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

The Mauthner fiber giant fiber synapses of the hatchetfish are chemically transmitting axo-axionic synapses in the medulla. Tetanic stimulation at room temperature depletes the presynaptic Mauthner terminal of vesicles and leads to the appearance of large numbers of irregular membraneous compartments in the terminal. Stimulation during cooling to 12 degrees C depletes the terminal of vesicles and greatly increases the external surface, which forms large whorls of invaginating double membranes. Many coated vesicles are attached to the surface and the invaginating whorls. It is concluded that vesicles are discharged by exocytosis and fusion of their membrane with the external surface, and that at room temperature, membrane is reinternalized by coated vesicles and formed into irregular compartments. In completion of the cycle, these compartments disappear, and the vesicle population recovers over an hour or two of rest. When the Mauthner fibers are stimulated at low rates, the p.s.p.'s in the giant fibers are large and suprathreshold. Minature p.s.p.'s are generated spontaneously or can be evoked by subthreshold depolarization or tetanic stimulation of the Mauthner fiber. Stimulation of the Mauthner fibers at gradually increasing frequencies depresses p.s.p. amplitude to or below the level of miniature p.s.p.'s, but no failures are observed. Small p.s.p.'s without failures suggest that the quantum number remains high but that quantal size is greatly reduced, either by partial filling, as is supported by the morphological observation of vesicle depletion, or by desensitization. When stimulation is stopped, recovery of p.s.p. amplitude occurs in 1 or 2 seconds, but if tetanic stimulation is resumed immediately, p.s.p. amplitude decreases again and much more rapidly than in the initial rundown. This result suggests that depression of p.s.p. amplitude is not due to desensitization and leaves partial filling as the most likely explanation of small quanta. Calculated quantal size following a tetanus recovers in 200-500 ms, which probably largely reflects the time for filling since enough vesicles can be supplied to prevent failures with much shorter intervals between stimuli. Because quantal size appears to decrease gradually as stimulation frequency increases, it appears that release of vesicles can interrupt filling, leading to the conclusion that filling and release sites are very close together. This conlusion is consistent with other data in the literature obtained by different techniques.
Cold Spring Harb Symp Quant Biol 1976
PMID:Stimulation-induced depletion of vesicles, fatigue of transmission and recovery processes at a vertebrate central synapse. 18 Nov 97

Trigeminal (V) tractotomy and cold block of synaptic transmission in V nucleus caudalis were used to show that caudalis modulates the responses to innocuous and noxious stimuli of single V main sensory-oralis neurones recorded in anaesthetized or decerebrate cats. Cold block caused a reversible depression of mechanosensitivity of 91 of 105 V-thalamic relay and non-relay cells tested; V tractotomy also decreased sensitivity. The possibliity that the effects observed with cold block of caudalis were caused by direct spread of cooling to the main sensory-oralis region, and not by depression of a tonic, net facilitatory influence of caudalis on main sensory-oralis cells, was ruled out by several controls. With cold block of caudalis there also occurred a reversible shrinkage in mechanoreceptive field size and reversible reduction in sensitivity of rapidly adapting and slowly adapting mechanoreceptive neurones. Occasionally no change or an increase in sensitivity occurred, the latter suggesting the liklihood of an inhibitory influence from caudalis as well as the facilitatory influence. The effects of interactions of innocuous and noxious V stimuli were likewise subject to ascending influences from caudalis. Cold block also reversibly depressed responses to tooth pulp and V cutaneous noxious stimuli, although pulp-evoked responses were depressed less than mechanical or infraorbital nerve-elicited responses. Our results indicate that caudalis, as well as acting as a relay site to thalamus, also exerts a predominantly facilitatory influence on the relay to the thalamus and local reflex centres of mechanoreceptive and nociceptive information through the V main sensory-oralis region. The findings also might in part explain the analgesia, partial loss of tactile sensibility, and relief from V neuralgia reported after V tractotomy.
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PMID:Inputs to trigeminal brain stem neurones from facial, oral, tooth pulp and pharyngolaryngeal tissues: II. Role of trigeminal nucleus caudalis in modulating responses to innocuous and noxious stimuli. 18 52

Haemodynamic adaptation was studied during the first 10 h after aorto-coronary bypass surgery. In a control group of 12 patients the heart was fibrillating and perfused during cardiopulmonary bypass (at 30 degrees C), and in 11 patients cold cardioplegic arrest was used. The first 4--5 h were characterized by rewarming, with increasing oesophageal temperature, cutaneous vasoconstriction and elevated systemic vascular resistance (SVR). A phase of vasodilation followed. In the control group the oxygen uptake index increased by 57% during rewarming, but the cardiac index (CI) was constant (about 2.9 l . min-1.m-2). The arterio-venous oxygen content difference (AVDo2) therefore increased (max. 3.0 mmol . l-1). The postoperative left ventricular performance was better and the serum levels of aspartate aminotransferase (ASAT) during the first 2 days postoperatively were lower in the cardioplegic patients than in the controls, indicating more efficient myocardial preservation. In the cardioplegic-hypothermic group, CI was constant at about 3.2 l . min-1.m-2 (significantly higher than in the control group) and AVDo2 remained normal during the rewarming period. The heart rate was lower initially in the cardioplegic patients than in the controls, implying a favourable influence on myocardial oxygen consumption. The better myocardial function in the cardioplegic-hypothermic group was associated with an only moderately increased SVR. This suggests that the elevated SVR in the control group could have been due to myocardial depression.
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PMID:Myocardial performance early after aorto-coronary bypass surgery. Cardioplegic arrest versus coronary perfusion. 31 58

1. Increasing the Mg2+ concentration results in a depression of succinoxidase-linked state 3 respiration of liver mitochondria from both control and cold-acclimated rats and hamsters. 2. It appears that in the cold-acclimated hamster, liver mitochondrial respiration is more sensitive to changes in Mg2+ levels than that of the rat.
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PMID:The effects of magnesium on state 3 respiration of liver mitochondria from control and cold-acclimated rats and hamsters. 31 42

Xanthogranulomatous pyelonephritis in children, contrary to adult onset, rarely is associated with non-function or calcification. The lesion is predominantly on the left side in children. There appears to be a normal humoral but temporarily impaired cellular immune response in addition to sustained depression of polymorphonuclear chemotaxis. The etiology of this is uncertain but may be attributed partially to hyperosmolarity of serum and urine, and to leukocyte specific antinuclear antibodies. The presence of leukocyte specific antinuclear antibody or cold agglutining may interfere with normal phagocyte chemotaxis requiring tissue macrophages to produce a xanthogranulomatous reaction to bacterial invasion.
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PMID:Xanthogranulomatous pyelonephritis in children. 32 Mar 49

Unanesthetized squirrel monkeys exposed to an ambient temperature of 10 degrees C showed elevations in total body oxygen consumption (VO2), arterial blood pressure (BP), and heart rate (HR) above values recorded at 28 degrees C. Further elevation of BP in the cold by intravenous infusion of phenylephrine was accompanied by immediate reduction in VO2, inhibition of shivering, and decrease in rectal temperature, as well as immediate reduction in HR. The magnitude of reduction in VO2 correlated with the magnitude of the concomitant baroreflexive bradycardia. When the pressor effects of phenylephrine were opposed by administration of diazoxide or phentolamine, the inhibitory effects of phenylephrine on both HR and VO2 were abolished. In animals previously subjected to bilateral sinoaortic denervation, both the bradycardia and depression in oxygen consumption normally associated with BP elevation were markedly reduced. These results suggest that elevation of blood pressuere can inhibit the thermoregulatory increase in total body oxygen consumption normally produced by cold exposure, and that this inhibition, like the concomitant bradycardia, is probably mediated via the sinoaortic baroreceptors.
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PMID:Baroreflexive depression of oxygen consumption in the squirrel monkey at 10 degrees C. 40 89

Oxygen consumption was monitored in fed and fasted, lean and obese mice of the ob/ob strain before and after subcutaneous injections of norepinephrine (NE). The increase in oxygen consumption after NE was of a similar magnitude in both lean and obese fed mice, but of a longer duration in the obese. Prior fasting caused a diminution of the response in the lean but was associated with an enhanced response in the obese mice. Fasting also resulted in a significant depression of the resting oxygen consumption of the obese mice but not of the lean. The relevance of these findings to the inability of the obese mouse to withstand cold exposure and to the maintenance of the obese state is discussed.
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PMID:Influence of norepinephrine and fasting on the oxygen consumption of genetically-obese mice. 44 Jun 28

Lean and genetically obese (ob/ob) male and female mice were given nicotine by subcutaneous injection. Nicotine treatment was found to raise plasma free fatty acids by similar amounts in both lean and obese mice. In lean mice, nicotine caused depression of rectal temperature at ambient temperatures 22-25 degrees C and partially prevented the hypothermia in these mice when exposed to cold (o-3 degrees C). In obese mice, nicotine treatment did not alter either rectal temperature at 22-25 degrees C or the severe hypothermia on cold exposure. It is proposed that the effect of nicotine on free fatty acids is due to release of adrenal catecholamines and that this mechanism operates in both lean and obese animals. It is also proposed that, in obese mice under normal circumstances, there is a defect in the central nervous control of this adrenergic mechanism which may contribute to the observed fall in body temperature at low ambient temperatures.
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PMID:Acute effects of nicotine on plasma free fatty acid concentrations and on the response to cold stress, in lean and obese (genotype ob/ob) mice. 52 20

1. Measurements of milk secretion, mammary oxygen consumption and blood flow, cardiac output and blood pressure have been made in lactating goats exposed to a thermoneutral environment and to two levels of cold stress which were sufficient to raise total body oxygen consumption by an average of 18 and 46% above that in a thermoneutral environment. 2. Mammary blood flow and oxygen consumption were not appreciably affected by the milder cold stress but fell to 63 and 70%, respectively, of their thermoneutral value in the moderately cold environment. Resistance to blood flow through the udder was increased by this level of cold stress and the gland took a smaller fraction of an increased cardiac output. 3. Both levels of cold exposure caused a reduction in milk secretion, to 80 and 40% of its thermoneutral value in the mild and moderate cold respectively. The amount of milk secreted per unit volume of blood flowing through the gland decreased as the severity of the cold stress increased. 4. Voluntary food intake was not affected by the change in environmental temperature but the intake of water was reduced to 55% of the thermoneutral value during mild cold exposure and to 40% of the thermoneutral value during the moderate cold stress. 5. It is concluded that a reduction in blood flow to the mammary gland could be one of several possible mechanisms underlying the depression of milk secretion during cold exposure.
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PMID:Effect of cold exposure on mammary circulation oxygen consumption and milk secretion in the goat. 56 44

In anaesthetized rabbits the influence of vagal cold-block on the ventilatory response to lowered arterial oxygen pressure was investigated. With intact carotid chemoreflexes, lowered PaO2 caused hyperventilation, which was progressively intensified with the degree of hypoxia, regardless of whether the alveolar PCO2 was uncontrolled or kept constant at the hyperoxic control. The V-PaO2 response was to a greater extent due to an increase of respiratory rate than to one of tidal volume. During hyperoxia, vagal cold-block caused a distinct increase in ventilation provided the alveolar PCO2 was not allowed to decrease. During moderate hypoxia, vagal block caused only a slight increase in ventilation, when PACO2 was not controlled, but a distinct decrease in ventilation, when PACO2 was maintained at the hyperoxic level. Without carotid chemoreflexes, lowered PaO2 did not change ventilation at any level, provided the vagus nerves were left intact. This was due to a substantial increase in respiratory rate counteracting a corresponding decrease in tidal volume. Then vagal block led to a ventilatory depression depending on the degree of hypoxia, which was due to a simultaneous decline in respiratory rate and tidal volume. It is concluded that during hypocapnic hypoxia the vagal stretch reflex primarily inhibits the carotid chemoreflex drive of ventilation. During normocapnic hypoxia, however, the mode of interaction between the peripheral and the central chemical drive has to be considered, which without vagal feed-back is occlusive. This occlusion appears to be counteracted by a vagal mechanism sensitive to CO2 in the airways--and possibly also to a lack of O2--, mainly shortening respiratory cycle duration.
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PMID:The role of the vagus nerves in the ventilatory response to lowered PaO2 with intact and eliminated carotid chemoreflexes. 57 48


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