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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The actions of various doses of haloperidol, pimozide, clozapine, and phenoxybenzamine were assessed on a conditioned-avoidance response (CAR) in control and 6-hydroxydopamine-treated rats, using a pole-climbing device. Haloperidol proved to be the most potent in disrupting the CAR. Pimozide was about 1.6 times less potent, and clozapine and phenoxybenzamine were approximately 52 and 155 times less potent than haloperidol, respectively. Prior treatment with 6-hydroxydopamine slightly enhanced the sensitivity to some of the doses of the DA and NE antagonists. Significantly lower levels of responding, however, were observed only after the highest dose of primozide. Clonidine was not only ineffective in reverting avoidance decrements, but also induced a further decline of the CAR. Apomorphine produced a partial, but significant, reversal of the haloperidol and pimozide-induced depression of conditioned responses. Regarding the clozapine-pretreated animals, a significant antagonism was observed only with the smaller dose of apomorphine. The highest dose induced a further decline of the CAR. The DA agonist was also ineffective in the phenoxybenzamine-injected rats. Amphetamine was effective in antagonizing the avoidance decrements produced by all the CA antagonists. Our results support the suggestion that CAR depends on both DA and NE mechanisms. DA seems to be more significant that NE, however, since the CAR was more depressed when receptors depending on the former neurotransmitter were blocked.
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PMID:The actions of dopaminergic and noradrenergic antagonists on conditioned avoidance responses in intact and 6-hydroxydopamine-treated rats. 10 52

D-Amphetamine (Amph) and p-chloroamphetamine (PCA) induced dose-dependent increases in oropharyngeal myocloniform twitch activity (MTA) in rats anesthetized with urethane. In doses of 80-120 mg/kg, gamma-hydroxybutyric acid (GHB) blocked Amph-induced MTA. The blockade was readily surmountable. Pretreatment with reserpine markedly enhanced the myoclonigenic effect of Amph and rendered it insensitive blockade by GHB, 160 mg/kg. PCA and tryptamine also effectively stimulated MTA, but unlike Amph were antagonized by low doses of the serotonin (5-HT) antagonist methysergide. In doses which blocked Amph, GHB failed to antagonize the myoclonigenic effect of PCA. It is concluded that: (a) the actions of Amph and PCA on MTA is less sensitive to GHB blockade than DA-mediated MTA; and (c) the GHB-Amph antagonism may be of a functional nature, i.e. result from a depression of the firing activity of DA neurons produced by GHB. Since reserpinization abolished the GHB effect on Amph-induced MTA, the functional integrity of granular DA binding and releasing mechanisms appears to be a pre-requisite for the antagonism between GHB and Amph.
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PMID:Pharmacological evidence for a selective antidopaminergic action of gamma-hydroxybutyric acid. 97 99

Amphetamine- and apomorphine-induced changes in the activity of neurons in the caudate-putamen of paralyzed, locally anesthetized rats were recorded in animals pretreated with 2.5 mg/kg d-amphetamine sulphate for 6, 18 or 36 days, or in animals pretreated with saline for 36 consecutive days. In saline-pretreated animals, 2.5 mg/kg d-amphetamine sulphate (IP) produced an initial, brief potentiation of neuronal firing that was followed by a marked depression of neuronal activity lasting for approximately 35 to 110 min after injection. In amphetamine-pretreated animals, this depression of neuronal activity to the same dose of the drug was markedly prolonged, especially in animals given 36 consecutive days of d-amphetamine pretreatment. A similar enhancement occurred in response to 0.25 mg/kg apomorphine (IP) in animals pretreated with amphetamine for 36 days compared to saline-pretreated control animals. These results are discussed in relation to the known behavioral and biochemical effects of acute and long-term amphetamine administration.
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PMID:Enhancement of effects of dopaminergic agonists on neuronal activity in the caudate-putamen of the rat following long-term d-amphetamine administration. 99 66

The L-Dopa-potentiating effects of the two optical isomers of amphetamine, as well as the effects of their own, were investigated in mice, using locomotor activity as test parameter. The study was performed in three steps. First, the time-course were studied for the effects of (+)- and (-)-amphetamine and L-Dopa. Second, dose-response relationships were established for the amphetamine enantiomers. Third, the L-Dopa-potentiating effects, of a few, selected doses of the amphetamine isomers were investigated by establishing dose-response curves for L-Dopa with and without the amphetamines. All animals given L-Dopa were pretreated with an inhibitor of extracerebral aromatic amino acid decarboyxlase. (+)-Amphetamine, 0.5-8 mg/kg, caused a dose-dependent stimulation of locomotoractivity, whereas (-)-amphetamine, 1-4 mg/kg, caused a dose-dependent depression. Doses higher than 8 mg/kg of the laevo-isomer caused stimulation of the activity. (+)-Amphetamine, 0.25 mg/kg, and (-)-amphetamine, 0.5 mg/kg, i.e. doses without any effect on locomotor activity of their own, caused virtually the same shift to the left of the dose-response curve for L-Dopa. (-)-Amphetamine, 4 mg/kg which per se caused depression of locomotor activity, caused a marked potentiation of the L-Dopa-induced stimulation of motor activity. Thus, there does not exist a close correlation between the L-Dopa-potentiating action of the amphetamines and their stimulating properties per se.
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PMID:Differences between (+)- and (-)-amphetamine in effects on locomotor activity and L-dopa potentiating action in mice. 114 58

The effect of post-footshock injections of (+)-amphetamine, the selective D2-receptor agonist quinpirole (LY 171555), and the D2-receptor antagonist metoclopramide, into the nucleus accumbens, on the formation of the open field deficit, has been studied in rats. Microinjections of (+)-amphetamine (10 micrograms) stimulated rat locomotor activity tested 5 min later, while quinpirole (10 micrograms) significantly inhibited animal motility in the test. The open field behaviour was not changed 24 h after injection of either drug. Amphetamine applied immediately after inescapable footshock did not modify stress-induced locomotor depression, when the rats' behaviour was examined 24 h later. On the other hand, post-shock injections of quinpirole significantly attenuated the long-term effects of the stressor, in the open field. Metoclopramide (10 micrograms) inhibited rat locomotor activity 5 min, but not 24 h, after local injection. Administration of a solution containing both quinpirole (10 micrograms) and metoclopramide (1 microgram) decreased motor activity of unstressed rats to a smaller degree than did quinpirole (10 micrograms) alone. Post-footshock injection of metoclopramide did not affect stress-induced hypomotility. It is concluded that the present data support the hypothesis that local depletion of brain dopaminergic stores causes some behavioural effects of stressors.
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PMID:Effects of intra-accumbens administration of dopamine agonists on stress-induced behavioural deficit. 197 6

Intracellular recordings were made from guinea-pig prepositus hypoglossi (PH) neurons in vitro. Neurons within this nucleus are innervated by terminals that release 5-HT (serotonin) to mediate an IPSP. Cocaine caused a concentration-dependent prolongation of that IPSP, while having no effect on either membrane potential or firing rate. Cocaine also caused an increase in the IPSP amplitude at lower concentrations (less than or equal to 1 microM) and a decrease at higher concentrations. The selective 5-HT uptake inhibitor fluoxetine also prolonged the IPSP duration but depressed the amplitude at all concentrations tested. The effects of cocaine on IPSP duration can be completely accounted for by inhibition of 5-HT uptake. The depression of the IPSP is most likely due to a presynaptic effect, because cocaine augmented the response to applied 5-HT. Amphetamine (3-300 microM), unlike cocaine, changed the membrane potential. At lower concentrations, it caused a ketanserin-sensitive depolarization, while higher concentrations resulted in a spiperone-sensitive hyperpolarization. The hyperpolarization was most likely caused by the evoked release of 5-HT, while the depolarization may have been due to a direct effect of amphetamine on 5-HT2 receptors. Amphetamine also acted as a weak uptake inhibitor. The effects of cocaine, but not those of amphetamine, were observed at concentrations that are attained during self-administration.
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PMID:Cocaine and amphetamine interact at 5-HT synapses through distinct mechanisms in guinea-pig prepositus hypoglossi. 206 79

After bilateral visual cortex ablation, cats show a transient deficit in tactile placing and a permanent deficit in visual placing of both forelimbs. Amphetamine administration (four doses, 5 mg/kg, i.p., spaced at 4-day intervals beginning 10 days after surgery) accelerated the rate of recovery of tactile placing compared with saline controls whereas visual placing was not affected. The catecholamine antagonist, haloperidol (0.4 mg/kg, i.p.), blocked the amphetamine-enhanced recovery of tactile placing. Additionally, the visual cortex lesions produced a depression of oxidative metabolism, measured by cytochrome oxidase histochemistry, in subcortical regions remote from the injury. Animals treated with amphetamine exhibited an alleviation of this metabolic depression in the superior colliculus but not in other regions.
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PMID:Recovery of tactile placing after visual cortex ablation in cat: a behavioral and metabolic study of diaschisis. 303 89

The effects of various alpha 2 adrenoceptor agonists on forced swimming-induced despair behaviour were studied in mice. Clonidine, B-HT 920 and guanfacine significantly prolonged the total immobility duration. Clonidine-induced behavioural despair was antagonized by prior treatment with yohimbine. The tricyclic antidepressants imipramine, desipramine, trimipramine, amitriptyline, nortriptyline and doxepin, the MAO inhibitor tranylcypromine, and the antimanic agent lithium reversed clonidine-induced behavioural despair. Chronic treatment with imipramine evoked more pronounced reversal as compared to acute treatment. Amphetamine, a psychostimulant, inhibited clonidine-induced enhancement of immobility duration but diazepam, a skeletal muscle relaxant was without any effect. On the other hand, adenosine showed potentiation of the submaximal response of clonidine. These observations suggest that clonidine-induced behavioural despair is probably mediated through its presynaptic action on alpha 2 adrenoceptors, resulting in reduced central noradrenergic outflow. The present data proposes a simple test system to induce depression-like syndrome in animals, sensitive to antidepressant therapy.
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PMID:Clonidine--induced behavioural despair in mice: reversal by antidepressants. 308 33

The behavioral and biological responses to d-amphetamine have been studied extensively in patients with schizophrenia and depression, and to a lesser degree in bipolar affective disorders. Because of theories linking borderline personality disorder to those illnesses, amphetamine, 30 mg, p.o., was administered to eight borderline patients in a double-blind, placebo-controlled study and the results were compared to the responses of normal subjects under identical conditions. Amphetamine led to symptoms of psychosis in four out of eight (50%) borderline patients. No normal subject became psychotic during the procedure. Global ratings of well-being were significantly elevated in the borderline group compared to the normal group. In addition the global response was highly inversely correlated with the patient's score on the Diagnostic Interview for Borderlines. Borderline patients had a nonsignificantly decreased growth hormone response following amphetamine compared to normals. Thus, borderline patients appear to be pharmacodynamically separable from normals.
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PMID:Amphetamine response in borderline patients. 386 51

1. The cervical sympathetic trunk of the isolated rat superior cervical ganglion was stimulated with short bursts of repetitive pulses. At room temperature with rates of stimulation of 4 Hz and above, the ganglionic action potentials were reduced in size.2. Amphetamine (2.7 x 10(-5)M), which caused some depression of transmission during stimulation at 0.1 Hz, caused a partial reversal of the depression of transmission occurring with rates of stimulation above 4 Hz.3. This action of amphetamine was mimicked by adrenaline (3 x 10(-5)M) and noradrenaline (9.6 x 10(-5)M) but not by isoprenaline (1.8 x 10(-5)M) and was unaffected by propranolol (1.4 x 10(-5)M) but was abolished by prior application of phenoxybenzamine (5.8 x 10(-6)M). Furthermore, this action of amphetamine was unaltered in ganglia taken from rats pretreated with reserpine (single dose of 6 mg/kg, 16 h before dissection).4. Amphetamine had no effect on the surface potentials of the ganglion or on changes in these potentials produced by concentrations of carbachol (5. x 10(-6)M to 5.5 x 10(-3)M).5. It is concluded that amphetamine has a direct action on alpha-adrenoceptors situated at presynaptic sites.
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PMID:Effect of amphetamine on the transmission of repetitive impulses through the isolated superior cervical ganglion of the rat. 433 52


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