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)

Verruculogen (V) and penitrem A (PA) represent a group of toxic secondary metabolites of mold contaminants of foodstuffs known as 'tremorgenic mycotoxins', which produce a unique neurotoxic syndrome characterized by sustained tremors, limb weakness, ataxia and convulsions. In the present study the intraperitoneal median tremogenic dose in mice for V was found to be 0.92 mg/kg and that for PA, 0.19 mg/kg. Behavioral and neurochemical parameters were assessed following acute exposure to varying neurotoxic and subneurotoxic doses of these mycotoxins. Measures of spontaneous motor activity (photoactometer) and exploratory reflex behaviors (open field) were markedly depressed by both V and PA. Notably, at dose levels of V or PA that were not accompanied by any overt signs of neurotoxicity, significant neuromotor depression was still observed. Acquisition of a conditioned avoidance shuttle response was disrupted, but only at a high neurotoxic dose level of V. Neurochemical analyses revealed no clear catecholaminergic or cholinergic involvement in the neurotoxic syndrome of eigher V or PA.
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PMID:Neurobehavioral studies of tremorgenic mycotoxins verruculogen and penitrem A. 64 98

Adult Richardson's ground squirrels were infected with western equine encephalomyelitis virus by intranasal instillation. Mortality followed the instillation of a minimum threshold of 4.7 logs of virus while infection was produced by a dosage of 2.3 logs. The incubation period was from four to seven days, being preceded by a viremic phase. Signs were depression, ataxia and paralysis of the limbs. Highest titres of virus were recovered from the brain and histopathological changes involving the central nervous system included meningitis, vasculitis, perivascular cuffing, gliosis, neuronophagia and neuronal degeneration. The virus was also found in a variety of extraneural tissues. Lesions in extraneural tissues included necrosis of brown fat and an apparent increase in number of Kupffer's cells in the liver. The lymphoid tissue was involved indicating a possible source for viremia. The duration and magnitude of viremia were ample enough to provide virus source for arthropods. The potential for transmission of the virus independent of arthropods was discussed in view of the pathogenesis demonstrated in the experimental infections.
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PMID:Intranasal exposure of the Richardson's ground squirrel to Western equine encephalomyelitis virus. 66 6

In 6 years snake bite was diagnosed in 41 cats, with an average age of 20 months. The commonest presenting signs were dilated pupils, absence of the pupillary light reflex, depression and generalised muscle weakness. Other frequent findings were vomiting, dyspnoea, hindlimb ataxia and complete flaccid paralysis. Thirty-seven cases (90%) occurred in the 6 warmer months of the year. Tiger snakes were positively identified in 7 cases. A recovery rate of 89% was obtained in cases receiving 3000 units Tiger snake antivenene, fluid therapy and nursing. Cases presenting with a complete flaccid paralysis and sub-normal temperatures were poor prognostic risks.
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PMID:Snake bite in cats. 74 57

Various nitrogen analogs of delta6a,10a-tetrahydrocannabinol were synthesized by a general procedure described in an earlier communication. Minimum effective doses (MED50's) and lethal doses (LD50's) were determined by a modified Irwin mouse screen after iv administration of compounds in PEG 200. The most potent compounds were the propargyl (5t), allyl (5m), and chloroallyl (5o-q) derivatives. Overt behavioral effects (CNS depression, static ataxia, and hypersensitivity) of 5t and Roger Adams' carbocyclic analog (III) were found to be similar in the mouse, cat, dog, and monkey. Dichloroisoproterenol prevented and reversed many of the depressant effects of both III and 5t but had no effect on the ataxia produced by these compounds. In antinociceptive tests, 5t was active in the phenylquinone and Eddy hot-plate tests but was inactive in the tail-flick test.
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PMID:Drugs derived from cannabinoids. 1. Nitrogen analogs, benzopyranopyridines and benzopyranopyrroles. 81 19

A systematic search for cases of adult-onset hereditary ataxia was conducted on location in Scotland. The investigation resulted in the discovery of eight pedigrees with 42 patients of whom 16 were alive in 1975. Nine patients were examined by the authors and recent hospital records were available on the remaining seven. The clinical features were quite variable. In declining order of frequency, findings were gait and limb ataxia, dysarthria, hyperreflexia, extrapyramidal motor disturbances, impaired vibratory sense, spasticity, defects of extraocular movements and nystagmus, reflex depression, Babinski signs, impaired joint position sense, muscle weakness, optic atrophy, and mental abnormalities. Foot deformity occurred only once. Inheritance was compatible with autosomal dominant transmission, but complicated by consanguinity in two families. The minimum prevalence was calculated as 0.31/100,000. Autopsy in two members in one family revealed olivopontocerebellar degeneration.
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PMID:Adult-onset hereditary ataxia in Scotland. 90 33

Guinea pigs treated with a single s.c. injection of a slowly released morphine suspension (300 mg/kg) exhibited a quantifiable withdrawal syndrome after naloxone injection (0.01-10 mg/kg s.c.). Ileum removed from such animals responded to naloxone (1-300 ng/ml) by contracting. These contractions could be blocked by scopolamine or tetrodotoxin. Both the in vivo and in vitro responses were specific for the opiate-dependent state and were dependent on naloxone dose. Time courses of the development and decline of the two responses were similar. Weaker opioids, pentazocine and codeine, were less effective than morphine in producing a dependent state and sensitizing ileum to naloxone. 1-(-)-delta9-Tetrahydrocann abinol [1-(-)-delta9-THC] antagonized the effect of naloxone on ileum without affecting responses to acetylcholine. 1-(-)-delta9-THC produced a stereospecific, dose-dependent (1-10 mg/kg p.o.) inhibition of naloxone-precipitated withdrawal in guinea pigs and rats that was more complete than and different from that produced by sedatives. Pentobarbital inhibited withdrawal only at doses that produced ataxia. 1-(-)-delta9-THC had a biphasic effect on locomotor activity of guinea pig in the dose range that inhibited withdrawal, stimulation at 1 mg/kg and depression at 3 to 10 mg/kg. Our results suggest that cannabinoids may be useful in opiate detoxification. The inhibition by 1-(-)-delta9-THC of the action of naloxone in "dependent" ileum seems to be via reduction in acetylcholine release. Whereas the end result of 1-(-)-delta9-THC action in brain may not necessarily be a reduction in acetylcholine release as in ileum, the mechanism by which it produces this effect in the ileum model may explain its ability to antagonize withdrawal.
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PMID:Correlation between the in vivo and an in vitro expression of opiate withdrawal precipitated by naloxone: their antagonism by l-(-)-delta9-tetrahydrocannabinol. 98 78

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

A calcifying aponeurotic fibroma involving the soft tissue and bone of the occipital area compressed and attenuated the cerebellum and brainstem of a 9-year-old female dog of mixed breeding. Clinical signs included a head tilt to the left; gait ataxia; anisocoria, with a midly dilated left pupil; horizontal nystagmus, with the fast phase to the right; and a mild depression of the level of consciousness. The signs were sequential and progressive.
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PMID:Calcifying aponeurotic fibroma in a dog. 111 57

Ataxia and depression developed in 21 of 50 (42%) laboratory cats wearing flea collars impregnated with 2,2-dichlorovinyl dimethyl phosphate (dichlorvos or DDVP) in a warm dry environment. Five (10%) of the cats died. Whole blood cholinesterase (ChE) activity was significantly (P smaller than 0.001) reduced in all cats and cervical dermatitis occurred in 37 (74%) of them.
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PMID:Ataxia, depression, and dermatitis associated with the use of dichlorvos-impregnated collars in the laboratory cat. 123 42

This paper reports findings relative to a simple, rapid and reproducible technique for the induction of physical dependence upon ethanol in the rat. The dependence was induced by intragastric intubation of 20% (w/v) ethanol solutions at 9-15 g/kg in 3-5 fractional doses daily for 4 days, maintaining blood ethanol concentrations above a threshold level sufficient to sustain observable sedation throughout the entire period of intubation. Two phases were distinguished during the withdrawal period: 1. Prodromal detoxication, characterized by a spectrum of signs and responses of diminishing severity, related to the decline in blood ethanol concentrations (mg/dl): death, greater than 640; coma, 780-460; loss of righting reflex, 640-400; ataxia 3-1, 570-250; sedation 340-190; neutrality, 220-130; 2. Ethanol dependence, characterized by a spectrum of withdrawal signs and reactions of progressively increasing severity as blood ehtanol concentration approached 100 mg/dl: hyperactivity, tremors, akinesia, spastic rigidity, and induced and spontaneous convulsions. A rapid sucession of two diverse clusters of signs and reactions represents a reversal of the central nervous system function from the extremes of ethanol intoxication (CNS depression) to the extremes of ethanol dependence (CNS hyperexcitability) during the withdrawal period. Both extremes may terminate in death.
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PMID:Induction of physical dependence upon ethanol and the associated behavioral changes in rats. 123 14


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