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)

Electrical stimulation of a lateral region of the cerebellar nodulus-uvula transition zone in anesthetized albino rabbits decreases mean arterial blood pressure in direct proportion to stimulus intensity. The hypotension has an abrupt onset and is phasic; heart rate is unaffected. Neural pathways that might mediate the depressor response were studied using autonomic-blocking agents. Pretreatment with 2 mg/kg iv of either propranolol HCl or atropine methyl nitrate did not alter the onset or duration of the hypotensive response. However, pretreatment with 2 mg/kg iv phentolamine HCl abolished the depressor response, and 7 mg.kg-1.min-1 iv tetraethylammonium infusion decreased the response by more than 50%. Ipsilateral injections of 200 ng bicuculline methiodide into an area immediately dorsal to the superior cerebellar peduncle or the dorsal aspect of the superior vestibular nucleus reversibly attenuated the nodulus-uvula evoked depression. Anterograde horseradish peroxidase-wheat germ agglutinin (HRP-WGA) transport experiments revealed that both these regions receive direct inputs from the nodulus-uvula. These data suggest that hypotensive events elicited by lateral nodulus-uvula stimuli represent a central, alpha-aminobutyric acid-mediated, phasic inhibition of vasomotor drive mediated through autonomic ganglia to alpha-adrenoreceptors in the vasculature.
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PMID:Nodulus-uvula depressor response: central GABA-mediated inhibition of alpha-adrenergic outflow. 247 76

Two experiments were conducted using corn from clean or aflatoxin B1 (AFB1)-contaminated (182 ppb) sources. Weanling pigs (28 d) were fed one of eight dietary treatments arranged in a 2 x 2 x 2 factorial design. In Exp. 1 (192 pigs), treatments varied in corn source (clean or AFB1-contaminated), CP level (18 or 20%) and added fat (0 or 5%). At the end of the 28-d growth trials, plasma samples were obtained. An AFB1 x CP level interaction was detected (P less than .05) for growth rate (ADG), feed intake (FI) and feed/gain ratio (F/G). Feeding AFB1 reduced (P less than .05) ADG (.30 vs .37 kg/d) and FI (.57 vs .66 kg/d) and increased F/G (1.88 vs 1.78) of pigs fed 18% CP diets. Performance of pigs fed 20% CP diets was not altered by AFB1. Adding 5% fat to diets improved (P less than .05) F/G but did not improve ADG of pigs fed AFB1. There was an AFB1 x CP x fat interaction (P less than .05) for plasma cholesterol. Adding fat or increasing the CP level prevented the depression of plasma cholesterol in pigs fed AFB1. In Exp. 2 (96 pigs), all diets contained 18% CP and the treatments varied in corn source (clean or AFB1-contaminated), added L-lysine HCl (0 or .25%) and added DL-methionine (0 or .15%). Feeding AFB1 reduced (P less than .05) ADG of pigs fed the 18% CP diet (.44 vs .50 kg/d) but not of pigs fed diets supplemented with .25% lysine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of dietary protein, fat or amino acids on the response of weanling swine to aflatoxin B1. 249 62

The surface structure of the connective tissue papillae (CP) of Suncus murinus tongue was observed by SEM after fixing with Karnovsky's fixative and removal of the epithelial cell layer with 3N or 8N HCl. On the surface of the slender conical tongue, there are densely distributed filiform papillae among which fungiform papillae are seen sporadically. A pair of vallate papillae are situated in the posterior region of the tongue. Filiform papillae appear somewhat different externally depending on the dorsal surface of the anterior tongue. At the tip of the tongue, filiform papillae are of a slender conical shape and have a slight depression in the anterior basal portion. The CP of these is seen as a spherical protrusion on which a shallow groove runs in the anteroposterior direction. In the middle region, somewhat large filiform papillae contain CP having one or two small round head-like structures on each spherical protrusion. These head-like structures are increased in number in the posterior region. In the most posterior region of the anterior tongue, there are distributed large filiform papillae having several slender protrusions that surround a basal anterior depression. These large branched filiform papillae have a glove finger like CP. Small conical filiform papillae are distributed in the posterior marginal region of the anterior tongue which have CP of a horse-shoe like protrusion that opens in the anterior direction. Spherical fungiform papillae have CP which are thick columnar in shape with many lateral thin folds running vertically and having a round depression on the top of each. CP of the vallate papillae appear as a beehive like structure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Three dimensional structure of the connective tissue papillae of the tongue in Suncus murinus]. 251 78

MK-801 is a ligand at phencyclidine recognition sites associated with NMDA-coupled cation channels, where it acts as a potent noncompetitive antagonist of central glutamate/aspartate (NMDA-type) receptors. Low doses (10-100 micrograms/kg IP) produced a dose-related and prolonged (greater than 1 h) enhancement of variable-interval self-stimulation responding. Higher doses (300 micrograms/kg) caused flaccid ataxia and disrupted responding. Ketamine HCl (3.0-100 mg/kg IP), a dissociative anaesthetic binding to the phencyclidine site, produced a similar response pattern, but facilitation was less prolonged and occurred over a narrower dose range. Kynurenic acid (3.0-300 mg/kg IP), a nonselective competitive antagonist of glutamate receptors, produced only depression of responding, possibly the result of kynurenate-induced blockade of central kainate and/or quisqualate receptors. The behavioural stimulant effects of MK-801 appear to be an intrinsic and essential feature of selective NMDA antagonists, and these effects of MK-801 differ qualitatively and quantitatively from the well-known facilitatory effects of dopamine-dependent stimulants.
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PMID:The effect of MK-801 and other antagonists of NMDA-type glutamate receptors on brain-stimulation reward. 255 Sep 89

The alpha-2 adrenoceptor agonists clonidine and xylazine were employed in chicks and rats to induce a loss of the righting reflex, a sign for depression of the central nervous system. These effects of clonidine and xylazine were antagonized by yohimbine, idazoxan and CH-38083 (7,8-(methylenedioxi)-14-alpha-hydroxyalloberbane HCl), compounds having alpha-2 adrenoceptor antagonist properties. Prazosin, an antagonist for alpha-1 adrenoceptors, enforced the alpha-2 adrenoceptor agonist-induced depression in both species. 6-Hydroxydopamine treatment, which reduced the norepinephrine concentrations in the rat cerebral cortex by 76%, increased the duration of the loss of righting reflex induced by xylazine indicating that central postsynaptic alpha-2 adrenoceptors might also be involved in this behavioral alteration. The electrically-stimulated tritium release was also determined from the isolated rat cerebral cortex slices which had been preloaded with 3H-norepinephrine. Clonidine and xylazine inhibited the stimulation-induced tritium release and this inhibition was counteracted by yohimbine, idazoxan or CH-38083, but not by prazosin. We have concluded from the present data that stimulation of alpha-2 adrenoceptors with pre- and postsynaptic locations or inhibition of alpha-1 adrenoceptors in the central nervous system may shift the depression/vigilance balance to the direction of depression which might be accompanied by a decreased activity of cortical noradrenergic neural transmission.
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PMID:Possible role of alpha-2 and alpha-1 adrenoceptors in the experimentally-induced depression of the central nervous system. 257 6

The ototoxicity of an otic drop preparation containing 2% acetic acid and 3% propylene glycol (VoSol, Denver Chemical Co., Humacao, PR) was investigated according to measurements of endocochlear potential (EP) and inner ear fluid pH. The application of this preparation to the round window membrane for 30 minutes caused a depression in EP from 80.5 +/- 2.5 mV (mean +/- SD; n = 6) to 11.7 +/- 7.7 mV, and lowered inner ear fluid pH from 7.55 +/- 0.09 to 5.06 +/- 0.19 (n = 6) in perilymph and from 7.52 +/- 0.07 to 5.88 +/- 0.63 (n = 6) in endolymph. Two percent acetic acid produced similar changes after 30 minutes: EP was reduced from 83.0 +/- 2.2 mV to 34.0 +/- 2.9 mV and endolymphatic pH from 7.49 +/- 0.04 to 6.83 +/- 0.21 (n = 4). However, the application of artificial perilymph of pH 4 titrated with HCl induced no significant changes in either EP or endolymphatic pH. We suggest that the mechanisms of ototoxicity in the otic drop preparation are Na+ and K+-ATPase inhibition, and that such inhibition is due to the intracellular acidification of strial cells resulting from the penetration of acetic acid across the cell membrane, and to the direct and synergistic actions of propylene glycol.
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PMID:The preparation of acetic acid for use in otic drops and its effect on endocochlear potential and pH in inner ear fluid. 259 25

Somatostatin (SRIF) (6 nmol) given intracisternally (i.c.) into the alpha-chloralose anaesthetized rat has recently been shown to cause apnoea with a latency of 5-10 minutes (Kalia et al. 1984a). The apnoea produced by SRIF is very rapid, irreversible and leads to the death of the animal. In view of the existence of SRIF nerve cell bodies and terminals in medullary respiratory nuclei such as the ventral and ventrolateral subnuclei of the nucleus of the tractus solitarius (nTS) (Kalia et al. 1984b, Johanson et al. 1984), we have proposed the existence of somatostatinergic mechanisms in the respiratory nuclei of the medulla oblongata involved in mediating apnoeic conditions (Kalia et al. 1984a). In the present study, we have analysed whether the SRIF induced apnoea could be counteracted by a previous i.c. administration of the highly selective alpha 2-adreno-receptor blocking agent RX 781094 (2-(2-(I,4 benzodioxanyl]2-imi-dazoline HCl) (Doxey et al. 1983), or an opiate receptor blocking agent such as naloxone. Thus, both alpha 2-adrenoreceptor agonists and opiates induce respiratory depression, and opiates in high doses cause apnoea (Bolme et al. 1974, Hassen et al. 1982, Sitsen et al. 1982). In addition, catecholamine (CA) and enkephalin immuno-reactive nerve terminal networks exist in high densities within the nucleus tractus solitarius (nTS) of the medulla oblongata and may therefore interact with somatostatin nerve terminals in regulation of respiratory activity (Kalia et al. 1984b).
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PMID:Somatostatin induced apnoea: prevention by central and peripheral administration of the opiate receptor blocking agent naloxone. 286 86

A study was carried out to evaluate the effect of cysteamine-HCl administration on gizzard ulceration and growth performance in broiler chicks. The effectiveness of the histamine H2-receptor antagonist, SKF 93479, in preventing gizzard ulcerations when given in combination with cysteamine-HCl was also examined. In the initial experiment cysteamine-HCl at the level of 2400 mg/kg of the diet caused severe gizzard ulceration and mortality and decreased feed intake and growth in chicks. The effect was not seen when cysteamine-HCl was administered at 600 or 1200 mg/kg of the diet. In Experiment 2 broiler chicks administered cysteamine-HCl at 1800 mg/kg of the diet had an increased incidence of gizzard ulceration and decreased growth performance. The severity of gizzard lesions and the depression of growth performance were not as great as in the group in Experiment 1 which received the 2400 mg/kg level of cysteamine-HCl. Addition of the H2 antagonist SKF 93479 at 54 mg/kg of the diet had no effect on improving gizzard ulcer score or growth performance in chicks which received cysteamine-HCl at the 1800 mg/kg of the diet level. From these data it appears that the administration of ulcerogenic levels of cysteamine-HCl in the chicken may involve a more complex pathogenesis in which factors other than acid hypersecretion are involved.
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PMID:Gizzard ulceration in chicks fed cysteamine alone or in combination with a histamine H2-receptor antagonist. 290 91

A double-blind cross-over study was performed in 12 healthy female volunteers comparing cetirizine di-HCl (10 mg) and sustained release dexchlorpheniramine maleate (6 mg) with respect to attentuation of histamine-induced skin wheals and subjective central nervous system (CNS) effects. Cetirizine was significantly more effective than dexchlorpheniramine in suppressing the size of wheals from 2 to 24 h after drug administration. In fact, at 24 h cetirizine was still as effective as 2 h after ingestion. Ten subjects receiving dexchlorpheniramine reported subjective symptoms relating to CNS depression, in contrast to only one subject given cetirizine.
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PMID:Attenuation of cutaneous reactivity to histamine by cetirizine and dexchlorpheniramine. 297 49

The acute effects of lead in the rat CNS in vitro were studied on synaptic transmission in the isolated hemisected spinal cord from newborn rats and on the transport of exogenous GABA, acetylcholine and cis-3-aminocyclohexane carboxylic acid (ACHC) from slices of cerebral cortex from adult rats. Lead had quite variable effects on monosynaptic reflexes and synaptic potentials. When it occurred, the depression of synaptic transmission by lead (typically at 18.5 mumol/liters of added lead acetate) was reversible provided exposure times were less than 15 min; furthermore, depression could be antagonised by increasing the external calcium concentration. Lead had no effect on the postsynaptic responses of motoneurons to the putative transmitters L-glutamate, GABA and glycine or to eledoisin-related peptide. The effects of lead on uptake and release of exogenous GABA and ACHC were dependent on the perfusion buffer employed: minimal effects were seen in solutions buffered with either phosphate or carbonate. When Tris HCl was used as buffer, lead inhibited the uptake of GABA and potentiated the spontaneous release of GABA with an EC50 = 50 mumol/liters as added lead acetate. In Tris HCl buffer, lead acetate (100 mumol/liters) produced a two-fold enhancement in the spontaneous release of acetylcholine under conditions where choline and acetylcholine re-uptake was blocked by hemicholinium. The availability of free lead cations in solution is highly dependent on the concentrations of other ions (particularly phosphates) and the pH. Under the appropriate conditions, lead can inhibit CNS synaptic function acutely in a manner consistent with lead competing with calcium ions in transmitter release processes as has been established for acetylcholine release at peripheral synapses.
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PMID:Acute effects of lead at central synapses in vitro. 298 66


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