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)

Previously accumulated GABA was released from isolated forebrain synaptosomes with repeated calcium stimulation in elevated-potassium medium. Fractional release (calcium-dependent) in response to a second calcium pulse (90-120 sec later) was depressed to approximately 60% of initial release. Neither initial GABA release nor the subsequent depression of release was affected by variations in the labelling duration. Stimulation-dependent depression of labelled GABA and norepinephrine release was demonstrated from both cerebral cortex and cerebellum synaptosomal preparations. In addition, depression resulted from prior stimulation in the presence of veratridine, A23187 or elevated-potassium. Although release of previously accumulated GABA was depressed by calcium stimulation, the release of GABA accumulated between stimulations was not. Release of this recently accumulated GABA was indistinguishable from the initial release of previously accumulated GABA and larger than the subsequently depressed release from the previously accumulated pools. These data imply (1) that the depressed release resulted from a decrease of available transmitter in pools that support secretion processes, (2) that depressed release did not result from a depression of stimulus-secretion coupling processes, and (3) that transmitter accumulated subsequent to release events is released preferentially to transmitter accumulated prior to the intervening stimulation.
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PMID:Stimulation-dependent depression of readily releasable neurotransmitter pools in brain. 78 58

The effect of diazepam, depakin, thiosemicarbazide (TSC) and bicucullin on the spontaneous and incuced (by stimulation of the sciatic nerve) activity of the cells of the sensory-motor cortex was studied on the unanesthetized immobilized (curarized) albino rats. Diazepam proved to intensify the inhibitory phenomena, i.e. decreased the frequency of spontaneous discharges and prolonged the postactivation depression of the neuron impulsation (the inhibitory pause. Depakin increasing the GABA content in the brain acted similarly. The GABA-ergic receptors blocker, bicucullin and TSC, decreasing its content, on the contrary, weakened the inhibitory phenomena. There was also revealed a reversible antagonism between diazepam and bicucullin in their effect on the neuronal activity. The data obtained confirmed the supposition put forward formerly on the capacity of diazepam to intensify the effect of GABA on the neurons of the cerebral cortex.
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PMID:[GABA-ergic mechanism of action of diazepam on cerebral cortex neurons]. 79 92

The effects of two diazepines (diazepam and Ro 11-7800) and 3 barbiturates (thiamylal, pentobarbitol and phenobarbital) on GABA-mediated recurrent inhibition were assessed on single hippocampal pyramidal cells and on population spikes using extracellular recording techniques. Recurrent inhibition was evoked in spontaneously active CA1 pyramidal cells by stimulation of the fimbria or the alveus with single shocks. Microiontophoretic application of Ro 11-7800 or systemic application of diazepines or barbiturates resulted in an increase of the duration of the inhibition and in a concomitant depression of the spontaneous firing in most neurones tested. When the firing rates were kept constant artificially, using excitant amino acids, a prolongation of the recurrent inhibition was observed with barbiturates but not with diazepines. The duration of the inhibition, which was assessed from CA1 population spikes elicited by double shocks to the fimbria, was prolonged following systemic application of diazepines or barbiturates. It is concluded that both diazepines and barbiturates are able to potentiate GABAergic recurrent inhibition in the hippocampus. The demonstration of this effect appears to depend critically on certain experimental conditions.
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PMID:Effects of diazepines and barbiturates on hippocampal recurrent inhibition. 92 49

The effect of electrical stimulation of the median raphe nucleus on the activity of spontaneously firing single neurones in the substantia nigra and mesencephalic reticular formation (MRF) has been investigated in urethane anaesthetized rats. Depression of activity was the predominant effect observed although this was sometimes accompanied by periods of excitation. Some neurones were only excited. The latency of inhibition of substantia nigra neurones was constant whereas that of MRF neurones was more variable. Microiontophoretically applied 5-hydroxy-tryptamine (5-HT) and dopamine (DA) produced mainly inhibition of neuronal activity, but excitation and biphasic effects were also seen. There was a good correlation between the direction of neuronal responses in the substantia nigra to median raphe stimulation and to the effects of 5-HT but not DA. Discrete electrolytic lesions of the median raphe nucleus were followed by a decrease in 5-HT but not GABA concentrations in the substantia nigra. In addition striatal 5-HT, GABA and NA concentrations were unchanged whereas striatal DA was increased. These observations strongly suggest that the substantia nigra receives a direct inhibitory input from the median raphe nucleus and this pathway uses a 5-HT-like neurotransmitter. This pathway probably contributes to the regulation of nigrostriatal dopaminergic transmission.
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PMID:Evidence for the existence of a raphe projection to the substantia nigra in rat. 95 33

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

(1) The effects of divalent cations (Ca++, Mg++, Sr++ and Co++) were studied on the post-synaptic responses of crustacean neuromuscular junctions and identified molluscan neurons to bath and iontophoretic application of putative transmitters. (2) The glutamate response of the crustacean muscle was parabolically dependent on [Ca++]0, while the ACh response of an identified molluscan neuron was inversely dependent on[Ca++]0. Elevated [Ca++]0 depressed both glutamate and ACh depolarizations in a concentration-dependent, reversible manner. Low concentrations of Co++ also depressed both depolarizations in a concentration-dependent, reversible manner. (3) Double-reciprocal plot analyses of the Ca++ and Co++ depressions indicate that these agents were apparently not acting to reduce the affinity of the receptor for the agonist. Elevated concentrations of both Ca++ and Co++ shifted the inversion potential of the ACh response in a hyperpolarizing direction, suggesting a preferential block of the receptor-coupled Na+ conductance. (4) Neither Ca++ nor Co++ depressed Cl- or K+-dependent responses coupled to the putative transmitters GABA, glutamate, dopamine or ACh. (5) The selective inhibition of the ACh and glutamate responses by the general anesthetic pentobarbital was examined as a function of[Ca++]0. Decreasing [Ca++]0 by 5-fold decreased the pentobarbital inhibition by about 50% while increasing [Ca++]0 by 5-fold produced an insignificant increase in the inhibition. (6) The data indicate that divalent cations, like general anesthetics, selectively depress post-synaptic excitatory responses that are primarily Na+-dependent. This selective depression by Ca++ could contribute to its anesthetic and anticonvulsant properties when present in elevated concentrations in the ventricular fluid. The mechanism by which divalent ions and general anesthetics selectively depress receptor-coupled conductances appear to be different: divalent ions preferentially attack the Na+ component while anesthetics block Na+ and K+ conductance equally (possibly by affecting the kinetics of the mechanism).
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PMID:Divalent cations: effects on post-synaptic pharmacology of invertebrate synapses. 117 55

Past research has demonstrated brain opioid and GABA release in response to ejaculation. In the present study we evaluated the potential role of these neurotransmitters in the postictal behavioral depression (PBD), after-discharge (AD) duration, and seizure intensity in rats kindled in the medial preoptic area (MPOA) and amygdala (AMG). The PBD, the AD duration and the seizure intensity were measured after a standard kindling stimulus and after a standard kindling stimulus applied 2 min after ejaculation. The PBD was significantly increased when the animals were stimulated 2 min after ejaculation. This increase was found in MPOA- but not in AMG-kindled rats. Ejaculation had no effect on AD duration or seizure intensity. Naloxone administration before the initiation of sexual behavior completely blocked the increase in PBD in MPOA-kindled rats. It is suggested, by indirect evidence, that opioid release during sexual behavior is added to the release associated with kindled seizures, increasing the duration of the PBD. Since sexual behavior lacked effect on AD duration or seizure intensity, no evidence could be found suggesting that functionally relevant amounts of GABA are released during this behavior.
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PMID:Sexual behavior enhances postictal behavioral depression in kindled rats: opioid involvement. 129 97

The effects of acute and chronic application of ketamine on the resting spontaneous motility, its development and reactivity was studied in chick embryos of white Leghorns. 1. Acute application of ketamine (Narcamon) in a dose of 12.5 mg/kg e.w. partially depressed spontaneous motility as early as in 11-day old chick embryos. From day 15 of incubation ketamine very effectively blocked spontaneous motility. 2. Ketamine was fully ineffective in spinal preparations (decapitation on day 2 of incubation) of 11- and 13-day-old embryos. It was not until day 15 evoked that it depressed motility as in normal embryos. 3. Chronic continuous supply of ketamine (average dose 6.34 +/- 0.72 mg/kg e.w./24 h) from day 4 of incubation till day 8, 12, or 16 of incubation reduced the developmental decrease of spontaneous motility by 23.1-6.0% as compared to the controls. This effect was already observed after the first 4 days of chronic application of ketamine. 4. Chronic application of ketamine significantly diminished the strychnine activation and GABA-mediated depression of spontaneous motility. The depressive effect of the acute application of ketamine itself was hardly affected. The results have shown that ketamine interferes with the development of the endogenous rhythm of intrinsic activity and with the development of reactivity of the generator of embryonic spontaneous motility.
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PMID:Influence of ketamine on the spontaneous motility of chick embryos and its development. 129 27

Paired-pulse depression (PPD) technique was used to investigate the potency of recurrent synaptic inhibition mediated by GABA in area CA1 of 54 hippocampal slices from coriaria lactone (CL)-kindled and control rats. When paired stimuli were sent to the axon of CA1 pyramidal cell and Schaffer collaterals, the effect of population spike PPD lasted about 40-60ms; no significant change was observed on PPD potency between kindled and control groups (P = 0.06, 2-way ANOVA). The results indicate that the GABA-ergic synaptic inhibition seemed not to play a key role in the maintenance of the chemical kindling induced by CL.
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PMID:[Observation of paired-pulse depression in CA1 region of hippocampal slices from coriaria lactone-kindled rats]. 130 44

Persistent changes in synaptic efficacy are thought to underlie the formation of learning and memory in the brain. High-frequency activation of an afferent excitatory fibre system can induce long-term potentiation, and conjunctive activation of two distinct excitatory synaptic inputs to the cerebellar Purkinje cells can lead to long-term depression of the synaptic activity of one of the inputs. Here we report a new form of neural plasticity in which activation of an excitatory synaptic input can induce a potentiation of inhibitory synaptic signals to the same cell. In cerebellar Purkinje cells stimulation of the excitatory climbing fibre synapses is followed by a long-lasting (up to 75 min) potentiation of gamma-aminobutyric acid A (GABAA) receptor-mediated inhibitory postsynaptic currents (i.p.s.cs), a phenomenon that we term rebound potentiation. Using whole-cell patch-clamp recordings in combination with fluorometric video imaging of intracellular calcium ion concentration, we find that a climbing fibre-induced transient increase in postsynaptic calcium concentration triggers the induction of rebound potentiation. Because the response of Purkinje cells to bath-applied exogenous GABA is also potentiated after climbing fibre-stimulation with a time course similar to that of the rebound potentiation of i.p.s.cs, we conclude that the potentiation is caused by a calcium-dependent upregulation of postsynaptic GABAA receptor function. We propose that rebound potentiation is a mechanism by which in vivo block of climbing fibre activity induces an increase in excitability in Purkinje cells. Moreover, rebound potentiation of i.p.s.cs is a cellular mechanism which, in addition to the long-term depression of parallel fibre synaptic activity, may have an important role for motor learning in the cerebellum.
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PMID:Synaptic excitation produces a long-lasting rebound potentiation of inhibitory synaptic signals in cerebellar Purkinje cells. 131 49


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