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)

Oxygen uptake, cardiac output, stroke volume and arterial and central blood pressures were measured before and after induction of neuroleptanaesthesia in 27 subjects. Nine were elderly patients operated on for obliterative arteriosclerotic disease, and the other 18--nine elderly and nine younger patients--underwent operation for varicose veins. Cardiac output, stroke volume and systolic arterial blood pressure decreased significantly with a corresponding decrease in oxygen uptake. The changes were most pronounced in the patients with arteriosclerotic disease. The arterio-venous oxygen difference was unchanged in the arteriosclerotics and decreased in the other two groups. The central pressures remained unchanged in all groups. It is concluded that the cardiovascular changes induced by neuroleptanaesthesia are due to a decrease in oxygen uptake and not to myocardial depression.
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PMID:The cardiovascular effects of neuroleptanaesthesia. 84 53

A case of upper gastrointestinal tract hemorrhage secondary to esophageal varices in a patient with Felty's syndrome prompted a review of the pathogenesis and treatment of this condition. Six previously reported cases of this association were found. The clinical picture is that of long-standing rheumatoid arthritis with severe articular and extraarticular manifestations including splenomegaly, depression of the blood elements, mild liver function abnormalities, portal hypertension without cirrhosis or portal vein obstruction, an elevated splenic blood flow, and a reduction in portal hypertension by simple splenectomy. The presence of portal hypertension with varices may be another indication of splenectomy in patients with Felty's syndrome.
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PMID:Esophageal varices in Felty's syndrome: A case report and review of the literature. 108 37

Synaptic connections between the sensory and motor neurons of Aplysia in culture undergo long-term facilitation in response to serotonin (5-HT) and long-term depression in response to FMRFamide. These long-term functional changes are dependent on the synthesis of macromolecules during the period in which the transmitter is applied and are accompanied by structural changes. There is an increase and a decrease, respectively, in the number of sensory neuron varicosities in response to 5-HT and FMRFamide. To determine whether macromolecular synthesis is also required for the structural changes, we examined in parallel the effects of inhibitors of protein (anisomycin) or RNA (actinomycin D) synthesis on the structural and functional changes. We have found that anisomycin and actinomycin D block both the enduring alterations in varicosity number and the long-lasting changes in synaptic potential. These results indicate that macromolecular synthesis is required for expression of the long-lasting structural changes in the sensory cells and that this synthesis is correlated with the long-term functional modulation of sensorimotor synapses.
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PMID:Inhibitors of protein and RNA synthesis block structural changes that accompany long-term heterosynaptic plasticity in Aplysia. 135 72

FMRFamide evokes both short-term and long-term inhibition of synapses between mechanosensory and motor neurons in Aplysia. We report here, using dissociated cell culture and low-light epifluorescence video microscopy, that depression lasting 24 hr of sensorimotor synapses evoked by four brief applications of FMRFamide is accompanied by a significant loss of sensory cell varicosities and neurites. These structural changes in the sensory cells require the presence of the target motor cell L7. Because the loss of structures known to contain transmitter release sites correlates significantly with the changes in the amplitude of the excitatory postsynaptic potential in L7, our results suggest that the structural changes evoked by FMRFamide reflect a loss of synaptic contacts. Thus, long-term depression parallels long-term facilitation of the sensorimotor synapse produced by serotonin in that both forms of heterosynaptic plasticity involve target-dependent modulation of the number of presynaptic varicosities.
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PMID:Target-dependent structural changes in sensory neurons of Aplysia accompany long-term heterosynaptic inhibition. 167 49

The central functions of norepinephrine (NE) are a recent discovery: regulation of alertness and of the wakefulness-sleep cycle, maintenance of attention, memory and learning, cerebral plasticity and neuro-protection. The anatomical, histological, biochemical and physiological properties of the central noradrenergic system: extreme capacity for ramification and arborization; slow conduction, non-myelinized axons with extrasynaptic varicosities producing and releasing NE; frequency of co-transmission phenomena, and; neuromodulation with fiber effect responsible for improvement in the signal over background noise ratio and selection of significant stimuli form a true interface between the outside world and the central nervous system, notably for the neocortex in the context of the cognitive treatment of information. This central noradrenergic system is involved in the neurophysiology and the clinical features of cerebral aging (ideation-motor and cognitive function slowing down, loss of behavioral adjustment), neuro-degenerative disorders (SDAT, Parkinson's disease), certain aspects of depression and less obvious conditions (head injuries, sequelae of cerebrovascular accidents, sub-cortical dementia). The recent development of medications improving alertness (adrafinil, modafinil) with a pure central action and specifically noradrenergic, may contribute to an improvement in these multifactorial disorders.
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PMID:[Noradrenaline and cerebral aging]. 186 52

Tonically and phasically active crayfish motor terminals have well-characterized differences in synaptic physiology. During repetitive activation, the tonic terminals show facilitation and no depression, while the phasic terminals show dramatic synaptic fatigue. It has been proposed that this greater capacity for transmitter release from tonic terminals may be largely due to the presence of large synaptic varicosities along tonic terminals that contain large mitochondria, synapses, and numerous synaptic vesicles. In addition, a recent study indicates that in vivo tonic stimulation of a phasic terminal in young animals increases the fatigue resistance of the neuromuscular synapses and increases the number of synaptic varicosities, as well as the size of mitochondria and synapses. Because these previous morphological studies of crustacean motor terminals were performed using transmission electron microscopy, only short lengths of terminal were observed, and changes in synaptic varicosity frequency and size could not be thoroughly examined. In order to examine the synaptic varicosities along the terminal, motor terminals were injected with HRP, and the morphology of contrast-enhanced light microscopic images was examined. We report here that tonic terminals have much larger and more numerous synaptic varicosities than phasic terminals. In vivo stimulation of a phasic motoneuron results in an increase in the frequency of synaptic varicosities. This represents an increase in the total number of varicosities because terminal length appears to remain constant. These synaptic varicosities appear to form along preexisting terminals and persist for days after the final in vivo stimulation. The results indicate that the greater transmitter-releasing capabilities of tonic terminals compared to phasic terminals are due to their larger and more frequent synaptic varicosities. In addition, the development of these synaptic varicosities is activity dependent.
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PMID:Activity-dependent development of synaptic varicosities at crayfish motor terminals. 201 Aug 3

To assess the role of peripheral sympathetic nerves in the regulation of calcitonin release, rats subjected to superior cervical ganglionectomy (SCGx) 16-28 h earlier were used. The time periods selected allowed us to examine C cell response during the supraliminal release of sympathetic transmitter that accompanies anterograde degeneration of nerve varicosities as well as during the neural paralysis that ensues thereafter. At the time intervals examined, SCGx did not result in significant changes of basal serum calcitonin or Ca levels. The intraperitoneal administration of CaCl2 brought about an impending increase of serum Ca to the same extent in SCGx and sham-operated rats. A significant depression of calcitonin release was observed in rats killed around the time of nerve terminal degeneration (16-21 h post SCGx) but not about 10 h later. Additionally a delay to achieve a maximal calcitonin response was apparent during nerve degeneration. Injection of the alpha-adrenoceptor blocker phenoxybenzamine significantly increased basal calcitonin levels and restored the depressed calcitonin response to hypercalcemia seen in SCGx rats. Treatment with the beta-adrenoceptor-blocker propranolol counteracted phenoxybenzamine activity but was unable to modify per se calcitonin release in SCGx or sham-operated rats. Basal Ca levels and their increase after intraperitoneal CaCl2 were similar in all examined groups regardless of the drug injected. In an additional experiment phenoxybenzamine injected into SCGx rats in doses one-fifth those employed earlier still reversed both the depression in maximal calcitonin response as well as the delay to attain maximal release after CaCl2, but was unable to affect basal calcitonin levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in calcitonin release during sympathetic nerve degeneration after superior cervical ganglionectomy of rats. 374 8

Medical histories of 436 patients treated with Ovulen after childbirth or an abortion were examined in order to collect a sample of women who had taken the orals for 6-12 cycles. A group of 70 patients was thus formed. The following parameters were investigated: weight variation; blood pressure; nausea and vomiting; varicosities; variation in menstrual flow and length of period; breast-related side effects; jaundice; psychic alteration, i.e., nervousness, anxiety, or depression; changes in libido; headaches; skin changes; and pregnancy. Results are presented both in graph and table form. Weight change was found to tend more to loss than to gain. No statistically significant changes in blood pressure were observed. Nausea and associated symptoms tended to disappear after the 9th cycle. Edema was present in only 6% of all cycles. The most common side effect was varicosities, present in 25% of the sample, but in no instance did thrombosis occur nor was varicosity a cause for discontinuation in any case. Breast-related side effects were more common at the outset. No jaundice was observed. Psychic alterations were not common and were mostly insignificant and tended to occur more frequently at the outset. 12% of the sample had headaches from the beginning of treatment up until the 8th month, after which they began to disappear. Only 1 patient had chloasma and then only during the 1st 2 cycles. There was a marked tendency toward menorrhagia which was thought to be beneficial due to the prevalence of anemia in the group. Changes in libido were minimal and tended to disappear after the 8th cycle. None of the patients became pregnant.
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PMID:[Secondary effects of ethynodiol diacetate plus mestranol]. 535 18

1. Chemical synaptic transmission develops between individual identified neurones dissected from leech ganglia and maintained in culture. Impulses in Retzius cells give rise to hyperpolarizing synaptic potentials in pressure (P) sensory cells. In suitable medium the potentials develop by 3 days and can be observed for more than 3 weeks. 2. The synaptic potentials occur after a synaptic delay, exhibit facilitation and depression and are reversed by hyperpolarization. The blocking effects of reduced calcium and raised magnesium concentrations in the bathing fluid provide additional evidence for the chemical nature of transmission. 3. An increase in chloride conductance is involved in the generation of the synaptic potential in the P cell. With high intracellular Cl in the post-synaptic cell, the synaptic potentials become reversed and amplified. The amplitudes of these reversed responses range from 1 to 20 mV with a falling phase lasting for seconds. 4. Changes in the membrane potential of the presynaptic cell that modify the amplitude and duration of the action potential influence the efficacy of transmission. In addition, impulses in Retzius cells initiated from hyperpolarized values of membrane potential evoke smaller synaptic potentials in the P cells than impulses arising from a depolarized level. 5. With neurones placed directly next to one another in the dish, maintained depolarization of the presynaptic Retzius cell in the absence of conducted action potentials gives rise to slow synaptic potentials in the P cells. In some pairs, the response in the P cell consists of a marked increase in 'noise'. 6. Injection of horseradish peroxidase into the Retzius cell reveals neurites with distinctive varicosities growing over the P cell.
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PMID:Chemical transmission between individual Retzius and sensory neurones of the leech in culture. 612 33

The muscarinic acetylcholine (ACh) receptor from rat brain has been partially purified and characterized. The molecular weight of the smallest subunit of the receptor protein obtained by a chaotropic agent is 30,000 dalton, while the protein found in sodium dodecyl sulphate polyacrylamide gels has a molecular weight of 80,000 dalton. The isoelectric point is in the range 4.5 to 5.1. The low affinity dissociation constant for agonists of the alpha-adrenoceptor from rat and guinea-pig brain, and of the muscarinic ACh receptor from guinea-pig ileum longitudinal muscle-myenteric plexus preparation, is increased 2-3-fold at potassium concentrations of 80-100 mM. The transmitter stores of noradrenergic nerves of guinea-pig vas deferens were labelled by preincubation with 3H-noradrenaline (3H-NA), and those of cholinergic nerves of guinea-pig ileum myenteric plexus were labelled by preincubation with 3H-choline. The mechanisms underlying frequency dependent facilitation and presynaptic receptor mediated depression of transmitter secretion were studied. The secretion evoked by electrical stimulation required both invasion of the nerve terminals and activation of the depolarization-secretion coupling in varicosities, while that evoked by high potassium (40-110 mM) was due to direct depolarization varicosities. Blockade of presynaptic alpha-adrenergic and muscarinic autoreceptors by phentolamine and atropine, respectively, caused 4-5-fold greater increase in the secretion of labelled transmitter evoked by electrical than by potassium stimulation from noradrenergic and cholinergic terminals. This suggests that depression of transmitter secretion is exerted mainly by control of the invasion of nerve terminals, and only to a minor extent by control of depolarization-secretion coupling in invaded terminals. Autoinhibition of transmitter secretion involves regulation of calcium availability and is antagonized by facilitation. Endogenous cyclic nucleotides are not critically involved in either facilitation, or alpha-adrenergic or muscarinic autoreceptor mediated control of transmitter secretion in these nerves.
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PMID:Mechanisms of facilitation and muscarinic or alpha-adrenergic inhibition of acetylcholine and noradrenaline secretion from peripheral nerves. 629 52


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