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

Pituitary glands of proestrous (PRO) rats display enhanced LH secretory response to LHRH when compared to pituitary glands of estrous (EST) rats. In addition proestrous pituitary glands display a self-potentiating (priming) response to LHRH, whereas estrous pituitary glands do not. This study addresses the role of the proestrous surge of progesterone in converting the proestrous-like LH secretory responses of the pituitary gland to those of estrus. Anterior pituitary glands were obtained from PRO and EST rats. In addition, Pro rats were treated with pentobarbital alone (PRO/PB) or with pentobarbital plus progesterone (PRO/PB-P4). Pentobarbital was given to prevent proestrous surges of LH and progesterone. Pentobarbital-treated animals were killed the day after treatment, estrus. Pituitary glands from each group were tested for LH secretory response in a superfusion chamber with exposure of two 15-min pulses of 10 nM LHRH separated by 90 min, or assayed for LHRH receptor content using iodinated D-Ala6-LHRH. Anterior pituitary glands from PRO rats secreted higher levels of LH than EST rats in response to an LHRH pulse. Only PRO anterior pituitary glands secreted priming responses to LHRH. Though anterior pituitary glands obtained from pentobarbital-treated rats showed LH responses of similar magnitude to anterior pituitary glands of PRO rats after initial LHRH challenge, they did not display priming responses. Progesterone replacement (PRO/PB-P4) led to depressed secretory responses when compared to PRO pituitary glands similar to EST rats. LHRH receptor concentrations in pituitary glands of EST rats was lower than those in pituitary glands of PRO rats. Depression of pituitary LHRH receptor concentration from proestrus to estrus was prevented by pentobarbital-treatment on proestrus. Estrus-like depression of receptor concentration was restored after progesterone treatment (PRO/PB-P4). These data suggest the LHRH receptor depression on estrus is a consequence of the secretion of progesterone on proestrus. Further, the declining magnitude of the in vitro LH-secretory response to LHRH follows a declining LHRH receptor concentration; however no correlation exists between receptor number and ability to prime.
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PMID:Secretion of luteinizing hormone (LH) and pituitary receptors for LH-releasing hormone as modified by the proestrous surge of progesterone. 609 51

In gross-behavioral observations, chlordiazepoxide, diazepam, meprobamate, and pentobarbital-Na produced excitatory behavior at 5 and 10, 1 and 2, 100 and 200, and 10 and 20 mg/kg p.o., respectively whereas afloqualone produced no excitatory behavior at doses up to 20 mg/kg p.o., these doses induce muscle relaxation and motor depression. Afloqualone depressed DRL response at 10 and 20 mg/kg p.o. Similar effects were seen with chlorpromazine (5, 10, 20 mg/kg p.o.). Chlordiazepoxide, meprobamate, and pentobarbital-Na facilitated DRL response at doses producing excitatory behavior. Methamphetamine (0.5, 1, 2 mg/kg p.o.) facilitated the response, dose-dependently. In CER, chlordiazepoxide (5, 10, 20 mg/kg p.o.), diazepam (1, 2, 5 mg/kg p.o.), and meprobamate (50, 100, 200 mg/kg p.o.) dose-dependently increased the response during the alarm period, regardless of the response during the safe period. Pentobarbital-Na (5, 10, 20 mg/kg p.o.) had much the same effect. Afloqualone slightly increased the response during the alarm period in one out of 3 rats at 5, 10, and 20 mg/kg p.o., respectively. Chlorpromazine and methamphetamine had no influence on the response during the alarm period at doses up to 20 and 2 mg/kg p.o., respectively. These results suggest that the pharmacological properties of afloqualone, as related to behavior differ from those of anti-anxiety drugs, hypnotics, and stimulants.
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PMID:[Effects of afloqualone, a new centrally acting muscle relaxant, on DRL response and CER in rats (author's transl)]. 612 Jan 27

Blockade of the spread depression [SD] in chemically or electrically stimulated areas of the cerebral cortex was analyzed in a series of experiments performed in 40 curarized, locally anaesthetised rats. Longlasting stimulation of the cerebral cortex (0.5 to 1.7 mA, 6 Hz, 0.1 ms) elicited recurrent episodes of enhanced evoked potentials propagating to remote cortical areas [Co], the caudate nucleus [Cd], the hippocampus [Hi] and the thalamus [Th] and was accompanied by marked slow potential shifts (4-6 mV amplitude, 2-3 min duration, at 2-5 min intervals]. The projected discharge interfered with SD initiation and propagation in all the examined structures. The SD blockade was most pronounced during the episodes and almost absent in the intervals between them. The block was manifested by reduced amplitude and duration of the slow potential of SD. Pentobarbital [20 mg/kg] suppressed the recurrent discharges and eliminated the corresponding SD blockade. Recurrent excitability changes induced by Cd and Th stimulation elicited similar effects but the threshold was higher in Cd and Th than in Co. SD was less effectively blocked by the projected discharge than by stimulation of the same structure, particularly in the vicinity of the recording electrodes, where the blockade could be observed even under pentobarbital. The SD blockade outlasted stimulation by a considerably longer period of time in Th (about 10 min) than in the Cd (about 3 min). The onset of stimulation and the projected episodes sometimes elicited SD waves but SD blockade prevailed with continued stimulation. The present findings support the hypothesis that excessive neural activity increases the potassium clearance and thus prevents the autoregenerative accumulation of potassium ions, mediating SD propagation.
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PMID:Stimulation induced recurrent epileptiform discharges block cortical and subcortical spreading depression in rats. 621 68

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

Calcium-dependent action potentials were recorded from mouse spinal cord neurons in primary dissociated cell culture following addition of the potassium channel blockers tetraethylammonium ion and 3-aminopyridine. The pharmacologically active barbiturates, pentobarbital and phenobarbital, but not the pharmacologically inactive barbiturate, barbituric acid, produced reversible, dose-dependent reduction of action potential duration at sedative-hypnotic and anesthetic concentrations. Pentobarbital reduced action potential duration at concentrations from 25 to 600 microM (50% reduction at 170 microM) while phenobarbital reduced action potential duration at concentrations from 100 to 5000 microM (50% reduction at 900 microM). The barbiturate concentrations which reduced calcium-dependent action potential duration in this study correlate with reduction of neurotransmitter release from other neuronal preparations and with reduction of calcium uptake by synaptosomes. The results suggest that barbiturates may produce anesthesia in part by reduction of presynaptic calcium entry and consequent reduction of neurotransmitter release in addition to postsynaptic increase of membrane chloride ion conductance. Barbiturate anticonvulsant actions are probably due to postsynaptic augmentation of GABA-mediated inhibition and depression of excitatory synaptic transmission. The major difference between anticonvulsant (phenobarbital) and anesthetic (pentobarbital) barbiturates was the dose-dependency of these actions. Phenobarbital produced postsynaptic modulation of neurotransmitter responses at low concentrations and decreased calcium-dependent action potential duration and increased chloride ion conductance at high concentrations. In contrast, pentobarbital produced all actions at low concentrations. Thus for phenobarbital there would be a large therapeutic index for anticonvulsant activity compared to anesthetic activity but for pentobarbital there would be a small therapeutic index.
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PMID:Barbiturate reduction of calcium-dependent action potentials: correlation with anesthetic action. 627 33

The effect of pentobarbitone on Ca2+ current (ICa), separated from other ionic currents was studied under voltage clamp using a suction pipette technique in Helix neurones. Pentobarbitone depressed the maximal peak amplitude (MPA) of ICa in a concentration-dependent manner without shifting the current-voltage (I-V) relationships along the voltage axis. Increases in external Ca2+-concentration [( Ca2+]o) overcame the inhibitory action of the agent on MPA. Pentobarbitone markedly accelerated the decay phase of ICa which took a distinctly different time course from that of the control. The accelerating action of the agent on the decay phase of ICa was not overcome by increases in [Ca2+]o. In the presence of internal EGTA (20 mM), pentobarbitone also accelerated the decay of ICa. Changes in pH of the external perfusing solution altered the potency of pentobarbitone in depressing MPA; in the presence of pentobarbitone (3 X 10(-4) M) at pH of 7.0, 8.0 and 9.0, fractional inhibition was approx. 46%, 21% and 4%, respectively. Internal application of pentobarbitone (10(-4)-10(-3) M) inhibited MPA, but exerted no effect on the decay phase of ICa. Pentobarbitone (10(-4) M) markedly accelerated the decrease of MPA of ICa induced by repetitive stimuli applied at an interval of 150 ms, indicating a use-dependent depression of MPA. Results provide evidence that pentobarbitone has a dual action on ICa, inhibiting MPA and accelerating the decay phase of ICa.
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PMID:Accelerating effects of pentobarbitone on the inactivation process of the calcium current in Helix neurones. 631 18

The effects of pentobarbital were studied on synaptic transmission in the rat hippocampal slice preparation. Low concentrations of pentobarbital (0.04 - 0.1 mM) produced an increase in the Schaffer collateral to CA 1 evoked EPSP and population field potential amplitudes. Higher concentrations of pentobarbital (0.2 - 1.0 mM) produced depression of field potential amplitudes. Pentobarbital altered synaptic transmission by affecting both pre- and post-synaptic functions. Analysis of input/output curves suggest the presynaptic site is most sensitive.
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PMID:Biphasic actions of pentobarbital on synaptic transmission. 632 Mar 7

The effects of naloxone, pentobarbitone, or their combination, on arterial blood gases were studied in urethane-anaesthetised rats. Naloxone itself did not significantly alter the blood gases. Pentobarbitone significantly decreased PO2 and elevated PCO2, and these effects were prevented by pretreatment with naloxone. Arterial blood pH was unaffected by any of the drugs. The findings suggest that naloxone lacks a specific analeptic effect, but can antagonise respiratory depression induced by pentobarbitone.
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PMID:Antagonism of pentobarbitone-induced respiratory depression by naloxone in rats. 641 81

The following three regimens of anesthesia in mice were compared: (1) Ketamine 100 mg--xylazine 5 mg/kg b.wt. i.m., (2) pentobarbitone 50 mg/kg b.wt. i.p., and (3) carfentanyl 0.003 mg--etomidate 15 mg/kg b.wt. i.m. For these dosage rates the respiratory variables, i.e., respiratory rate, paO2, paCO2, pHa, BEa, HCO-3a, and the circulatory parameters, i.e., heart rate, mean arterial pressure and hematocrit, were determined during the conscious state, during surgical anesthesia, and at waking time. With ketamine and xylazine, the respiration was moderately decreased whereas the cardiovascular system was strongly depressed. Pentobarbitone induced a high respiratory depression but a lesser degree of circulatory depression. Analgesia was inadequate. Although there was a moderate respiratory and circulatory depression during anesthesia with carfentanyl and etomidate the drug-induced excitation and muscle spasms do not recommend this anesthetic combination for mice. Of these three methods, the combination of ketamine and xylazine is considered the most reliable for anesthesia of mice.
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PMID:A comparative study with various anesthetics in mice (pentobarbitone, ketamine-xylazine, carfentanyl-etomidate). 647 5

Local rates of glucose utilization in the spinal cord and brain were measured with the 2-[14C]deoxyglucose method in conscious and in paralyzed and mechanically ventilated pentobarbital- or 70% nitrous oxide-treated rats. In conscious animal lumbar spinal cord glucose utilization is only 40-50% that of the cerebral cortex and shows little laminar heterogeneity. Pentobarbital reduces and nitrous oxide increases the cerebral glucose utilization of most structures. The effect of paralysis and nitrous oxide analgesia on lumbar spinal cord glucose utilization is quantitatively similar to that produced in brain; 15-25% increases occur in most spinal cord laminae and cerebral structures. In contrast, the 10-20% reduction in spinal cord gray matter metabolism in the paralyzed and pentobarbital-treated animals is considerably less than the 20-50% depression measured in most brain structures. From these data the authors conclude that, relative to that of most cerebral structures, spinal cord metabolism is less sensitive to depression by barbiturates and suggest that differences in the cell populations of these tissues may account partially for this observation.
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PMID:A comparison of local rates of glucose utilization in spinal cord and brain in conscious and nitrous oxide- or pentobarbital-treated rats. 648 5


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