Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The midpontine decerebrate dog, immobilized with gallamine, was used to determine the changes in the transcallosally evoked potential (TEP) produced by intravenous infusions of various drugs. A total of 50 TEPs, recorded from the g. ectolateralis, was computer analyzed before, during and after administration of the drugs. Changes in the TEP were also correlated with changes in the EEG recorded from the g. ectolateralis. The EEG was analyzed by inspection and amplitude integration (electrogenesis). LSD (30 microng/kg) significantly depressed the TEP, and the effect persisted for at least 80 min. DMT (1 mg/kg) caused a significant and reversible increase in the amplitude of the TEP. LSD and DMT reduced the alpha activity of the EEG and enhanced the amplitude of the low-frequency waves. DMT produced a significant and LSD a marginal increase in electrogenesis. Tryptamine (10 and 20 mg/kg), mescaline (6 mg/kg), methoxamine (0.88 mg/kg) and apomorphine (5 mg/kg) had no significant effect on the TEP or EEG. These results suggest that depression of the TEP is not related to spinal reflex facilitation in the dog or hallucinogenic activity in man.
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PMID:Transcallosally evoked potentials and the EEG in the decerebrate dog: actions of tryptaminergic, dopaminergic and adrenergic agonists. 6 32

Rats given quipazine (5 mg/kg) or LSD (0.05 mg/kg), were decapitated at the time of maximum of behavioral effect of drugs (head twitches), resp. 30 and 15 min, or when the behavioral effects disappeared (resp. 60 and 30 min), and concentrations of dopamine (DA), noradrenaline (NA), serotonin (5HT) and 5-hydroxyindole-3-acetic acid (5-HIAA) were assayed in the striatum. Quipazine significantly elevated the DA level at both periods tested. LSD at the peak of its action depressed the level of 5-HIAA, and in the next period produced a significant depression of striatal levels of NA, 5HT and 5-HIAA.
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PMID:The effect of quipazine and LSD on monoamines in the rat striatum. 9 44

Electrolytical lesions of the dorsal raphe nucleus in the rat did not change frequency of head twitches produced by codeine and apocodeine. The action of serotonergic drugs was affected differently: the lesion depressed the frequency of head twitch episodes produced by 5-hydroxytryptophan (5-HTP), LSD and quipazine, but did not change the frequency of head twitches produced by 5-methoxytryptamine. On the other hand, the lesions protected against high mortality produced by combined treatment with tranylcypromine and 5-methoxytryptamine. There was a good correlation between the extent of lesion, measured by the depression of the level of prosencephalic serotonin, and the depression of head twitch frequency produced by 5-hydroxytryptophan and quipazine, while the correlation was not significant for the action of LSD. It is concluded that presynaptic serotonergic structures belonging to the mesostriatal serotonergic system are necessary for appearing of head twitches after treatment with 5-HTP, LSD and quipazine, and therefore these compounds have a presynaptic action in this test.
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PMID:Head twitches produced by serotonergic drugs and opiates after lesion of the mesostriatal serotonergic system of the rat. 31 25

Pentazocine, cyclazocine, and nalorphine are narcotic antagonists that also have analgesic activity of their own. The present investigation compared the stimulus properties of these three drugs in rats. Each drug was used as a discriminative stimulus for a separate group of rats. Depression of one lever resulted in food reinforcement following the administration of drug, and the opposite lever was reinforced after saline. Each drug readily acquired control of discriminated responding. The specific narcotic antagonist, naloxone, which antagonizes many of the effects of pentazocine, cyclazocine, and nalorphine, also antagonized the discrimination of these drugs. Stimulus generalization tests to each other narcotic antagonist, d-amphetamine, morphine, and LSD, showed that each narcotic antagonist has highly specific stimulus properties. Clear generalization occurred only to pentazocine and cyclazocine in the nalorphine-saline group, but neither cyclazocine nor pentazocine generalized to nalorphine.
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PMID:Pentazocine, cyclazocine, and nalorphine as discriminative stimuli. 41 47

The effects of systemic LSD (10--25 micrograms/kg) on visually evoked [K+]o responses from the striate cortex have been investigated in cats. Elevation of [K+]o was dependent on the orientation, and direction of stimulus movement and showed ocular dominance. LSD most commonly produced a depression of [K+]o transients and a deterioration in their directional selectivity. These observations suggest that the effect of LSD is to produce a net depression in visually evoked neuronal firing.
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PMID:LSD's effect on neuron populations in visual cortex gauged by transient responses of extracellular potassium evoked by optical stimuli. 53 Apr 63

The effects of antidepressant drugs on central 5-HT receptor activity were studied in rats and mice. Antidepressant drugs were evaluated for their ability to displace 3H-5-HT and 3H-d-LSD from membrane binding sites in the dorsal neocortex of rats in vitro and for their ability to block 5-HTP and d-LSD induced behavioral effects in mice. The degree of blockade of head-twitches in mice produced by the antidepressants was highly correlated with their affinity for 3H-d-LSD binding sites. A number of antidepressant drugs such as amitriptyline, nortriptyline, mianserine, doxepine, nomifensine and dibenzepine appear to possess marked 5-HT receptor blocking activity at some type of 5-HT receptors in brain. New antidepressant drugs such as zimelidine, which specifically inhibit 5-HT reuptake and do not block 5-HT receptor sites, may after chronic treatment also reduce the functional activity of 5-HT systems by producing adaptive changes in postsynaptic 5-HT mechanisms. Thus, a new indoleamine hypothesis of depression is presented: the therapeutic action of antidepressant drugs may in part be due to a reduced functional acitivity of some central 5-HT systems.
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PMID:Reevaluation of the indoleamine hypothesis of depression. Evidence for a reduction of functional activity of central 5-HT systems by antidepressant drugs. 57 36

It was found that spiperone and pimozide in doses which themselves do not influence the flexor reflex of the hind limb of the spinal rat inhibit stimulation of this reflex induced by serotoninomimetic drugs (LSD and fenfluramine). Higher doses of spiperone depress the flexor reflex and inhibit the stimulating effect of clonidine. Pimozide has no such effect. Haloperidol in doses which do not influence the action of LSD and fenfluramine produces a depression of the flexor reflex and antagonizes the action of clonidine. Our findings indicate that, irrespective of their antidopamine action, spiperone has a central antiserotonin effect and an antinoradrenaline one, pimozide--an antiserotonin one and haloperidol--an antinoradrenaline one.
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PMID:The effect of haloperidol, spiperone and pimozide on the flexor reflex of the hind limb of the spinal rat. 73 Dec 32

Ten rats were given 9.1 to 82 mg/kg of 2,4-dimethyl-3-ethylpyrrole (kryptopyrrole) and the behavioral and electroencephalographic effects were studied. Kryptopyrrole was found to decrease EEG voltage, disrupt synchronization and induce abnormal spiking at a variety of cortical sites. Intermittent periods of low frequency hypersynchronous EEG activity was consistently elicited by kryptopyrrole. These waves bear a resemblance to the hypersynchronous EEG patterns associated with hallucinatory agents such as LSD-25. Marked behavioral alterations were observed following the initial injection including ataxia, hyperventilation, locomotor depression and catelepsy. Kryptopyrrole causes major central nervous system dysfunction, and these findings are discussed in the context of a drug-induced model of psychoses.
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PMID:Neurological and behavioral toxicity of kryptopyrrole in the rat. 109 75

23 cases are demonstrated, in which the connection between drug use and sudden death is to be accepted. The victims are only males and juveniles. It is demonstrated by the cases reported, that upon the sudden death of a juvenile increased consideration must also be given to a possible connection between death and drug use. First and foremost the drug used is susceptible of leading to death by way of an intoxication due to too large a dosage or owing to oversensitiveness. Far advanced putrefaction, the combined effects of several drugs including alcohol, the difficulty in furnishing chemical proof of the presence of hashish and LSD in body-fluids and organs can make it nearly impossible to clarify the cause of death. Only what has been related in respect of the manner of living and drug use by members of the family, mates and friends makes the connection between death and drug use appear quite likely. The indirect connection between drug use and the juvenile's death is to be accepted if it comes to the accident under the influence of drugs - be it under the impression of invulnerability or omnipotence or in a state of hallucinations. Depressions under the influence of drugs are also susceptible of resulting in real suicidal actions. In case of inexplicable accidents or entirely unexpected suicide drug effects must, therefore, nowadays be thought of.
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PMID:[Drug use leading to death (author's transl)]. 112 Dec 98

Successive daily injections of LSD-25 and UML (1-methyl-d-lysergic acid butanolamide) caused progressive depression of brain 5-HT levels in the rat. On the fourth day, the decrease was significant with respect to the highly significant fall observed after a single administration, whereas it had been shown earlier that conditioned behaviour is no longer affected by LSD-25 after 3 days and that simultaneous administration of a single dose of LSD-25 and UML is equally ineffective in this respect. Its depression of 5-HT levels, however, has now been shown to be equal to that of LSD-25 alone at doses that influence conditioned behaviour. The findings indicate that changes in such behaviour are not dependent on brain 5-HT levels and that no link exists between such levels and the psychotomimetic effect of LSD-25 in man.
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PMID:The relation between cerebral serotonin levels and conditioned behaviour in the rat following the administration of LSD-25 and UML. 115 13


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