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

Repetitive stimulation of the locus coeruleus evoked strong inhibition of the firing rate of about 50% of cells of the cingulate rat cortex. Forty per cent of the cells were not affected and 9% were excited by stimulation of the locus coeruleus. Pretreatment of the rats with reserpine and alpha-methyl-p-tyrosine drastically reduced the percentage of cells inhibited by locus coeruleus stimulation. The cells inhibited in response to stimulation of the locus coeruleus as well as those not inhibited were depressed by microiontophoretically applied norepinephrine. This inhibitory action of NE was observed in rats anesthetized either with urethane, chloral hydrate or with Nembutal. The transsynaptically elicited, as well as the norepinephrine elicited, depression of the cells' discharge rate was antagonized by the microiontophoretically applied beta-receptor blocking drug MJ 1999. These data suggest that the inhibitory action on cingulate cortical cells of locus coeruleus stimulation is mediated by the dorsal ascending noradrenergic pathway.
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PMID:Activation of an inhibitory noradrenergic pathway projecting from the locus coeruleus to the cingulate cortex of the rat. 69 22

The toxicity of pentobarbital was examined in male Wistar rats pretreated with a non-toxic dose of imipramine (10 mg/kg, po). Pentobarbital (70 mg/kg, ip) lethality was enhanced up to 6 hr after imipramine administration, and pentobarbital (45 mg/kg, ip) sleeping time was prolonged up to 12 hr after imipramine. Physiological measurements showed that imipramine pretreatment 2 hr prior to pentobarbital (70 mg/kg, ip) enhanced barbiturate depression in mean blood pressure, oxygen consumption and respiration rate, but not in heart rate or back skin temperature. Analysis of brain radioactivity after [14C] pentobarbital indicated that these effects of imipramine were not solely the result of inhibition of liver metabolism.
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PMID:Imipramine enhancement of pentobarbital toxicity in rats. 93 31

Guinea pigs treated with a single s.c. injection of a slowly released morphine suspension (300 mg/kg) exhibited a quantifiable withdrawal syndrome after naloxone injection (0.01-10 mg/kg s.c.). Ileum removed from such animals responded to naloxone (1-300 ng/ml) by contracting. These contractions could be blocked by scopolamine or tetrodotoxin. Both the in vivo and in vitro responses were specific for the opiate-dependent state and were dependent on naloxone dose. Time courses of the development and decline of the two responses were similar. Weaker opioids, pentazocine and codeine, were less effective than morphine in producing a dependent state and sensitizing ileum to naloxone. 1-(-)-delta9-Tetrahydrocann abinol [1-(-)-delta9-THC] antagonized the effect of naloxone on ileum without affecting responses to acetylcholine. 1-(-)-delta9-THC produced a stereospecific, dose-dependent (1-10 mg/kg p.o.) inhibition of naloxone-precipitated withdrawal in guinea pigs and rats that was more complete than and different from that produced by sedatives. Pentobarbital inhibited withdrawal only at doses that produced ataxia. 1-(-)-delta9-THC had a biphasic effect on locomotor activity of guinea pig in the dose range that inhibited withdrawal, stimulation at 1 mg/kg and depression at 3 to 10 mg/kg. Our results suggest that cannabinoids may be useful in opiate detoxification. The inhibition by 1-(-)-delta9-THC of the action of naloxone in "dependent" ileum seems to be via reduction in acetylcholine release. Whereas the end result of 1-(-)-delta9-THC action in brain may not necessarily be a reduction in acetylcholine release as in ileum, the mechanism by which it produces this effect in the ileum model may explain its ability to antagonize withdrawal.
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PMID:Correlation between the in vivo and an in vitro expression of opiate withdrawal precipitated by naloxone: their antagonism by l-(-)-delta9-tetrahydrocannabinol. 98 78

1 The effects of general anaesthetics on the responses of neurones to iontophoretically applied L-glutamate have been examined in slices of the guinea-pig olfactory cortex in vitro. 2 Concentrations of pentobarbitone, ether, methoxyflurance, trichloroethylene and alphaxalone that are known to depress synaptic transmission in the prepiriform cortex also depressed the sensitivity of prepiriform neurones to L-glutamate. 3 Halothane, in concentrations that depress synaptic transmission (less than 1%) did not alter sensitivity of neurones to glutamate. Higher concentrations (greater than 1% produced a dose-related depression of the glutamate sensitivity of neurones. 4 All four volatile anaesthetics tested caused some cells to alter their glutamate-evoked firing pattern to one in which the spike discharges were more closely grouped. Pentobarbitone and alphaxalone had no such effect. 5 If the sensitivity of the neurones to the endogenous excitatory transmitter is affected by anaesthetics in the same way as the glutamate-sensitivity, these results suggest that halothane depresses synaptic transmission by decreasing the amount of transmitter released from the nerve terminals, whereas the other anaesthetics depress the sensitivity of the post-synaptic membrane to the released transmitter.
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PMID:Anaesthetics depress the sensitivity of cortical neurones to L-glutamate. 99 May 90

The canine right atrium was perfused with arterial blood led from a carotid artery of the heparinized support dog and suspended in a bath filled with blood. In 5 non-spontaneously beating preparations, the frequency-force relationship was investigated by electric stimulation at a frequency range from 0.017 to 3 Hz. At a low frequency level, a large peak tension developed. At 0.5 Hz, minimum values of developed tension were obtained. At a range of 0.5-3 Hz, the developed tension increased with the frequency. Higher frequencies than 4 Hz usually caused pulsus alternans. The staircase phenomena were not influenced by treatment with propranolol or atropine. Therefore, there may be no participation of the autonomic nerve stimulation on the frequency-force relationship. Effects of pentobarbital, (+/-)-verapamil and manganese on the frequency-force relationship were investigated with both the blood-perfused, isolated atrium preparations and isolated ventricular preparations. Pentobarbital and manganese chloride produced a uniform depression of the developed tension at all frequencies but the depression with (+/-)-verapamil was greater at higher frequencies in both atrial and ventricular muscles.
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PMID:Effect of pentobarbital, verapamil and manganese on the frequency-force relationship of the isolated atrium and ventricle of the dog heart. 99 33

To ascertain whether neuroleptics act on the caudate nucleus itself, the effects of these compounds as well as other centrally acting drugs were examined in relation to caudate spindle and EEG arousal responses (sciatic nerve stimulation) in gallamine-immobilized cats. Haloperidol and chlorpromazine enhanced the caudate spindle at a dose which had no effect on the EEG arousal response. On the other hand, clozapine and a higher dose of chlorpromazine enhanced the caudate spindle, but depressed the arousal response. High frequency stimulation of the sciatic nerve suppressed the caudate spindle. Pentobarbital, biperiden and diazepam, while depressing the arousal response, caused an enhancement of the caudate spindle. Imipramine at a low dose had no effect on either response, whereas at a high dose this drug enhanced the caudate spindle with concomitant depression of the arousal response. From these results, it may be concluded that the enhancing action on the caudate spindle induced by haloperidol and a low dose of chlorpromazine is due to an increase in susceptibility of the caudate nucleus itself. In addition, it is suggested that depression of the activating system is involved in an appearance of the caudate spindle.
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PMID:Effect of psychotropic drugs on caudate spindle in cats. 100 8

Pentobarbital depressed macromolecular synthesis in Ehrlich ascites cells in vitro, and this depression was proportional to a decrease in oxygen consumption. However, survival time of animals bearing Ehrlich ascites cells was unaffected by pentobarbital. The acute toxicity of the drug was greatly enhanced by the presence of the tumor. Sleeping time was prolonged in mice carrying the following tumors: Ehrlich ascites, Sarcoma 180 ascites, and Yancy plasma cell solid. Seven-day Ehrlich ascites tumor-bearing animals treated with pentobarbital slept about three times longer than normal mice, but both groups awoke at the same plasma levels of the unbound drug. The plasma half-life of unchanged pentobarbital was about four times as long in tumor-bearing mice as it was in controls. No qualitative difference in catabolism other than rate was detected. Renal excretion of unchanged pentobarbital in tumor-bearing animals was 50% of control animals during the first 4 hr. In tumor-bearing mice the sleeping time of the nonmetabo ble barbiturate, barbital, was identical with that in normal animals. These data suggest that the tumor affected mainly pentobarbital metabolism. Tumor-bearing mice still responded to the pharmacological challenge of phenobarbital with the apparent induction of drug metabolizing enzymes. The prolonged pentobarbital sleeping time in tumor-bearing mice required the development of some type of tumor-host relationship.
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PMID:Physiological disposition of pentobarbital in tumor-bearing mice. 112 Mar 16

Eleven sheep were prepared with cannula guides directed toward four areas within the ventricular system to determine effective sites of action of chemicals which when injected into the cerebrospinal fluid produce changes in feeding behavior and temperature regulation. Pentobarbital, barbital, calcium chloride, and magnesium chloride elicited feeding in sheep when injected into the third ventricle or into the cerebral aqueduct; however, feeding response was less after injections into the latter. Pentobarbital and magnesium chloride elicited an increase in body temperature when injected into the third ventricle but not when injected into the cerebral aqueduct. Perfusions (push-pull) of the lateral and third ventricles with calcium chloride and magnesium chloride solutions (50 mM) resulted in feeding while similar perfusions of the fourth ventricle resulted in no response. Responses to lateral and third ventricular injections presumably involved effects on both anterior and posterior hypothalamic areas while injections into the cerebral aqueduct, due to the caudal flux of the cerebrospinal fluid, may have affected primarily only the posterior hypothalamus and more caudal structures. The feeding response probably resulted from depression of neural fibers which inhibit feeding.
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PMID:Feeding and temperature changes in sheep following injections of barbiturates, Ca-++, or Mg-++ into the lateral, third, or fourth ventricle or cerebral aqueduct. 112 57

In acute experiments on cats under deep Nembutal anesthesia punctures of the cortex caused a prolonged negative shift of its surface potential (up to 15 mv, 5.5 min), which was followed by a prolonged positive shift. During these shifts of the potential, both components of the direct response were depressed. The changes in potential and the depression of electric activity spread over the cortex at a mean rate of 65 micrometers/s. The phenomenon arised when the punctures are made with a pipet 20 micrometers and above in diameter. A puncture of the surface structures was critical; passage of the pipet through the middle and deep layers was ineffective. It is assumed that when cortical punctures are made the SD is caused by K(+) ions which leak out of the destroyed glial structures.
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PMID:Spreading depression resulting from cortical punctures. 121 Dec 54

1. The effects of BRL 34915 (cromakalim), a potassium channel opener, have been tested on the epileptiform activity elicited by high dose/concentrations of some calcium antagonists in in vivo (diltiazem) and in vitro (diltiazem and verapamil) experiments in rats. 2. Diltiazem (150-300 mg kg-1, i.p.) induced behavioural and electroencephalographic (EEG) seizures that were completely prevented by cromakalim (10 nmol/10 microliters, i.c.v.). Whereas, pentobarbitone (5-10 mg kg-1, i.p.) only prevented the behavioural component of the seizures. 3. In hippocampal slices, verapamil (1.5-2.0 mM) produced, within 30-60 min of perfusion, a CA1 epileptiform bursting in 80% of the experiments. This epileptiform activity was prevented by the cromakalim concentration (50 microM) that did not affect the control CA1 synaptic transmission per se. Pentobarbitone also prevented verapamil-induced epileptiform bursting only at the concentration (100 microM) that also reduced control CA1 synaptic transmission. 4. Diltiazem (1.5 mM) produced a biphasic excitatory-depressant effect within 60 min of perfusion. A CA1 epileptiform bursting appeared in 100% of the experiments within 30 min of perfusion. These excitatory effects were followed by a depression phase, characterized by a reduction of the magnitude of CA1 excitatory postsynaptic potentials (e.p.s.ps) and population spike. 5. The diltiazem-induced epileptiform bursting was prevented by cromakalim at a concentration (50 microM) that did not affect the control CA1 synaptic transmission per se. Pentobarbitone also prevented the diltiazem-induced epileptiform bursting only at a concentration (100 microM) that also reduced the control CA1 synaptic transmission. Both cromakalim (50 microM) and pentobarbitone (100 microM) failed to affect the depressant effects of diltiazem on CA1 hippocampal area. On the contrary, high (3.3mM) calcium solutions prevented both the excitatory and the depressant effects of 1.5 mm diltiazem within 60 min.6. These data indicate an involvement of potassium currents in the epileptiform activity elicited by high doses of diltiazem and verapamil.
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PMID:Cromakalim (BRL 34915) counteracts the epileptiform activity elicited by diltiazem and verapamil in rats. 166 91


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