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

Since its first characterization as a model for the detection of antidepressant drugs (van Riezen et al., 1976) a large body of data now supports the view that olfactory bulbectomy produces changes in animal behavior that are reversed by chronic treatment with antidepressants. The behavioral deficits seen in olfactory bulbectomized rats (such as irritability, deficits in acquisition of avoidance and of appetitive motivated conditioning and hyperactivity in a new environment) are probably the results of a reduced ability to adapt to environmental changes. These behavioral changes, their biochemical consequences and the effects of treatments with psychotropic drugs are reviewed. These studies suggest that the olfactory bulbectomized rat is a model of depression useful to detect antidepressant drugs.
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PMID:Effects of psychotropic drugs on the behavior and neurochemistry of olfactory bulbectomized rats. 219 55

The prevalence of abnormal perceptual experiences as symptoms of migraine attacks was determined in a consecutive series of 46 new female referrals to a migraine clinic. All patients met the diagnostic criteria of the International Headache Society for migraine with aura or migraine without aura and had no other serious physical illness. Seven patients (15%) reported abnormal perceptions (olfactory and/or gustatory hallucinations and distortions of body image) as part of most migraine attacks. A statistically significant association was found between these abnormal perceptual experiences and complaints of mood change, particularly increased depression and irritability, as part of most migraine attacks. It is suggested that spreading depression of cortical electrical activity may be responsible for the manifestations of temporal lobe and limbic system dysfunction.
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PMID:Abnormal perceptual experiences in migraine. 228 27

To evaluate the contribution of extracellular H+ activity toward depression of brain electrical activity during anoxia, extracellular pH (pHe) and field potentials were measured in turtle and rat olfactory bulbs with ion-selective microelectrodes. This study tests the hypothesis that unique regulation of pHe contributes to the remarkable tolerance of turtle brain to prolonged anoxia. Hypercapnea (20% CO2 ventilation) depressed olfactory bulb evoked potentials 25-30% in both rat and turtle. During anoxia, evoked potentials were completely abolished within 1 min in rat olfactory bulb but decreased to only 40% of control after 4 h in the turtle despite similar changes in brain pHe. Anoxia-induced acidification of turtle brain was exacerbated by hypercapnea and was attenuated by hypocapnea or by hypocapnea plus intravenous infusion of sodium bicarbonate. However, these manipulations of pHe during anoxia in turtle brain had little effect on depression of evoked potentials. We conclude that energy failure, rather than extracellular acidification, is the major contributor toward suppression of electrical activity in mammalian brain and that preservation of energy balance, rather than unique pH regulation, is responsible for protection of turtle brain during anoxia.
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PMID:Extracellular pH and suppression of electrical activity during anoxia in turtle and rat brain. 230 33

Studies on humans and rats have suggested that neuropeptide Y (NPY) is involved in major depression and anxiety. Therefore, we conducted the present study in order to elucidate the effect of repeated (13 or 14 days) treatment of rats with electroconvulsive shocks (ECS) on the concentration of NPY-like immunoreactivity (-LI) in various brain regions, adrenals and plasma. In addition, the effect of ECS on 125I-NPY binding was studied in 3 brain regions. The effects of ECS were compared to effects of 3 control treatments: one group not being handled at all during the time period, one group handled like the ECS-group but not receiving shocks, and one group receiving shocks below the threshold for induction of convulsions. The latter group developed behavioral signs reminiscent of the inescapable shock-induced 'learned helplessness' syndrome (a proposed animal model of depression). We found that the concentration of NPY-LI in the frontal and parietal cortex and in the hippocampus were approximately doubled in the ECS-group as compared to the 3 control groups. No changes in NPY-LI were detected in the striatum, hypothalamus, pons, olfactory bulbs or cerebellum, nor in plasma or adrenals. In spite of the marked changes in NPY-LI concentration, the binding characteristics of 125I-NPY in the frontal and parietal cortex and in the hippocampus were similar in all 4 groups of rats. Finally, we confirmed the previous observation that ECS increase [3H]prazosin binding in cortex. In conclusion, ECS treatment increases neocortical and hippocampal NPY-LI concentrations, while leaving 125I-NPY binding unaffected. Subconvulsive shocks were without effect.
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PMID:Electroconvulsive shocks increase the concentration of neocortical and hippocampal neuropeptide Y (NPY)-like immunoreactivity in the rat. 230 81

The effect of the muscarinic agonist oxotremorine-M has been studied on the surface-negative field potential (N-wave) evoked by orthodromic stimulation of the lateral olfactory tract in slices of guinea-pig olfactory cortex. Bath-application of oxotremorine-M (5-80 microM) or carbachol (10-300 microM) produced a reversible depression of the N-wave amplitude without affecting the lateral olfactory tract compound action potential. Oxotremorine-M was approximately 5 times more potent than carbachol in this respect, and the effects of both agonists were competitively blocked by telenzepine (5-100 nM), a selective M1-receptor antagonist. In contrast, methoctramine or AF-DX 116, two 'cardioselective' M2-receptor antagonists, had little or no blocking effect on the agonist responses. It is suggested that oxotremorine-M (like carbachol) inhibits the evoked field potential by activating presynaptic M1-type muscarinic receptors in the olfactory cortex slice.
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PMID:Muscarinic suppression of the evoked N-wave by oxotremorine-M recorded in the guinea-pig olfactory cortex slice. 233 31

A decreased rate of uptake of serotonin (5HT) into platelets is recognized as a possible marker of the depressed state, being normalized only by effective antidepressant treatment. Fluoxetine is a novel antidepressant, with 5HT uptake inhibitory properties. In this study, treatment of depressed patients with fluoxetine for up to 6 months did not normalize the decreased platelet 5HT uptake rates associated with depression, although the patients showed a clinical recovery. The olfactory bulbectomized (OB) rat shows a characteristic hyperactivity in a stressful environment, which can be reversed only by chronic treatment with most antidepressants. OB rats have been found to exhibit a decreased rate of platelet 5HT uptake, similar to depressed patients, which is normalized by chronic antidepressant treatment. However, 3 weeks treatment with fluoxetine failed to reverse the hyperactivity of the OB rat and the decreased rates of uptake of 5HT. We also examined the rate of uptake of serotonin into the synaptosomes of the OB rats, in order to elucidate whether platelet 5HT uptake reflected central activity. Chronic fluoxetine treatment failed to normalize high affinity synaptosomal 5HT uptake in the OB rat. Fluoxetine, therefore, unlike most other antidepressants, does not normalize the decreased rates of platelet 5HT uptake in depressed patients on clinical recovery. OB rats also showed a deficit in their platelet and synaptosomal 5HT uptake rates, following 3 weeks treatment with fluoxetine.
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PMID:Clinical and experimental studies on fluoxetine: effects on serotonin uptake. 233 7

1. The effects of low-frequency stimulus trains on synaptically evoked responses in piriform cortex pyramidal cells were studied by the use of intracellular recording techniques in an in vitro slice preparation. Afferent and association fiber systems were differentially stimulated with electrodes placed in layer 1a or layer 1b, respectively. To quantify synapse modifiability, the heights of postsynaptic potentials (PSPs) elicited by paired-pulse stimulation (100-ms interval) were averaged over a 50-s period before and after a set of 10 stimulus trains (10 pulses each, 20 Hz, 5-s interpulse interval). 2. Afferent and association fibers showed consistent differences in their response to stimulation during the period lasting from approximately 10 to 200 s after presentation of trains. During this time period, the responses to stimulation of association fibers in layer 1b displayed a short-term potentiation, which over the 10 posttrain trials, produced an average increase in PSP height of 23.2 +/- 3.7% (mean +/- SE). On the other hand, responses to layer 1a stimulation showed an average depression of 10.9 +/- 3.6%. Layer 1b potentiation decayed with time constant roughly estimated at 79 s. Layer 1b potentiation appeared even at very low stimulus voltages and after local association fiber input had been cut, suggesting that it was largely a monosynaptic effect. 3. In the period immediately after train presentations, responses evoked by both layers showed a short-term augmentation with a time constant around 3 s. In layer 1a, this augmentation was superimposed on a depression with slow recovery. At longer times after train presentation (greater than 5 min), 2 cells out of 46 showed changes (increases) in synaptic efficacy in response to layer 1b stimulation. 4. In the current experiments both layers 1a and 1b showed statistically significant facilitation before the presentation of stimulus trains. However, layer 1b facilitation decreased from 22.7 +/- 3.5% to a statistically insignificant 3.9 +/- 3.3% after the presentation of trains, whereas layer 1a facilitation remained at a statistically significant level of 23.1 +/- 5.7%. 5. These experiments show that pyramidal cell responses to stimulation of the afferent and association fiber systems are affected differently by the previous presentation of trains of stimuli. This suggests that mechanisms of synaptic modification may differ between the afferent and intrinsic association synaptic projections onto single pyramidal cells in olfactory cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Afferent and association fiber differences in short-term potentiation in piriform (olfactory) cortex of the rat. 238 64

The rat olfactory bulb is an area displaying a particularly high density of substance P receptors in the glomerular cell layer whose functions are unknown. In pilot in vivo experiments we discovered that iontophoretically administered substance P potently depressed the spontaneous firing rate of most unidentified neurons of the rat olfactory bulb. To further elucidate the mechanism of this unexpected depressant effect, we studied the peptide's action in vitro on coronal sections of this brain region. Bath applied and microiontophoretically administered substance P depressed the spontaneous discharge of unidentified glomerular neurons in a dose-dependent fashion. This inhibiting effect is mediated indirectly via the release of another transmitter because it was abolished completely if the standard perfusion medium was replaced by a medium containing zero calcium and high magnesium. It appears that substance P acts by means of releasing GABA which in turn evokes the observed cell depression because the depressant effects were completely abolished by bath-applied bicuculline (10 microM) and picrotoxin (100 microM). In conclusion we propose that substance P indirectly depresses neuronal activity in the glomerular cell layer of the rat olfactory bulb by releasing gamma-aminobutyric acid.
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PMID:Substance P depresses neuronal activity in the rat olfactory bulb in vitro and in vivo: possible mediation via gamma-aminobutyric acid release. 244 May 22

Spreading depression in the olfactory bulb of rats is an elusive phenomenon, the demonstration of which requires specific conditioning procedures. The present paper describes a simple technique for reliable initiation of bulbar spreading depression with microinjections of potassium acetate. Adult hooded rats were anesthetized with pentobarbital (50 mg/kg) and slow potential changes accompanying spreading depression were recorded with capillary microelectrodes stereotaxically inserted into the olfactory bulb and adjacent forebrain structures. KCl microinjection (0.5-1.0 microliter, 0.134-0.670 mol/l) into the olfactory bulb elicited local depolarization which only exceptionally developed into a propagating spreading depression. Potassium acetate (0.5-1.0 microliter, 0.15 mol/l) injected into the rostral olfactory bulb evoked a negative slow potential wave (amplitude of around 25 mV and duration 30-50 s) propagating at a rate of 3-4 mm/min through all the olfactory bulb layers. Low positive (5 mV) instead of negative waves were recorded in the superficial olfactory nerve layer with reversal in the glomerular layer (200-300 micron). The slow potential decreased in the rostrocaudal direction and expired at the caudal boundary of the olfactory bulb. Bulbar spreading depression never spread to neocortex, and cortical spreading depression never entered into the olfactory bulb but stopped in the anterior olfactory nucleus 7 mm rostral to bregma. Repeated potassium acetate injections into the olfactory bulb occasionally elicited a series of spreading depression waves recurring at regular intervals, probably reflecting reverberation of scroll-shaped waves around the rostrocaudal axis of the olfactory bulb.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spreading depression in the olfactory bulb of rats: reliable initiation and boundaries of propagation. 244 64

Slices of isolated olfactory cortex from guinea-pig have been used to study the action of adenosine at synapses between axons of the lateral olfactory tract and neurons in the olfactory cortex. Adenosine depressed the excitatory postsynaptic potential, and, with paired or multiple stimuli, the reduced excitatory postsynaptic potentials in adenosine showed more synaptic facilitation. Very small excitatory postsynaptic potentials which were estimated not to be affected by postsynaptic membrane conductance changes were highly sensitive to adenosine. Both observations indicate a presynaptic action of adenosine. To test whether a conductance increase to potassium ions mediated adenosine action, the K-channel blockers, 3,4-diaminopyridine (1-100 mumol/l) or 4-aminopyridine (100-500 mumol/l) were applied or Cs partially substituted for K. These substances reduced or prevented adenosine from having its depressant effect on synaptic transmission. These particular K-channel blockers also prolonged the action potential propagating along the lateral olfactory tract. When the increased excitability was counteracted by high Mg or low concentrations of tetrodotoxin, 3,4-diaminopyridine still blocked adenosine action. UO2 ions prolonged the lateral olfactory tract action potential without blockade of K-conductance, but still supported an adenosine depression of the excitatory postsynaptic potential. Veratridine also supported the adenosine depression. These observations suggest that the action of 3,4-diaminopyridine on adenosine was not solely the result of increased tissue excitability. In contrast, tetraethylammonium (20 mmol/l), Ba (0.5-4 mmol/l) or Rb replacement for K had a negligible effect on the duration of the presynaptic action potential and had no effect on the depressant action of adenosine. These data are compatible with the idea that adenosine enhances an aminopyridine-sensitive potassium conductance in nerve terminals and changes in Ca influx are consequential to this.
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PMID:Presynaptic K-channel blockade counteracts the depressant effect of adenosine in olfactory cortex. 245 96


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