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)

Dynamics of spatial temperature distribution over the dorsal surface of the cerebral cortex was studied through the skull with the thermovision technique on immobilized white rats. Direct cortical stimulation revealed local thermoresponses (up to +0.2 degrees C) under electrodes, in the symmetrical point in the opposite hemisphere as well as in some other cortical zones. The response latency was within the limit of 160 ms, peak latency--2-5 s and relaxation time 2-3 min. Nembutal caused depression of thermoresponses, increase in their thresholds, limitation in size as well as slowing down of the development and prolongation in time.
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PMID:[Temperature distribution on the surface of the rat brain during direct electric stimulation]. 360 Aug 73

Whole mice on normal or vitamin E deficient diet were immobilized by Nembutal anaesthesia and exposed to a stationary magnetic field of 1.4 tesla for up to 60 min. Thymidine kinase (TdR-K) was assayed in the high-speed supernatant of bone marrow cells which were collected into optimally adjusted nutrient medium of pH 7.3-7.4 containing 1350 mg NaHCO3 per litre and were then destroyed by sonication. In parallel, uptake of 125I-labelled 5-I-2'-deoxyuridine (125IUdR) into DNA of whole bone marrow cells, of various tissues and of the whole body was measured. The results indicate the following. The magnetic field exposure caused in bone marrow cells an increase of activity of TdR-K and of uptake of 125IUdR to about 130 per cent of control. The effect depended on immobilization of the mice in the field and on the presence of NaHCO3 in the nutrient medium used for cell collection. There was no field-induced change in body temperature. The effect on 125IUdR uptake was similar in isolated tissues and the whole body following intraperitoneal injection of the tracer. It increased to a maximum of about 135 per cent of control, during exposure times over 30 min. This effect is not explained as a result of a temporary change in the rate of cell proliferation. Vitamin E deficiency caused a depression of activity of TdR-K and of uptake of 125IUdR in bone marrow cells to about 75 per cent of control. This depression was similar to that observed after whole body gamma-irradiation with about 0.01 Gy (1 rad). The inhibitory effects of vitamin E deficiency on TdR-K were overcome by exposure to the magnetic field. Immediately after cessation of the magnetic field for 60 min, 125IUdR uptake was normal; normalization of uptake was delayed with exposure times shorter than 60 min. A 60 min exposure to the magnetic field had no long term effect on turnover of labelled cells in the mice. The data imply the non-specific control of thymidine kinase by charged molecular species and the modification of this control by the magnetic field.
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PMID:Magnetic field affects thymidine kinase in vivo. 387 39

Muscle potentials were recorded in the soleus muscle of Wistar rats anesthetized with urethane or Nembutal. The time course of their changes induced by repetitive stimulation of sciatic nerves at 5 Hz for 10 min was compared for young and aged rats. When stimulation commenced, muscle potentials from young rats were somewhat facilitated, followed by slight depression below control values, and thereafter they were gradually potentiated. On the contrary, muscle potentials from aged rats were rapidly reduced, attaining plateau levels 2 min or so after the onset of repetitive stimulation at 5 Hz.
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PMID:Patterns of soleus muscle potentials to repetitive stimulation in young and aged rats. 406 83

The effects of pentobarbital (Nembutal) on synaptic transmission and postsynaptic potentials were studied by the use of several invertebrate preparations. Pentobarbital selectively and reversibly depressed both excitatory postsynaptic potentials and sodium-dependent postsynaptic responses to putative excitatory transmitters without affecting either inhibitory postsynaptic potentials or chloride- and potassium-dependent postsynaptic responses to putative transmitters. A selective depression of postsynaptic excitatory events was also observed with other central nervous system depressants (ethanol, chloroform, chloralose, diphenylhydantoin, and urethane). The results suggest that central and peripheral depression observed during general anesthesia is due to a selective depression of excitatory synaptic events.
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PMID:Pentobarbital: selective depression of excitatory postsynaptic potentials. 435 18

1. The effects of pentobarbitone (0.05-0.6 mM in saline solution) on the evoked field potentials of in vitro preparations of guinea-pig olfactory cortex were studied.2. The evoked field potentials comprised an initial diphasic wave - the lateral olfactory tract (l.o.t.) compound action potential - followed by a surface negative wave (e.p.s.p) of 1-3 mV amplitude and about 10 msec duration. Superimposed on the negative wave were a number of positive peaks (population spikes).3. Pentobarbitone depressed the e.p.s.p. but not the l.o.t. compound action potential. The number and size of the population spikes were progressively reduced as the e.p.s.p. became depressed, indicating a failure of transmission through the cortical relay. The e.p.s.p. depression increased with increasing concentrations of pentobarbitone.4. Pentobarbitone had no effect on the threshold to electrical stimulation of the l.o.t. fibres or on that of the post-synaptic cells to synaptic excitation.5. Post-tetanic potentiation and frequency potentiation were either of normal magnitude or were enhanced in the presence of 0.2-0.3 mM pentobarbitone.6. It is concluded that pentobarbitone probably reduces the output of transmitter from the presynaptic nerve terminals of the olfactory cortex and that this mechanism could be the basis of the depressant action of the barbiturates.
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PMID:On the mechanism of barbiturate anaesthesia. 440 54

1. The cerebellar integration of sensory inputs to Deiters neurones was studied in cats under Nembutal anaesthesia.2. Stimulation of peripheral nerves produced in the Deiters neurones a sequence of an initial excitatory post-synaptic potential (e.p.s.p.) and a later inhibitory post-synaptic potential (i.p.s.p.), or a relatively small e.p.s.p.3. The Deiters neurones were classified as forelimb (FL)- or hind limb (HL)-type cells according to the location of the most effective peripheral nerve. In the FL cells stimulation of the forelimb nerves produced the e.p.s.p.-i.p.s.p. sequence (dominant response), while stimulation of the hind limb nerves was ineffective or produced the small e.p.s.p. (non-dominant response). In contrast, in the HL cells the non-dominant response was evoked from the forelimb nerves, and the dominant response from the hind limb nerves.4. The stimulus intensity-response relation indicates that Group I and II muscle afferents and low and high threshold cutaneous afferents contribute to the dominant and non-dominant responses.5. Antidromic identification of these Deiters neurones revealed that 90% of the HL cells and 85% of the FL cells project to the lumbo-sacral and cervico-thoracic segments of the spinal cord, respectively, while 10% of the HL cells and 15% of the FL cells innervate the cervico-thoracic and lumbo-sacral segments, respectively.6. The mean latency of the e.p.s.p. evoked from the forelimb nerves was 14 msec in the FL cells and 13 msec in the HL cells, and the latency of the e.p.s.p. evoked from the hind limb nerves was 17 msec in the FL cells and 18 msec in the HL cells. The later i.p.s.p. regularly followed the onset of the e.p.s.p. with a delay of 3-5 msec.7. The dominant and non-dominant responses in both types of cells exhibited the following three characteristic features: (i) a strong depression after conditioning stimulation of the inferior olive, (ii) an increase of the inferior olivary excitability during the responses, and (iii) a striking frequency depression with stimulation at relatively low frequency (5-10/sec).8. Consequently it was concluded that all of the responses were produced through the climbing fibres originating from the inferior olive, the i.p.s.p.s due to inhibition from Purkyne cells activated by the climbing fibres and the e.p.s.p.s due to excitation from the collaterals of the climbing fibres.
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PMID:Synaptic actions of peripheral nerve impulses upon Deiters neurones via the climbing fibre afferents. 456 27

1. In the unanaesthetized cat, an injection of 0.75 mg of morphine into a lateral cerebral ventricle produced strong hyperglycaemia; on intravenous injection, 10 to 30 times larger doses were required. Other effects produced with both injections were shivering, pupillary dilatation, opening of the eyes, miaowing, periods of excitation, and analgesia. Between the periods of excitation the cat did not react to objects moving in front of its eyes and it had a vacant stare.2. Noradrenaline, adrenaline, and 5-hydroxytryptamine (5-HT) injected intraventricularly (250 mug, twice) depressed the hyperglycaemia due to intraventricular morphine, and noradrenaline also depressed the hyperglycaemia due to intravenous morphine. Adrenaline produced the strongest and 5-HT the weakest depression. 5-HT did not depress the other effects of morphine, but the catecholamines depressed most of them; only analgesia and the vacant stare appeared to be unaffected.3. Reserpine injected intraventricularly (0.5 mg, twice) greatly accentuated the hyperglycaemia as well as the other effects produced by intraventricular morphine, but pupillary dilatation and opening of the eyes no longer occurred; the protrusion of the nictitating membranes produced by the reserpine persisted.4. Pentobarbitone sodium injected intraperitoneally in an anaesthetizing dose practically abolished the morphine hyperglycaemia, but injected intraventricularly in a dose of a few milligrammes, it had a two fold effect: depression followed by enhancement of the morphine hyperglycaemia. The enhancement may be due to sensitization of the effect of the adrenaline released by morphine, since adrenaline hyperglycaemia was enhanced as well.5. Morphine did not seem to act on structures in the walls of either the lateral or third ventricle when producing its hyperglycaemic effect on intraventricular injection. The action may therefore be on more caudally situated parts of the neuro-axis, on the central grey, on structures in the floor of the fourth ventricle or of the lateral recesses, or even on structures near the ventral surface of the brain stem.
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PMID:The hyperglycaemic effect of morphine. 465 65

1. The effect of haemorrhage on minute ventilation, arterial blood pH and end-tidal CO(2) has been investigated in cats anaesthetized with Nembutal. There was no change in minute ventilation with alteration of blood pressure above 100 mm Hg. Below this level ventilation progressively increased, the minute ventilation at 60 mm Hg being 33% above that at 100 mm Hg. The increase in minute ventilation was always associated with a fall in end-tidal CO(2) and a decrease in arterial blood hydrogen ion concentration.2. The effects were not influenced by vagotomy, but were abolished by carotid sinus denervation or carotid body destruction. After vagotomy and sinus denervation or aortic and carotid chemoreceptor destruction, haemorrhage resulted in a depression of respiration.3. The changes in arterial blood pH and end-tidal CO(2) did not occur without a change in minute ventilation.4. When the changes in arterial blood pH during haemorrhage were prevented by administration of CO(2) there was a marked increase in minute ventilation. It is concluded that the respiratory drive to respiration in the cat during haemorrhage is controlled mainly by carotid body chemoreceptors and that the resultant alkalaemia decreases the respiratory response.
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PMID:The effects of acute haemorrhage on respiration in the cat. 597 78

Earlier experiments have shown that afferent electrical stimulation of the sciatic nerve for 30 min induces a long-lasting post-stimulatory endorphin-dependent decrease in blood pressure in awake spontaneously hypertensive rats (SHR). In the present study we have examined whether this depressor response can be observed also in anesthetized SHR. The sciatic nerve was stimulated for 30 min with low-frequent (3 Hz) trains of impulses and the changes in blood pressure, heart rate and renal nerve activity were observed during the stimulation and in the post-stimulatory period. Animals anesthetized with Nembutal, Althesin and N2O did not show any post-stimulatory depression. In contrast, during chloralose anesthesia combined with muscle paralysis with Flaxedil, sciatic nerve stimulation induced a long-lasting post-stimulatory decrease in blood pressure due to central inhibition of sympathetic activity. The decrease in blood pressure could be prevented by naloxone and was therefore likely to be mediated via activation of central endorphin systems.
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PMID:Circulatory depression following low frequency stimulation of the sciatic nerve in anesthetized rats. 608 5

1 It has been suggested that the depression of excitatory synaptic potentials produced by general anaesthetics can be attributed to a partial blockade of impulse conduction in the terminal branches of axons. This hypothesis has been tested by comparing the actions of pentobarbitone, procaine and tetrodotoxin (TTX) on synaptic transmission in the guinea-pig olfactory cortex. 2 Pentobarbitone (0.1-0.3mM) depressed the evoked synaptic potentials without any significant depression of impulse conduction in the afferent fibres of the lateral olfactory tract (1.o.t). It had no effect on the electrical excitability of either the l.o.t axons or the postsynaptic neurones. 3 Tetrodotoxin (TTX; 1-5x10(-8 M) slowed conduction of impulses in the l.o.t. and decreased the amplitude of the l.o.t compound action potential in proportion to the concentration applied. All concentrations of TTX elevated the electrical threshold of the l.o.t. axons and there was evidence to suggest that the threshold of the postsynaptic neurones was also elevated. The synaptic potentials were depressed in direct proportion to the depression of the l.o.t. compound action potential. 4 Procaine (0.1-0.5 mM) exhibited a pattern of activity intermediate between pentobarbitone and TTX. The most marked effect, seen at all concentrations tested, was a slowing of impulse conduction and a decrease in the electrical excitability of the l.o.t. axons. 5 It is concluded that general anaesthetics (exemplified by pentobarbitone) depress synaptic transmission by interfering with the processes involved in chemical transmission and not by blocking impulse conduction in the terminal branches of afferent nerves.
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PMID:The actions of pentobarbitone, procaine and tetrodotoxin on synaptic transmission in the olfactory cortex of the guinea-pig. 627 19


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