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)

Experiments were carried out on cats under Nembutal anaesthesia. The electrodes were placed on the gyrus suprasylvius. The recording macroelectrode and the K+--sensitive microelectrode were placed between two stimulating electrodes (S1 and S2). A strong stimulus applied through S1 elicited a slow surface negative potential (SNP) and an increase in [K/]0. The change of K+ potential correlated in time with SNP but the decay of K+ potential lasted longer. At this time depression of the dendritic potential (DP)--EPSP of apcial dendrites--evoked by stimulation through S2 took place. The greater the negative shift and the [K/]0 increase the greater was the depression. Tetraethylammonium increased SNP and this correlated with a strong depression of DP. Application of KCl or acetylcholine solutions resulted in DP depression. It may be supposed that the depression of dendritic potentials expresses presynaptic inhibition in the cortical neuropile based on the action of K+ ions.
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PMID:On the process of inhibition in the superficial neuropil of the cerebral cortex. 294 82

Pentobarbitone depresses synaptic excitation in the guinea-pig olfactory cortex slice in vitro. A study has been made to elucidate the possible role of gamma-aminobutyric acid (GABA) in this depression by testing pentobarbitone in the presence of high concentrations of the GABA blockers, i.e. picrotoxin or bicuculline. These blockers reduced the action of pentobarbitone; the dose-depression curve for pentobarbitone was shifted to the right by a factor of 2.3. It is concluded that pentobarbitone has a bimodal action, one action via GABA and another unrelated to GABA or Cl- conductances.
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PMID:gamma-Aminobutyric acid partly mediates the pentobarbitone depression of synaptic excitation in the guinea-pig olfactory cortex in vitro. 298 34

It has been reported that pentobarbital facilities binding to benzodiazepine receptors binding at anesthetic concentrations and that this action may play a role in the anesthetic potency of this barbiturate. The interaction between pentobarbital and benzodiazepine receptors was tested with Ro 15-1788 which is reported to be a pure benzodiazepine antagonist and 3-hydroxymethyl-beta-carboline (3-HMC), an antagonist which has inverse activity alone. Cerebral blood flow (CBF) and cerebral oxygen consumption (CMRO2) were measured in rats after injections of pentobarbital with and without the antagonists. Pentobarbital produced dose-dependent decreases in cerebral blood flow and cerebral oxygen consumption at 15 and 30 mg/kg. The antagonist Ro 15-1788 (10 mg/kg) stimulated cerebral blood flow and cerebral oxygen consumption alone but did not alter the cerebral depression produced by pentobarbital. The cerebral metabolic stimulation produced by Ro 15-1788 was unexpected since the drug is reported to be a pure antagonist without agonistic activity, but the lack of effect on pentobarbital-induced cerebral depression is consistent with other reports. 3-Hydroxymethyl-beta-carboline at 10 mg/kg did not stimulate cerebral blood flow and cerebral oxygen consumption but significantly antagonized the decrease in cerebral oxygen consumption produced by 15 mg/kg pentobarbital. 3-Hydroxymethyl-beta-carboline had no significant effect on decreases in cerebral blood flow and cerebral oxygen consumption produced by phenobarbital, a barbiturate which is reported not to alter binding to benzodiazepine receptors. The ability of 3-HMC to antagonize the effects of pentobarbital would be consistent with an action of both drugs at the benzodiazepine receptor but not by altering binding to an endogenous receptor.
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PMID:The interaction between benzodiazepine antagonists and barbiturate-induced cerebrovascular and cerebral metabolic depression. 299 34

4,6,6-Trimethylcaprolactam antagonised GABAA receptor-mediated contractile responses in guinea-pig isolated ileum, displacing the GABA dose-response curve to the right in a non-parallel manner, and causing a depression of the maximum response. Pentobarbitone not only potentiated the GABAA receptor-mediated contractions but also reversed this non-competitive antagonism by 4,6,6-trimethylcaprolactam, shifting the dose-response curve for GABA to the left and restoring the maximum response. It is conclude that this caprolactam acts at the picrotoxin-barbiturate site on the Cl(-)-ionophore complex.
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PMID:Caprolactam-barbiturate interaction at the GABAA receptor complex in the guinea-pig intestine. 301 60

The present study investigated the effect of systemically administered pentobarbital on the tail-flick (TF) reflex in rats, the neurochemical mechanism of action and the role of descending influences. Pentobarbital produced a clear inhibition of the TF response. Systemic administration of naloxone did not significantly alter this effect, thus it appears to be independent of endogenous opioid systems. Complete spinal transection resulted in a marked potentiation of pentobarbital-induced TF inhibition, demonstrating a spinal locus of action. Moreover, this observation suggests the existence of a tonic descending excitatory influence, opposing the pentobarbital-produced depression of nociceptive transmission in the intact animal. Intrathecal administration of pentobarbital caused a much more pronounced TF inhibition in transected than in intact animals, lending further support to this hypothesis. To identify the neurochemical mechanisms involved in pentobarbital-produced antinociception, the gamma-aminobutyric acid (GABA) antagonists bicuculline and picrotoxinin were administered intrathecally in spinalized animals. Both substances caused an attenuation of the pentobarbital effect, demonstrating the involvement of GABAergic transmission. The proposed descending excitatory system may act either presynaptically and cause a decreased release of GABA into the synapse or postsynaptically via endogenous GABA antagonistic neurotransmitters, which may change the conformation of the GABA-barbiturate receptor complex.
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PMID:Barbiturate-induced inhibition of a spinal nociceptive reflex: role of GABA mechanisms and descending modulation. 303 63

Barbiturate actions on excitatory synaptic responses in CA 1 and dentate regions of hippocampal slices were studied to determine whether different effects occur on anatomically distinct synaptic pathways. Pentobarbital facilitated transmission between stratum radiatum inputs and CA 1 neurons at low concentrations (0.02-0.08 mM) and produced postsynaptic depression at higher concentrations. Only depression was observed for stratum oriens inputs to CA 1 and perforant path inputs to dentate granulae neurons. The (+) isomer of pentobarbital was approximately four times more potent than the (-) isomer of racemic mixture. Phenobarbital (0.04-0.12 mM) produced only depression of synaptic responses in CA 1 and dentate pathways. Comparison of effect on field excitatory postsynaptic potentials and population spike responses indicated that the barbiturates act at selective and pathway-specific sites. The results provide further evidence for specific cellular and membrane recognition sites for barbiturate action.
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PMID:Barbiturate effects on hippocampal excitatory synaptic responses are selective and pathway specific. 303 90

Extracellular single unit recordings were made in the brain stem reticular formation (RF) of urethane-anesthetized rats. Minaprine (cumulative i.v. dose of 10 mg/kg, given as 2.5, 2.5 and 5 mg/kg) has no significant effects on the RF neurons. Pentobarbital (10 mg/kg, i.v.) and scopolamine (5 mg/kg, i.v.) reduced the firing rate of the RF neurons. Minaprine (cumulative i.v. dose of 10 mg/kg, given as 2.5, 2.5 and 5 mg/kg) reversed the effects of pentobarbital and scopolamine. These observations indicate that minaprine has an ameliorating effect on the drug-induced depression of neuronal activity in the RF.
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PMID:Effect of minaprine on neuronal activity in the brain stem reticular formation of the rat. 324 20

A method is described for the measurement of cardiac output and oxygen saturation in closed-chest rats using a small (2.4 F) commercially available fiberoptic catheter and a reflection-spectral-photometer. Positioned in the aortic arch, the catheter functions as an oxymeter for oxygen saturation and as a densitometer for measurement of indocyanine green, obviating the need for blood removal and passage through a densitometer. The sensitivity and reproducibility of this method were characterized in 90 rats by thermodilution, radiolabeled microspheres, and electromagnetic flow methods as standard references. Basal cardiac output as well as changes in cardiac output during isoproterenol infusion and blood removal and replacement were measured. In addition, multiple measurements of cardiac output over 1 min were used to document the method's suitability in constructing a ventricular function curve. With the fiberoptic catheter, cardiac output varied predictably with anesthesia, with rats on dial-urethane (n = 23) having values of 150 +/- 39 (SD) ml/min/kg and 2 and 1% enflurane (18-35 rats per group) yielding cardiac outputs of 190 +/- 60 and 236 +/- 77 ml/min/kg, respectively. Pentobarbital produced the least cardiovascular depression (n = 15) with an average cardiac output of 322 +/- 22 ml/min/kg. The average cardiac output with this method in 90 rats (regardless of anesthesia) was 214 +/- 91 (SD). This value was comparable to cardiac output values determined in paired experiments from radiolabeled microspheres (9 rats) 220 +/- 43, electromagnetic flow (11 rats) 177 +/- 33, and a subset of rats with thermodilution (231 +/- 45 ml/min/kg). The within measurement (repeat measurements) variability with the fiberoptic method was consistently less than the rat-to-rat variability when compared to the thermal and radiolabeled microsphere methods, but it was comparable to electromagnetic flow. The method can be used when rapid measurements (4 measurements within 60 s) of cardiac output are required, as in constructing a ventricular function curve, and can readily detect small changes in cardiac output during controlled hemorrhage and isoproterenol infusion. In summary, this method gives measurement of oxygen saturation and cardiac output by dye dilution without blood removal. There is less surgical preparation than required for electromagnetic cardiac output, and it is an alternative to the thermodilution method.
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PMID:Measurement of cardiac output in anesthetized rats by dye dilution using a fiberoptic catheter. 330 43

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

Drug dependence tests on a new intravenous anesthesia inducer midazolam were performed in comparison with triazolam in male cynomolgus monkeys utilizing the intravenous route of administration. In the animals trained to self-administer sodium pentobarbital (0.6-1 mg/kg/inj) under FR1 and FR10 reinforcement schedules, 0.01 midazolam and 0.001 mg/kg/inj triazolam maintained self-administration in more than 4 out of 5 animals under FR1. Doses of 0.03 and 0.001 mg/kg/inj, respectively, were required under FR10. The intradaily progressive ratio test revealed that midazolam maintained self-administration only weakly (equivalently as or more weakly than triazolam did). Midazolam at 0.003-0.1 and triazolam at 0.0003-0.01 mg/kg/inj initiated self-administration, respectively, in 3 and 1 out of 4 naive animals, but the numbers of self-administration responses were only slightly higher than the vehicle control level. Pentobarbital at 0.1-3 mg/kg initiated self-administration in all of 4 animals with a high level of self-administration. In the single dose suppression test in physically pentobarbital-dependent animals, an ED25 value of midazolam for the suppression of the withdrawal signs was 0.30 mg/kg, i.v., which was almost equivalent to that for the central nervous system depression (0.27 mg/kg, i.v.). This was in clear contrast to the results of triazolam and pentobarbital, of which the ED25 values for the suppression were lower than those for the central nervous system depression. In naive animals, after the chronic administration of midazolam at 0.9, triazolam at 0.09, pentobarbital at 60 mg/kg/day (the doses inducing intermediate sedation) intravenously for 4 weeks, withdrawal signs were found respectively in 0, 1 and 3 out of 4 animals. After the chronic administration of higher doses of the compounds (1.2, 0.12 and 80 mg/kg/day) for 4 weeks, the withdrawal signs were found respectively in 1 and 2 out of 3 and 3 out of 4 animals. The benzodiazepine antagonist Ro 15-1788 (1 and 3 mg/kg, i.v.) precipitated clear withdrawal signs in none of 3 midazolam animals and 2 out of 3 triazolam animals. From these results, it can be concluded that the drug dependence liability of midazolam is within the range of those of most benzodiazepines.
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PMID:[Drug dependence tests on a new anesthesia inducer, midazolam]. 377 May 90


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