Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microwave irradiation of 6 kw at 2450 MHz for 300 msec was sufficient to completely inactivate mouse brain cholinesterase and choline acetyltransferase. After this method of sacrifice, the acetylcholine contents of mouse brain regions, given in nanomoles per gram, were found to be: striatum, 81; medulla-pons, 44; diencephalon-midbrain, 34; hippocampus, 31; cerebral cortex, 26; and cerebellum, 17. Sodium pentobarbital caused a dose-dependent increase in whole brain acetylcholine. A maximal increase of 81% in whole brain was seen at 15 minutes with 80 mg/kg of sodium pentobarbital. The increase in acetylcholine after sodium pentobarbital treatment was not caused by anoxia from respiratory depression or by hypothermia. All brain regions except the cerebellum exhibited an increase in acetylcholine after pentobarbital treatment. Fifteen minutes after treatment, cerebellar acetylcholine was significantly decreased. However, at the time when half of the animals had regained the righting reflex, the unconscious mice showed an increase in cerebellar acetylcholine which was statistically significant as compared to control. The relative accumulation rate of acetylcholine calculated for cerebral cortex and hippocampus was higher than that for striatum although the absolute rate of accumulation of ACh was higher in the striatum. Thus, after sodium pentobarbital treatment, the cerebral cortex and hippocampus exhibit a greater cholinergic response than the striatum.
 ...
PMID:Use of 300-msec microwave irradiation for enzyme inactivation: a study of effects of sodium pentobarbital on acetylcholine concentration in mouse brain regions. 0 94

Interaction between epileptic foci and spreading depression (SD) was studied in the cerebral cortex of rats anesthetized with Nembutal. At comparable discharge rates, picrotoxin and penicillin caused complete and partial SD blockade respectively, strychnine and Metrazol were ineffective and Aldactone facilitated SD. Conversely, the duration of SD-induced blockade of epileptic activity was maximal for Aldactone and minimal for picrotoxin. Treatment of the picrotoxin focus with tetrodotoxin (10(-4)M) reduced the discharge rate and reinstated SD propagation into the focus. [K+]e measured with ion-selective K+ electrodes 1 mm below the cortical surface increased to 8 mM in penicillin foci blocking SD and remained below 5 mM in Aldactone foci. It is concluded that the differential effect of various convulsants on SD propagation depends on the potassium concentration in the depth of the focus rather than on the discharge rate or on the mechanism of the the epileptogenic effect.
 ...
PMID:Differential effects of cortical speading depression on epileptic foci induced by various convulsants. 7 46

1. Pentobarbitone or phenobarbitone, in increasing concentrations up to 0-5 mM, progressively reduced the amplitude of miniature end-plate potentials (min.e.p.p.s). Pentobarbitone was the more potent of the two barbiturates in this regard. 2. Both barbiturates produced a monotonic increase in mean quantum content of the end-plate potential (e.p.p.) with increasing concentrations up to 0-5 mM. Pentobarbitone and phenobarbitone were equally potent in their action on evoked transmitter release. 3. The effect, if any, of increasing concentrations of barbiturates on the e.p.p. amplitude was depression. Therefore, over the range of concentrations examined the enhancement of transmitter release was quantitatively less than the reduction in responsiveness of the post-synaptic membrane. 4. Because of the greater ratio of post-synaptic to presynaptic actions, pentobarbitone was more potent than phenobarbitone in reducing synaptic efficacy (e.p.p. amplitude). 5. It is concluded that the presynaptic actions of pentobarbitone and phenobarbitone contribute significantly to barbiturate-induced changes in synaptic efficacy at low levels of transmitter release in the frog neuromuscular junction.
 ...
PMID:A comparison of the presynaptic and post-synaptic actions of pentobarbitone and phenobarbitone in the neuromuscular junction of the frog. 18 66

In order to study the J-reflex, monosynaptic reflexes were recorded from L7 or S1 ventral root after stimulation of the posterior biceps, and semi-tendinosus nerve (PBST) from the lower limb in cats anaesthetized with Pentobarbitone sodium. Intratracheal CO2 (60 ml, 100%) depressed the monosynaptic reflexes, and the depression was comparable to the effects of right atrial phenyl diguanide injection. Bilateral vagotomy did not abolish the response showing that the afferent pathway of this depression does not travel via the vagus nerve. Thus it is concluded that CO2 cannot be used to study the J-reflex.
 ...
PMID:Limitations in the use of CO2 as a method for studying the J-reflex. 61 82

1. A study has been made of the effect of barbiturates on membrane constants and synaptic potentials of neurones in the isolated guinea-pig olfactory cortex slice. 2. Normally, a long depolarizing i.p.s.p. follows the e.p.s.p. Pentobarbitone (0.1 mM) produced a tenfold increase in the duration of the high conductance phase of this i.p.s.p. 3. The i.p.s.p. was potentiated increasingly with higher barbiturate concentrations from 0.02 to 1.0 mM-pentobarbitone and 0.2 to 5 mM-phenobarbitone. 4. The resting membrane conductance, the initial phase of the e.p.s.p. and the threshold for the action potential were unaffected at lower concentrations. 5. The highest barbiturate doses increased the resting membrane conductance. This was associated with a depolarization of about 14 mV maximally and resulted in smaller synaptic potentials. The effect was probably generated by the same mechanism as the i.p.s.p. 6. This fortifies the idea that barbiturates have a primary action on prolonging inhibition rather than a depression in the excitatory potential.
 ...
PMID:A barbiturate induced intensification of the inhibitory potential in slices of guinea-pig olfactory cortex. 63 56

1. Interactions of bath-applied pentobarbitone and gamma-aminobutyric acid (GABA) on neurones in isolated superior cervical ganglia of the rat have been examined with intracellular microelectrodes. 2. Pentobarbitone itself (30 micrometer-1 mM) showed no clear or consistent GABA-like effects: changes in resting input conductance and membrane potential were small and variable. 3. Pentobarbitone (100 micrometer) strikingly enhanced the conductance increases produced by GABA and 3-aminopropanesulphonic acid, and reversed the depression of GABA-evoked responses by bicuculline. 4. It is concluded that reversal of bicuculline action at the membrane conductance level might be explained by augmentation of GABA-action. This augmentation cannot be attributed to 'partial agonist' properties of pentobarbitone or to interference with glial transport processes.
 ...
PMID:Interaction of pentobarbitone and gamma-aminobutyric acid on mammalian sympathetic ganglion cells. 64 60

1. The effects of the barbiturate anaesthetic pentobarbitone on the membrane properties and amino acid pharmacology of mammalian C.N.S. neurones grown in tissue culture were studied using intracellular recording coupled with bath application, extracellular ionophoresis, or focal diffusion. 2. The addition of an anaesthetic concentration of pentobarbitone to the bathing medium abolished all spontaneous synaptic activity, but did not render individual cells electrically inexcitable nor prevent evoked synaptic acitivity. 3. Focal ionophoresis of pentobarbitone or diffusion from blunt micropipettes reversibly increased membrane conductance, effectively dampening excitability without directly affecting individual action potential characteristics. 4. Pentobarbitone-induced membrane conductance was reversibly blocked by picrotoxin. The inversion potential of the pentobarbitone voltage response depended on Cl- ion gradients and was similar to that of GABA. 5. Pentobarbitone reversibly enhanced the conductance increase produced by GABA with a variable slowing of response kinetics, shifting GABA dose-response curves to the left. Responses to glycine and beta-alanine were not affected. 6. Higher ionophoretic currents of pentobarbitone, which measurably increased membrane conductance, attenuated and markedly slowed GABA responses. Similar effects on GABA responses were observed by superimposing GABA pulses on low level GABA currents. 7. Pentobarbitone, in the absence of an increase in membrane conductance, reversibly depressed depolarizing responses to glutamate without changing response kinetics. Slower responses to acetylcholine which were associated with an apparent decrease in membrane conductance were not affected by the drug. 8. Analysis of double-reciprocal plot data suggested a non-competitive type of antagonism between pentobarbitone and glutamate. Pentobarbitone depression of glutamate was not affected by picrotoxin. 9. Both GABA and glutamate responses appeared to be equally sensitive to pentobarbitone. Specific interaction of the drug with amino acid receptor-coupled events is indicated by the requirement for pentobarbitone pipette placement close to the amino acid response site. 10. The results suggest that pentobarbitone depresses neuronal excitability by (1) directly activating post-synaptic GABA-receptor coupled Cl- conductance, (2) potentiating post-synaptic GABA-induced conductance events, probably at the level of the GABA receptor, and (3) depressing post-synaptic glutamate-induced excitation, probably at the level of the conductance mechanism.
 ...
PMID:Pentobarbitone pharmacology of mammalian central neurones grown in tissue culture. 69 Aug 85

To check up the value of atrial pacing (AP) in estimating the degree of healing in myocardial necrosis, an ECG study was carried out in 20 dogs with experimental myocardial infarction induced by ligation of the left descending coronary artery. The main ECG changes recorded after ligation i.e., Q waves in 14 animals (73%), S-T segment elevation in 14 (74%) and decrease of QRS voltage in 12 (63%), disappeared within a 7-day interval. Anesthesia with Nembutal 56--57 days after ligation and before AP application induced the occurrence of Q waves in 6 animals, S-T segment depression in 18 and T wave inversion in 12. AP during 20 minutes, at a heart rate of 200 beats/min, produced the appearance or the increase of S-T segment depression in 14 animals and T wave inversion in 12. These findings support the assumption that the AP stress test can be used for the evaluation of the necrosis degree in the healing stages of experimental myocardial infarction, but a correct interpretation of the ECG changes induced by AP should also take into account the previous abnormalities due to anesthesia.
 ...
PMID:Value of the electrocardiographic stress test by atrial pacing in the healing stages of experimental myocardial infarction. 69 92

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.
 ...
PMID:Activation of an inhibitory noradrenergic pathway projecting from the locus coeruleus to the cingulate cortex of the rat. 69 22

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.
 ...
PMID:Anaesthetics depress the sensitivity of cortical neurones to L-glutamate. 99 May 90


1 2 3 4 5 Next >>