar radioemission. In the case of oblique magnetic moment the equation for the capture surface has been obtained. The capture region is formed around this surface. Expressions for jumps of the electromagnetic field, the current density and the charge density on the capture region boundary have been obtained. The problem of the pulsar magnetosphere is stated mathematically in the case of oblique magnetic moment and ejection of only electrons.