Bilateral changes in striatal dopamine metabolism after unilateral intracarotid and intrastriatal administration of apomorphine.

Following cannulation of the common carotid artery of female Sprague-Dawley rats, 3 microCi (10 micrograms) of [3H]apomorphine were infused. At various time intervals, drug concentrations were determined in the right and left striata, anterior forebrains, posterior forebrains and cerebella. One minute following intracarotid infusion of apomorphine, approximately a 65-fold right/left difference in apomorphine concentrations was attained in all forebrain structures, and this difference steadily diminished with time as a result of declining drug levels in the infused hemisphere.

Effects of prenatal phencyclidine on 3H-PCP binding and PCP-induced motor activity and ataxia.

Either phencyclidine hydrochloride (PCP) (5, 10, or 20 mg/kg) or saline was administered by subcutaneous injection to gravid CF-1 mice during either Mid (E6-15) or Late (E12-18) gestation. A nontreated control group (UTC) was left undisturbed during pregnancy. All treated and control litters were fostered at birth to untreated dams.

Dopamine autoreceptor agonists attenuate spontaneous motor activity but not spontaneous fighting in individually-housed mice.

The present study was conducted to determine whether or not two behavioral characteristics of individually-housed mice, hyperactivity in a novel environment and intermale fighting, are attenuated by the dopamine (DA) agonists, apomorphine, (+)- and (-)-3-(3-hydroxyphenyl)-N-n-propylpiperidine (3-PPP). Autoreceptor-activating doses of these drugs which reduced spontaneous activity in a novel environment did not inhibit spontaneous fighting with conspecific olfactory bulbectomized males. Individually-housed mice were more active in a novel environment and showed a significant reduction of activity at lower doses of apomorphine, (+)- and (-)-3-PPP than group-housed mice.

Phencyclidine during pregnancy: fetal brain levels and neurobehavioral effects.

Either phencyclidine (PCP) (5, 10, or 20 mg/kg) or saline was administered SC to pregnant CF-1 mice during either MID (E6-E15) or LATE (E12-E18) gestation. Because of the reported prolonged persistence of PCP in adult tissues we first determined its half-life in fetal brain for both treatment periods. PCP appeared rapidly in fetal tissues after maternal administration but was not detected after 8 hours.

The effects of phencyclidine on fighting in differentially housed mice.

The effects of phencyclidine (PCP) on the fighting of individually housed male mice were examined (1) after different lengths (5-35 days) of individual housing, and (2) in mice of different ages (35, 70 or 170 days old) at the onset of individual housing. Significant increases in the total time spent fighting in a 10-minute aggression test were observed at 19-21 and 32-35 days of individual housing with 1.25 mg/kg PCP and at 10 and 32-35 days with 2.

Behavioral and biochemical studies of dopamine receptor sensitivity in differentially housed mice.

Group housed and individually housed mice were compared in (1) the motor activity responses to direct and indirect dopamine (DA) agonists, (2) in vivo presynaptic autoreceptor sensitivity and (3) in vitro binding of 3H-spiperone. Relative to group housed mice, individually housed mice showed an increased motor activity response to amphetamine, 1.25 and 0.

Morphine enhances high-affinity choline uptake in mouse striatum.

The effects of morphine (2 mg/kg-60 mg/kg) on cholinergic neuronal activity were examined by the method of high-affinity, Na+-dependent [3H]choline uptake into synaptosomes isolated from mouse corpus striatum. Acute administration of analgesic doses of morphine (10 mg/kg, 20 mg/kg) significantly stimulated choline uptake into synaptosomes in a naloxone-reversible manner. When synaptosomes were directly exposed to pharmacologically effective concentrations of morphine (0.

Cocaine potentiates ketamine-induced loss of the righting reflex and sleeping time in mice. Role of catecholamines.

Cocaine in graded doses potentiated ketamine-induced loss of the righting reflex and sleeping time. Potentiation of drug-induced sleep with cocaine was not a generalized phenomenon inasmuch as it had no effect on sleep induced by pentobarbital or hexobarbital and decreased sleep induced by phenobarbital. Pentylenetetrazole reduced ketamine sleep but d-amphetamine had a potentiative action.

Effect of narcotics on monoamine oxidase activity of mouse brain.

The effect of morphine, levorphanol and methadone on the monoamine oxidase (MAO) activity of mouse brain was studied. Both methadone and levorphanol produced a concentration-dependent inhibition of whole brain mitochondrial MAO in vitro with an IC50 of approximately 7.4 x 10(-4) for levorphanol and 2.

Studies on the role of dopaminergic systems in morphine-induced motor activity. Comparison with noradrenergic and cholinergic systems.

The role of dopaminergic, noradrenergic and cholinergic systems in morphine-induced motor activity was investigated in mice using both blockers and stimulators of the receptors of the respective systems. The dopaminergic blocking drugs, spiroperidol and clothiapine, significantly reduced while stimulating dopaminergic receptors with amantadine significantly increased morphine-induced motor activity. Blockade of noradrenergic receptors with phenoxybenzamine and cholinergic receptors with atropine significantly reduced morphine activity whereas stimulation of either of these systems with DOPS and physostigmine respectively, had no effect.