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

Acrylonitrile (VCN) is an aliphatic nitrile which is used extensively in manufacturing of synthetic fibers, plastics, and rubber. Although the neurotoxicity of VCN is recognized, no thorough characterization of this effect has been reported. Current studies were designed to quantitatively characterize the acute phase of VCN-induced cholinomimetic neurotoxicity, and to determine the effects of dose, route of administration, and atropine on such toxicity. Administration of a single gavage or subcutaneous doses of 20, 40, or 80 mg VCN/kg to male Sprague-Dawley rats causes two distinctive phases of acute neurotoxic effects. Signs observed in the early phase had a rapid onset, and were cholinomimetic in nature. They included salivation, lacrimation, chromodacryorrhea, polyuria, miosis, vasodilatation in face, ears and extremities, increased gastric secretion, and diarrhea. A late phase developed hours after VCN dosing, and the toxic signs included depression, convulsions, and respiratory failure followed by death at high doses. These results revealed that the cholinomimetic toxicity induced by VCN was dose related regardless of the route of administration. In another study, rats were pretreated with atropine (1 mg/kg, IP) prior to VCN (40 mg/kg) in order to investigate the role of the cholinergic system. Atropine protected rats against VCN-induced cholinomimetic neurotoxicity, suggesting possible involvement of the cholinergic system. Finally, this work provides essential basic information for studying the biochemical, pharmacological, and neurological basis of VCN-induced neurotoxicity in the rat.
 ...
PMID:Assessment of the acute acrylonitrile-induced neurotoxicity in rats. 175 2

Polygraphic sleep exploration is usually not necessary to evaluate and treat such dyssomnias as nightmares or anguish dreams, but it may be indispensable in case of severe repeated or refractory sleep disorders, particularly in patients with concomitant depression. Two cases of major depression (DSM III R) associated with wakings during the night and dreams of death are reported. In both cases, polygraphic sleep exploration performed after complete, two-weeks long discontinuation of medicines revealed sinus bradycardia during paradoxical sleep, particularly in pre-waking periods. Heart rates ranged from 33 to 43 beats/minute in the most pronounced bradycardic episodes. The possibility of organic cardiac pathology was excluded by additional examinations. Atropine (175 mg) administered alone resulted in complete disappearance of bradycardic episodes and in improvement of objective and subjective sleep parameters. In these two cases bradycardia seemed to be due to vagal dysfunction with exaggeration of the "rebound" bradycardia which follows the initial tachycardia that occurs during the phasic phenomena of paradoxical sleep.
 ...
PMID:[Sleep disorders with nocturnal bradycardia in 2 depressed patients]. 183 64

The intermediary pathways in the bombesin-induced somatostatin release were examined in isolated perfused rat stomach obtained from male rats that were fasted overnight. The stomachs were perfused by way of the celiac artery. On coinfusion of 1.0 mumol/L tetrodotoxin and 1 nmol/L bombesin, a significant depression in release of somatostatin was observed compared with that observed with bombesin alone. The 5-minute integrated somatostatin response after treatment with tetrodotoxin and bombesin was 173% +/- 14% of basal, which was significantly lower than that observed with bombesin alone (394% +/- 59% of basal, P less than 0.05) but significantly higher than that observed with medium-199 alone (95% +/- 7% of basal, P less than 0.05); this indicated that approximately 70% of the bombesin-stimulated somatostatin release was indirectly mediated through neural pathways, while a significant (approximately 30%) segment of it was mediated by nonneural mechanisms. To test if the 30% somatostatin release was secondary to gastrin release in response to bombesin, gastrin antiserum and bombesin (1 nmol/L) were coadministrated in the presence or absence of tetrodotoxin (1 mumol/L). Gastrin antiserum alone did not significantly affect basal release of somatostatin but caused a significant inhibition (approximately 23%) of bombesin-provoked somatostatin release. Coadministration of gastrin antiserum and tetrodotoxin attenuated bombesin-stimulated somatostatin release. Gastrin (1 mumol/L) alone significantly stimulated somatostatin release (150% +/- 10% of basal), which was completely attenuated in the presence of gastrin antiserum. Tetrodotoxin did not affect bombesin-elicited gastrin release, confirming that bombesin-stimulated gastrin release was directly mediated. To determine the nature of the neural pathways mediating the bombesin-induced somatostatin release, atropine (100 nmol/L) was used. Atropine inhibited bombesin-induced somatostatin release to the same extent as tetrodotoxin, indicating that cholinergic pathways mediated bombesin-induced somatostatin release. These results show that almost all the somatostatin response to bombesin is indirectly mediated, and is composed of a major neural (cholinergic) and a minor nonneural pathway. The nonneural mechanism appears to be contributed primarily by gastrin released in response to bombesin, which apparently has a short paracrine positive feedback effect on somatostatin release.
 ...
PMID:Role of gastrin in bombesin-stimulated somatostatin release. 197 61

The autonomic components of the baroreflex control of heart rate were evaluated in conscious mongrel dogs before and after 4-6 weeks of ventricular pacing (250 beats/min). Arterial baroreflex sensitivity (BRS) was determined by the slopes of linear regression of pulse interval versus the preceding systolic arterial pressure in response to bolus injections of either phenylephrine or nitroglycerin. BRS was significantly depressed in the heart failure state [nitroglycerin slope, 5.0 +/- 2.7 (mean +/- SD) versus 16.6 +/- 5.1 msec/mm Hg, p less than 0.005; phenylephrine slope, 15.0 +/- 14.8 versus 32.0 +/- 26.7 msec/mm Hg, p less than 0.005]. There was no depression in BRS in dogs that were used as time controls or were acutely paced for 30 minutes. After beta 1-adrenergic blockade with metoprolol, the resting heart rate in the heart failure state was depressed more than in the normal state (-17.0 +/- 5.0% versus -3.2 +/- 3.4%, p less than 0.001). Atropine significantly increased resting heart rate more in the normal state than in the heart failure state (115.8 +/- 36.7% versus 25.4 +/- 14.5%, p less than 0.005). Thus, dogs in the heart failure state appear to have high resting cardiac sympathetic tone and low resting vagal tone. For nitroglycerin administration, metoprolol depressed BRS by 47.6 +/- 26.3% in the normal state and by 63.6 +/- 58.5% in the heart failure state. Atropine decreased the BRS by 86.7 +/- 7.8% in the normal state and by 39.5 +/- 30.2% in the heart failure state.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Analysis of baroreflex control of heart rate in conscious dogs with pacing-induced heart failure. 198 84

We studied the ontogeny of muscarinic depression in the developing rat visual cortex using carbachol (a nonhydrolyzable cholinergic agonist) application to neocortical slices obtained from four postnatal age groups: 9-10 days, 15 days, 30-40 days and 18 months. Carbachol suppressed the evoked synaptic response of layers II-III to stimulation of layer II-III afferents. Atropine eliminated the carbachol effect, suggesting that it is mediated by muscarinic receptors. The results indicate a significant increase in muscarinic efficacy in the developing rat visual cortex.
 ...
PMID:Ontogenesis of the depressant activity of carbachol on synaptic activity in rat visual cortex. 201 80

The cardiovascular changes induced by several sedatives were investigated in five ponies with a subcutaneously transposed carotid artery by means of cardiac output determinations (thermodilution technique), systemic and pulmonary artery pressure measurements (direct intravascular method) and arterial blood analysis (blood gases and packed cell volume). The cardiovascular depression (decrease in systemic blood pressure and cardiac output) was long lasting (greater than 90 min) after administration of propionylpromazine (0.08 mg/kg intravenous (i.v.)) together with promethazine (0.08 mg/kg i.v.). The phenothiazine-induced sedation was not optimal. alpha 2-Agonists (xylazine (0.60 mg/kg i.v.) and detomidine (20 micrograms/kg i.v.)) induced initial but transient cardiovascular effects with an increase in systemic blood pressure and a decrease in cardiac output for about 15 min. Second degree atrioventricular blocks and bradycardia were seen during this period. The cardiovascular depression was more pronounced during detomidine sedation. Atropine (0.01 mg/kg i.v.) induced a tachycardia with a decrease in stroke volume but did not alter the cardiac output or other cardiovascular parameters. It prevented the occurrence of the bradycardia and heart blocks normally induced by xylazine or detomidine. Atropine potentiated the initial hypertension induced by the alpha 2-agonistic sedatives (especially detomidine). The decrease in cardiac output induced by xylazine, and to a lesser extent by detomidine, was partially counteracted when atropine was given in advance. The atropine-xylazine combination seemed the best premedication protocol before general anaesthesia as it only resulted in minor and transient cardiovascular changes.
 ...
PMID:Haemodynamic changes during sedation in ponies. 239 24

The role of the vagus nerve and adrenoceptor stimulation in acid secretion after pylorus-ligation in the rat has been examined. All drugs were administered intraperitoneally. Atropine (5 mg kg-1) depressed the H+ output (111 mumols +/- 33.8 vs 412.5 mumols +/- 62.2, mean +/- s.e.m., n = 10, P less than 0.001); cimetidine (40 mg kg-1) did not enhance this action, while vagotomy was more effective than atropine (32.7 mumols +/- 4.9, mean +/- s.e.m., n = 10, P less than 0.05). Atropine (10 mg kg-1) produced a similar depression to the 5 mg kg-1 dose. Cimetidine (100 mg kg-1) depressed the H+ output (248.5 mumols +/- 46.8, mean +/- s.e.m., n = 10, P less than 0.05). Propranolol (5-20 mg kg-1) had no significant effect on the H+ output but dose-dependent inhibition was produced by phenoxybenzamine or phentolamine; an inhibition similar to that achieved by vagotomy was seen with the 20 mg kg-1 dose. Both these drugs (5 or 10 mg kg-1) had no significant effect on the H+ output when given with atropine (5 mg kg-1) but the H+ output was significantly lower than that produced by either drug at the same dose given alone. Atropine (5 mg kg-1) with phenoxybenzamine or phentolamine (20 mg kg-1) produced H+ output not significantly different from that with vagotomy or either alpha-adrenoceptor given alone at 20 mg kg-1, but the result was significantly (P less than 0.05) lower than the H+ output with atropine (5 mg kg-1) alone.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The role of vagal adrenergic activity in the mechanism of gastric acid secretion after pylorus-ligation in the rat. 257 4

The existence of presynaptic muscarinic acetylcholine receptors on motor nerve terminals of the isolated frog sartorius muscle was investigated. The modulatory role of these receptors was studied by observing the effects of muscarinic ligands on the frequency of miniature endplate potentials and on the quantal content of endplate potentials. The agonist oxotremorine reduced in concentration-dependent fashion the frequency of spontaneous potentials and the amplitude of evoked potentials. Also, high concentrations of oxotremorine depolarized the postsynaptic membrane and reduced the amplitude of the miniature endplate potentials. The depolarizing action of the drug was blocked by D-tubocurarine. The muscarinic antagonist atropine attenuated agonist-induced reductions in endplate potential amplitude and miniature endplate potential frequency but did not affect the depression in amplitude of the spontaneous potentials evoked by oxotremorine. It is concluded that activation of presynaptic muscarinic receptors inhibits the release of acetylcholine from motor nerve terminals. Atropine itself had no effect on the quantal content of evoked potentials or on the frequency of spontaneous potentials suggesting that the nerve terminal is not affected by non-quantal acetylcholine.
 ...
PMID:Muscarinic inhibition of quantal transmitter release from the magnesium-paralysed frog sartorius muscle. 278 30

Intravenous administration of physostigmine has been found to produce dose- and time-dependent alterations of the lumbar monosynaptic and polysynaptic reflexes in spinal cats. A small dose of physostigmine (0.8 mg/kg) enhanced the monosynaptic reflex for 3 hr, while a larger dose (2.0 mg/kg) produced a pattern of initial depression which peaked at 5 min, followed by an increase which was maintained for 3 hr after injection. Both doses of physostigmine were found to produce a similar pattern of enhancement of the polysynaptic reflex. Atropine and mecamylamine antagonized the increase of the monosynaptic reflex produced by both doses of physostigmine. The initial depression of the monosynaptic reflex produced by the large dose of physostigmine was blocked by mecamylamine, but unaffected by atropine. The enhancement of the polysynaptic reflex, produced by both doses of physostigmine, was antagonized by atropine but not by mecamylamine. In addition, nicotine and oxotremorine were found to mimic the initial effects of physostigmine in the presence of the appropriate antagonist. These data show that both muscarinic and nicotinic receptors are involved differentially in the modulation of spinal reflexes and that physostigmine had an additional late effect which consistently occurred at 20 min after administration.
 ...
PMID:Electrophysiological evidence for nicotinic and muscarinic modulation of spinal cord reflexes. 281 87

Single intraperitoneal doses of various antipsychotic drugs (clozapine 6, 12, 25 mg/kg, sulpiride 100 mg/kg, haloperidol 0.5, 1.0, 2.0 mg/kg, fluphenazine 0.5, 1.0, 2.0 mg/kg) induced a depression of the spontaneous chewing movement (SCM) rate in rats during the first 6-8 hours. Haloperidol and fluphenazine elicited a rebound increase in SCM on day 2-5, while clozapine and sulpiride did not. Atropine (5 mg/kg) reduced the SCM rate. During chronic administration for 10 months clozapine (50 mg/kg/day) caused no changes in the SCM rate. Sulpiride (120 mg/kg/day) gave a marginal rise above control levels, while thioridazine (40 mg/kg/day), chlorpromazine (30 mg/kg/day), fluphenazine (0.6 mg/kg/day) and haloperidol (0.4 mg/kg/day) produced highly significant increases in SCM rates. It is suggested that the present animal model may prove useful for monitoring the risk of tardive dyskinesia with individual drugs.
 ...
PMID:Spontaneous chewing movements in rats during acute and chronic antipsychotic drug administration. 287 45


<< Previous 1 2 3 4 5 6 7 8 9 Next >>