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 conducted on rats; a study was made of methionineS35 incorporation into the sum total proteins isolated from various portions of the brain after a single administration of chlorpromazine, majeptil and tricedil. A generalized depression of protein synthesis in all the structures, except the medulla oblongata, followed chlorpromazine administration in one and three hours. A stimulating effect is characteristic of majeptil in the majority of the brain portions. The action of tricedil was accompanied by reduction of methionine-S35 incorporation into the proteins of the majority of the brain structures and by an increase in its incorporation into the olfactory lobes. As supposed, changes in the protein synthesis in individual structures of the brain served as an important link in the action mechanism of psychotropic preparations on the organism.
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PMID:[The effect of psychotropic substances (aminazin, majeptil, trisedil) on protein synthesis in different regions of the rat brain]. 0 90

1. The actions of ether and methoxyflurane on the evoked potentials of in vitro preparations of the guinea-pig olfactory cortex were studied. Following stimulation of the lateral olfactory tract (l.o.t.) evoked potentials could be recorded from the cortical surface; these potentials consisted of an initial wave (the compound action potential of the l.o.t.) followed by a negative field potential which was associated with the synchronous excitation of many superficial excitatory synapses (population e.p.s.p.). Superimposed on the population e.p.s.p. was a number of positive peaks. These positive peaks reflect the synchronous discharge of many neurones and so have been called population spikes. 2. When ether or methoxyflurane was added to the gas stream that superfused the surface of the preparations, the population e.p.s.p.s. and population spikes were depressed at lower concentrations than those required to depress the compound action potential of the afferent fibres. 3. The evoked activity of individual cells in the cortex was depressed by ether and methoxyflurane. However, five of the twelve cells tested in ether showed an increase in their evoked activity at concentrations below 4-5%, but at higher concentrations these cells also became depressed. 4. Both ether and methoxyflurane depressed the sensitivity of cortical neurones to iontophoretically applied L-glutamate and may similarly depress the sensitivity of the post-synaptic membrane to the released transmitter substance. 5. Neither anaesthetic appeared to increase the threshold depolarization required for nerve impulse generation. Thus, the decrease of the discharge of the post-synaptic cells was primarily caused by a depression of chemical transmission. 6. Ether caused some cells in the cortex to alter their normal pattern of synaptically evoked discharge and both anaesthetics induced similar changes during excitation by glutamate.
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PMID:The action of ether and methoxyflurane on synaptic transmission in isolated preparations of the mammalian cortex. 16 56

1. Silices of guinea-pig olfactory cortex were cut at 550 micrometer nominal thickness and preincubated at 24 +/- 0.5 degrees C for than 2 1/2 hr. They were then stimulated via the lateral olfactory tract, and field potential recordings were made from all regions of the slice. 2. Potentials recorded resembled those described previously, but it was noticed the early N-wave had two distinct components, which we designated the N'a' wave (earlier) and N'b' wave (later). Evidence was obtained that this was not a consequence of the division of a single population e.p.s.p. (N-wave) into two by a P notch (synchronous discharge of post-synaptic action potentials). 3. In some slices the N'a' wave and N'b' wave had similar thresholds, and in others the N'a' wave had the slightly lower threshold. 4. The N'b' wave was best developed at low frequencies of stimulation (less than 0.1 Hz), and considerably depressed with stimulation above 1 Hz. This was most evident with submaximal stimulation. 5. Exploration of the distribution of peak amplitudes and latencies of the N'a' and N'b' waves showed that the N'a' wave could have been directly initiated by lateral olfactory tract action potentials, while the N'B' wave could not. The N'b' wave amplitude was relatively larger towards the periphery of the slices, away from the tract. In a few cases, an N'b' wave could be recorded in the absence of an N'a' wave at that site. 6. Depth studies showed that the origin of the N'b' wave lay deeper in the slice than that of the N'a' wave. 7. The effect of conditioning stimulation on the N'a' and N'b' waves was examined. The N'b' wave was more depressed at short conditioning intervals than the N'a' wave, and showed less later potentiation. The recovery of the N'b' wave from conditioning was much slowed with submaximal stimulation, and when trials were repeated at low frequency. 8. The N'a' and N'b' components persisted when the slice was warmed to near-physiological temperatures, and showed a similar pattern of response to conditioning stimulation as had been found at lower temperatures. 9. N'a' and N'b' waves could still be recorded when slices were incubated in a medium containing 1.2 mM-Mg2+ and 1.2 mM-Ca2+. These physiological concentrations were about half those routinely employed. There was little or no depression of the N'b' component by conditioning stimulation in this medium. 10. The N'a' wave is probably a result of e.p.s.p.s in apical dendrites of superficial pyramidal cells, initiated by transmitter release from lateral olfactory tract axon collaterals. The N'b' wave may reflect e.p.s.p.s in the apical dendrites of deeper pyramidal cell elicited by firing in recurrent collaterals from superficial pyramidal cell axons.
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PMID:Mono-and multi-synaptic origin of the early surface-negative wave recorded from guinea-pig olfactory cortex in vitro. 50 82

From the following three lines of evidence, it is proposed that at least part of the convulsant activity of naloxone is a result of GABA receptor blockade. Firstly, iontophoretic naloxone reversibly antagonized GABA-evoked depression of firing rate in 21 of 27 neurons tested in the rat olfactory tubercle-nucleus accumbens region, without blocking inhibition evoked in the same cells by glycine (15 cells) or morphine (6 cells). Secondly, i.p. naloxone in high doses caused convulsions in mice, and potentiated the convulsant activity of bicuculline, but not that of strychnine. Diazepam, which protected mice against convulsions elicited by bicuculline, but not by strychnine, also protected mice against naloxone. Thirdly, naloxone, morphine, levorphanol and its non-analgesic enantiomer dextrorphan displaced 3H-GABA from GABA receptor sites in homogenates of human cerebellum, all with comparable low potencies (IC50 = 250--400 micron). There was no correlation with affinities at the stereospecific receptor sites that mediate opiate-induced analgesia, since the potent opiates etorphine and diprenorphine were relatively inactive (IC50 greater than 3 mM). In addition naloxone displaced 3H-GABA from receptor sites in rate forebrain and cerebellum, with similar low potency.
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PMID:Naloxone as a GABA antagonist: evidence from iontophoretic, receptor binding and convulsant studies. 61 28

1. Stable intracellular recordings were obtained from neurones in slices of the guinea-pig olfactory cortex maintained in vitro. 2. Single stimuli applied to the lateral olfactory tract (l.o.t.) produced an excitatory post-synaptic potential (e.p.s.p.) usually generating a single spike. 3. The e.p.s.p. was followed by a long (200-500 msec) after-depolarization (l.a.d.) of peak amplitude 5-16 mV. This was accompanied by a very large conductance increase and was associated with an inhibition of the intracellularly recorded e.p.s.p. and of spike generation. 4. The l.a.d. was more susceptible than the e.p.s.p. to depression by (i) repetitive l.o.t. stimulation and (ii) raising external [Mg2+]. The l.a.d. could be generated without a preceding spike. 5. At an average resting membrane potential of -74 mV the average reversal potential for the l.a.d. (El.a.d.) was -63 mV.El.a.d. became more positive on reducing [Cl-]out or on using KCl-filled electrodes. 6. It is concluded that the l.a.d. represents a Cl- -mediated inhibitory post-synaptic potential, generated through deep-lying recurrent inhibitory loops.
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PMID:A depolarizing inhibitory potential in neurones of the olfactory cortex in vitro. 63 55

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.
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PMID:A barbiturate induced intensification of the inhibitory potential in slices of guinea-pig olfactory cortex. 63 56

A 37-year-old woman had bilateral anygdalotomy for psychomotor and minor motor seizures and long periods of very pronounced mental depression. The patient has been seizure-free for four years postoperatively. A preoperative left temporal spike focus disappeared after extensive left anygdalotomy. Of particular interest in this case is the recovery of olfactory and memory functions which were partially impaired by the bilateral lesions. Bilateral anygdalotomy is effective in relieving temporal lobe seizures without the complications and deficits that usually occur with resections of the bilateral temporal lobe.
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PMID:Amygdalotomy for bilateral temporal lobe seizures. 80 18

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

Explants of 18- or 19-day fetal mouse olfactory bulb have been maintained in culture for periods up to 5 weeks. Compound action potentials can be evoked in the bulb explants by 1 day in vitro, and by 3-4 days, synaptically mediated slow wave discharges can be domonstrated in bicuculline (10(-5) m). The capability of the bulb explants to generate these slow-wave discharges has also been revealed by the introduction of picrotoxin (10(-5)m, d-tubocurarine (10(-4)m) and chloride-free medium, but not of strychnine (up to 3 X 10(-5)M. The data indicate early functional development of inhibitory, as well as excitatory, synaptic systems. In addition, the selective and reversible depression of these slow wave potentials by GABA (1-5 X 10(-4)M), but not by glycine (up to 3 X 10(-3)M), indicates a GABA-ergic component in the inhibitory network. Single unit extracellular recordings have been obtained from the presumptive mitral cells which, in culture, are spontaneously active even as early as 1-2 days after explantation. Correlative Bodian silver-impregnations demonstrate the presence of neurons in these explants which resemble typical mitral cells. Studies of mitral cells using paired stimuli suggest the development in vitro of an inhibitory system analogous to that known to suppress the excitability of their in situ counterparts following orthodromic or antidromic activation. These data, as well as the pharmacological sensitivities of the mitral cells in culture to GABA (5 X 10(-4)M) and bicuculline (10(-5)M), indicate that granule-to-mitral synapses may develop characteristic functions in olfactory bulb explants.
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PMID:Electrophysiological studies of fetal mouse olifactory bulb explants during development of synaptic functions in culture. 100 99

Slices from guinea pig brain containing the lateral olfactory tract (LOT) and the prepiriform cortex were studied in vitro. Field potentials, evoked by stimulation of the LOT, were recorded extracellularly. This field potential comprises a compound action potential, a surface negative wave (identified as EPSP), and superimposed positive peaks ("population spikes" or PSs) reflecting postsynaptic activity. In a previous article the penicillin-induced increase of EPSP and of both amplitude and number of PSs was described. Now we are reporting the slight depression of EPSP and PSs and the prevention of the appearance of penicillin-induced PSs by an antiepileptic drug sodium dipropylacetate (Depakine). The effect was dose-dependent. Models explaining the effects of penicillin and dipropylacetate are discussed.
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PMID:Actions and interactions of dipropylacetate and penicillin on evoked potentials of excised prepiriform cortex of guinea pig. 110 21


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