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)

The investigation employed monorhinic (single nostril) olfactory testing to decide whether patients with unilateral anterior temporal lobe resection (N = 16) and patients with unoperated temporal lobe epilepsy (N = 18) have impaired ability to detect, remember, and identify odors. A shape memory task accompanied the odor memory task for comparison. The lobectomy patients showed a minor bilateral depression of absolute sensitivity but still fell within the clinically normal range. The lobectomy patients showed impairment of odor recognition memory but strictly via the nostril ipsilateral to the resected lobe. A similar ipsilateral-contralateral asymmetry characterized the performance of these patients in odor identification. In that case, however, performance via the contralateral nostril showed some impairment too. Nonsurgery patients also exhibited some impairment in odor identification, but bilaterally. Finally, both groups of patients fell somewhat below normals in recognition memory for amorphous shapes. The various results implied that temporal lobe epilepsy alone takes some toll on olfactory information processing and that temporal lobe resection exacerbates the problem, but only on the side of surgery.
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PMID:Odor perception in temporal lobe epilepsy patients with and without temporal lobectomy. 377 40

The time course of terminal anoxic depolarization and of the concomitant [K+]e increase was compared in the cerebral cortex and olfactory bulb of rats anesthetized with pentobarbital. Respiration arrest elicited by (+)-tubocurarine induced a negative slow potential shift which reached 50% of maximum after 90 s in the cortex and after 180 s in the olfactory bulb (n = 10). Bulbar [K+]e increased slowly to 16 mmol/l, then more rapidly to 40 60 mmol/l and reached 90 mmol/l after 10 min asphyxia (n = 10). While the resting and maximal [K+]e levels were the same in the cortex and olfactory bulb, the fast [K+]e rise started in the olfactory bulb at a higher level (16 mmol/l) and proceeded at a slower rate (doubling time 14 s) than in the cortex, where the same values were 11 mmol/l and 5 s, respectively. It is argued that the olfactory bulb resistance to asphyxia is due to a powerful GABAergic inhibition which counteracts the autoregenerative ionic shift and accounts for the absence of spreading depression in this structure.
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PMID:Terminal anoxic depolarization proceeds more slowly in the olfactory bulb than in the cerebral cortex of rats. 379 89

Removal of the main olfactory bulbs in rats has been shown to alter neuronal function in brain areas involved in emotional regulation and homeostasis. These neuronal alterations result in maladaptive behavioral patterns and elevated plasma corticosterone that are suggestive of the symptom profile of patients with primary unipolar depression. Moreover, the endocrine and behavioral deficits of bulbectomized rats are reversed by the chronic administration of drugs that reverse the symptoms of depression in people when given chronically. However, the therapeutic improvements seen in patients with depression are not directly due to molecules of the antidepressant drug but rather to some relatively long-lasting compensatory change induced in the neuronal substrate by the drug. The present research demonstrates that the reversal of the olfactory bulb lesion deficits following chronic antidepressant drug administration in rats is not due to molecules of the drug per se but rather to some drug-induced change in the neuronal substrate that continues for at least 5 days after the last dose of drug. These endocrine, behavioral, and pharmacological similarities suggest that the study of rats with olfactory bulb ablation may make significant contributions to the understanding of the neuroscience of primary unipolar depression in humans.
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PMID:Effects of antidepressant drugs on the behavior of olfactory bulbectomized and sham-operated rats. 396 27

Evoked potentials (EP) due to the stimulation of the upper incisor tooth pulp were recorded from the somatosensory cortex of the freely moving adult rats. Background EEG, motor activity of an animal and respiratory potentials of the olfactory bulb were recorded simultaneously. EP configurations and mean amplitudes of primary complex (P1 + N1) differed significantly during states of sleep, drowsiness, relaxed wakefulness, grooming and exploratory behaviour; primary complex amplitude during intensive motor activities was several times less than during periods without movements. Negative correlation of the EP amplitude and instant respiration rate was found during relaxed wakefulness: it was less pronounced during periods with motor activities. At the same time direct parallelism between changes in EP and respiration rate was absent: the EP depression was maximal during grooming, while the respiration rate was minimal during exploratory behaviour.
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PMID:[Variability of cortical evoked potentials in response to tooth pulp stimulation in the freely moving rat]. 397 56

Bicuculline methiodide (0.5-3 nmol) and picrotoxin (0.5-4 nmol) were injected uni- or bilaterally into the rat amygdala and the resulting behavioural, electroencephalographic and morphological alterations were studied. In rats treated unilaterally with lowest doses of either bicuculline or picrotoxin (0.5 and 1 nmol) increase in the locomotor activity, occasional myoclonus of the hindlimbs and wet dog shakes were observed. At doses of 2-3 nmol, both gamma-aminobutyrate antagonists produced a sequence of repetitively occurring behavioural alterations including limbic gustatory automatisms, tremor and myoclonus of the forelimbs, head nodding and rearing, that developed over 15-30 min and built up progressively into the recurrent motor limbic seizures lasting for 1-6 h. In animals injected bilaterally with either bicuculline (0.5-3 nmol) or picrotoxin (0.5-3 nmol) motor limbic seizures rapidly developed into the status epilepticus lasting for several hours. Bicuculline and picrotoxin produced both ictal and interictal epileptiform activity in the electroencephalogram. A spectrum of electroencephalographic changes consisted of high voltage fast activity, slow and fast voltage spiking, paraoxysmal bursts and periods of postictal depression. The earliest electrographic alterations appeared in the amygdala and then rapidly spread to cortical areas. Electrographic seizures started 1-10 min after unilateral injections of large doses of bicuculline and pictrotoxin (2-4 nmol). Ictal periods lasted for 1-2 min, recurred every 5-10 min and were followed by periods of depression of the electrographic activity. Bilateral injections of large doses of both gamma-aminobutyrate antagonists (2-3 nmol) resulted in the status epilepticus. Morphological examination of frontal forebrain sections with light microscopy revealed a widespread damage to the amygdala, olfactory cortex, substantia nigra, thalamus, hippocampus and neocortex. Pretreatment of animals with diazepam prevented the build-up of convulsive activity and brain damage produced by bicuculline or picrotoxin. Muscimol retarded the appearance and shortened the duration of convulsive activity, but did not alter the sequence and intensity of seizures. The results indicate that gamma-aminobutyrate antagonists, bicuculline and picrotoxin when directly applied to the amygdala can elicit in rats motor limbic seizures, epileptic changes in the electroencephalogram indicative of repetitive limbic seizures, and status epilepticus accompanied by seizure-related brain damage.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Injections of picrotoxin and bicuculline into the amygdaloid complex of the rat: an electroencephalographic, behavioural and morphological analysis. 397 84

Disorders of taste and smell are underrecognized and often misdiagnosed. Two cases are described in which patients mistakenly thought to suffer from depression actually had unnoticed drug-induced dysosmia and dysgeusia. Also reviewed are psychiatric, neurologic, and medical disorders and drugs that cause abnormalities of taste and smell, and some behavioral aspects of food aversions. Three groups, all of whom may superficially appear depressed, must be distinguished from each other: 1) patients with dysosmia or dysgeusia, 2) patients with primary neuropsychiatric illness with olfactory or gustatory hallucinations, and 3) patients with conditioned taste aversions.
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PMID:Dysosmia and dysgeusia presenting as depression. 399 7

1. The extracellular field potentials of the olfactory cortex evoked by stimulation of the lateral olfactory tract (l.o.t.) were studied in in vitro preparations from the olfactory cortex. The field potentials comprised an initial diphasic wave - the l.o.t. compound action potential - followed by a negative wave of about 10 msec duration which in turn was followed by a low amplitude positive wave of long duration (100 msec or more). In this paper, the size of the negative field potential (extracellularly recorded EPSP) has been studied during and after periods of repetitive stimulation of the l.o.t.2. If two identical volleys were delivered to the l.o.t. the second evoked EPSP was not the same size as the conditioning EPSP. At brief conditioning intervals (up to 10 msec) the second (test) EPSP was smaller than the control. For conditioning intervals between 10 and 200 msec, the test EPSP was potentiated over the control. For long conditioning intervals (300 msec up to 5 sec) the test EPSP was again slightly smaller than the control EPSP. After a brief conditioning train, the depression of a test EPSP (elicited 300 msec or more after the conditioning train) was more pronounced and lasted longer. These changes of test EPSP size were attributed to the presence of two opposing processes: an initial potentiation superimposed on a more prolonged but less pronounced depression.3. During prolonged repetitive stimulation the final steady amplitude of an EPSP varied with the frequency of stimulation. At low frequencies (0.5-2/sec) the steady EPSP amplitude was 90-95% of the initial control amplitude. At moderate frequencies (5-20/sec) the steady EPSP amplitude was greater than the initial control. At high frequencies (above 20/sec) the steady amplitude of the EPSPs declined with increasing frequency of stimulation. Potentiation of EPSPs was observed early in a train of impulses when the stimulation frequency was 5-70/sec.4. After a large number of stimuli at frequencies from 20 to 100/sec the amplitude of individual, infrequently evoked, EPSPs passed through a phase of depression that lasted about 30 sec. This depression was followed by a phase of potentiation (post-tetanic potentiation). The amplitude and duration of post-tetanic potentiation appeared to depend on the characteristics of the conditioning train.5. The discussion compares the results obtained with those obtained for other mammalian synapses. It is suggested that the transmitter in the presynaptic terminals could be in three parts, (a) immediately available transmitter (b) conditionally available transmitter requiring a single nerve impulse for its availability and (c) main depot transmitter which replenishes the other two stores. Potentiation and depression of evoked EPSPs were interpreted in terms of changes in the amount of transmitter released by the test volley. According to this analysis, a fixed proportion (about 10%) of the immediately available transmitter is released by each nerve impulse.
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PMID:Potentiation and depression of synaptic transmission in the olfactory cortex of the guinea-pig. 433 92

1. The effects of pentobarbitone (0.05-0.6 mM in saline solution) on the evoked field potentials of in vitro preparations of guinea-pig olfactory cortex were studied.2. The evoked field potentials comprised an initial diphasic wave - the lateral olfactory tract (l.o.t.) compound action potential - followed by a surface negative wave (e.p.s.p) of 1-3 mV amplitude and about 10 msec duration. Superimposed on the negative wave were a number of positive peaks (population spikes).3. Pentobarbitone depressed the e.p.s.p. but not the l.o.t. compound action potential. The number and size of the population spikes were progressively reduced as the e.p.s.p. became depressed, indicating a failure of transmission through the cortical relay. The e.p.s.p. depression increased with increasing concentrations of pentobarbitone.4. Pentobarbitone had no effect on the threshold to electrical stimulation of the l.o.t. fibres or on that of the post-synaptic cells to synaptic excitation.5. Post-tetanic potentiation and frequency potentiation were either of normal magnitude or were enhanced in the presence of 0.2-0.3 mM pentobarbitone.6. It is concluded that pentobarbitone probably reduces the output of transmitter from the presynaptic nerve terminals of the olfactory cortex and that this mechanism could be the basis of the depressant action of the barbiturates.
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PMID:On the mechanism of barbiturate anaesthesia. 440 54

The effects of the dopamine agonist bromocryptine on several measures dopaminergic function were assessed in the rat. Following inhibition of impulse flow with gamma-butyrolactone, and after dopa decarboxylase inhibition, dopa accumulation and its reversal by dopamine agonists is easily studied. In this model, bromocryptine (10 mg/kg, i.p.) caused a significant decrease in dopa accumulation in both the striatum and olfactory tubercle which was prevented, but not reversed, by the dopamine antagonist (+)-butaclamol (4 mg/mg, i.p.). The inactive isomer, (-)-butaclamol was without effect. Analysis of an vitro 3H-spiperone binding 2h after bromocryptine (10 mg/kg, i.p.) revealed a 30% decrease in the number of striatal dopamine receptors labelled (Bmax), with no change in receptor affinity for 3H-spiperone. No changes in binding were seen when animals were sacrificed 30 min or 48 h after bromocryptine. In extracellular single unit recording experiments, bromocryptine-induced depression of nigrostriatal dopamine cell firing was found to be largely reversible by the dopamine antagonist haloperidol when injected within 5 min of intravenous bromocryptine. However, when haloperidol was injected more than 20 min after bromocryptine, no reversal of bromocryptine-induced depression of cell firing was obtained. These results strongly suggest that bromocryptine interacts in an irreversible fashion with central dopaminergic receptors.
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PMID:Evidence for an irreversible interaction of bromocryptine with central dopamine receptors. 610 95

The rat olfactory cortex slice has been used to investigate the effects of chlordiazepoxide on evoked field potentials and the release of endogenous amino acid neurotransmitters (aspartate, glutamate, GABA and possibly taurine) which accompany electrical stimulation of the lateral olfactory tract. When single, low frequency stimuli were employed, chlordiazepoxide (2 microM-1 mM) depressed the amplitude of the field potential correlate of the depolarizing actions of the lateral olfactory tract excitatory transmitter (aspartate?) although aspartate release was unaffected. The field potential correlate of GABA-mediated presynaptic inhibition (late N-wave) was also depressed in amplitude but low drug concentrations (between approximately 2 and 50 microM) increased its peak duration . Effects of chlordiazepoxide on evoked inhibition were analyzed by giving paired stimuli such that the second stimulus occurred during the field potentials evoked by the first stimulus. Chlordiazepoxide (1-20 microM) increased the depression in amplitudes of the presynaptic massed action potential and late N-wave evoked by the second of a pair of stimuli compared with those evoked by the first stimulus suggesting that presynaptic inhibition was potentiated. These effects of chlordiazepoxide were accompanied by a significant reduction in aspartate release from the lateral olfactory tract terminals. Moreover, the drug effects on presynaptic inhibition and aspartate release were antagonized by picrotoxin (5 microM). On the other hand, chlordiazepoxide (1-50 microM) had no significant effect on postsynaptic inhibition. The results are discussed in terms of both the sites (presynaptic or postsynaptic) and mechanisms of action of chlordiazepoxide.
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PMID:The effects of chlordiazepoxide on synaptic transmission and amino acid neurotransmitter release in slices of rat olfactory cortex. 611 29


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