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)

Patients with seasonal affective disorder (SAD) selectively eat more carbohydrates (CHO), particularly sweets but also starch-rich foods, during their depression in winter. The Dutch Eating Behaviour Questionnaire (DEBQ) was administered to female SAD patients, healthy female controls, and female medical students to determine their eating style, together with the modified Seasonal Pattern Assessment Questionnaire (SPAQ+). SAD patients showed higher values for "emotional" (EMOT) eating than the students, and these in turn had higher values than the controls. In comparison to controls, SAD patients and students head high values for the factor "external" (EXT) eating, but there was no difference between the groups with respect to "restraint" (REST) eating. This is in strong contrast to patients with bulimia and anorexia nervosa, who are high REST eaters, indicating that SAD patients do not have a similar eating disorder. Additional items showed that SAD patients selectively eat sweets under emotionally difficult conditions (when depressed, anxious, or lonely). Configural frequency analysis showed that seasonal body weight change (SBWC) is high in subjects with high EMOT and REST eating together with a high body mass index (BMI). This result is in accordance with the concept of disinhibition of dietary restraint in extreme emotional situations, e.g., the depressive state.
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PMID:Eating style in seasonal affective disorder: who will gain weight in winter? 905 25

The effects of olfactory bulbectomy on the acoustic startle reflex and shock-induced sensitization of the startle reflex were examined in 3 experiments. In Experiment 1, bulbectomized animals showed a modest increase in baseline startle responding following surgery, and normal acquisition of fear-potentiated startle, but a pronounced increase in baseline startle responding during the course of conditioning relative to sham-operated controls. In Experiments 2 and 3, bulbectomized animals showed shock-induced sensitization of the startle reflex to shock intensities that did not produce sensitization in sham and unoperated controls. These data suggest that olfactory bulbectomy results in an increased vulnerability to stressors, which may be mediated by a disinhibition of the amygdala or other structures involved in mediating stress and anxiety. Thus, the olfactory bulbectomy model of depression may share some similarities with other stress-induced models of depression.
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PMID:Olfactory bulbectomy enhances sensitization of the acoustic startle reflex produced by acute or repeated stress. 910 26

Rat neocortical brain slices generated rhythmic extracellular field [microelectroencephalogram (micro-EEG)] oscillations at theta frequencies (3-12 Hz) when exposed to pharmacological conditions that mimicked endogenous ascending cholinergic and GABAergic inputs. Use of the specific receptor agonist and antagonist carbachol and bicuculline revealed that simultaneous muscarinic receptor activation and gamma-aminobutyric acid-A (GABA(A))-mediated disinhibition were necessary to elicit neocortical oscillations. Rhythmic activity was independent of GABA(B) receptor activation, but required intact glutamatergic transmission, evidenced by blockade or disruption of oscillations by 6-cyano-7-nitroquinoxaline-2,3-dione and (+/-)-2-amino-5-phosphonovaleric acid, respectively. Multisite mapping studies showed that oscillations were localized to areas 29d and 18b (Oc2MM) and parts of areas 18a and 17. Peak oscillation amplitudes occurred in layer 2/3, and phase reversals were observed in layers 1 and 5. Current source density analysis revealed large-amplitude current sinks and sources in layers 2/3 and 5, respectively. An initial shift in peak inward current density from layer 1 to layer 2/3 indicated that two processes underlie an initial depolarization followed by oscillatory activity. Laminar transections localized oscillation-generating circuitry to superficial cortical layers and sharp-spike-generating circuitry to deep cortical layers. Whole cell recordings identified three distinct cell types based on response properties during rhythmic micro-EEG activity: oscillation-ON (theta-ON) and -OFF (theta-OFF) neurons, and transiently depolarizing glial cells. Theta-ON neurons displayed membrane potential oscillations that increased in amplitude with hyperpolarization (from -30 to -90 mV). This, taken together with a glutamate antagonist-induced depression of rhythmic micro-EEG activity, indicated that cholinergically driven neocortical oscillations require excitatory synaptic transmission. We conclude that under the appropriate pharmacological conditions, neocortical brain slices were capable of producing localized theta frequency oscillations. Experiments examining oscillation physiology, pharmacology, and topography demonstrated that neocortical brain slice oscillations share many similarities with the in vivo and in vitro theta EEG activity recorded in other brain regions.
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PMID:Physiology, pharmacology, and topography of cholinergic neocortical oscillations in vitro. 916 68

The purpose of the present study was to investigate in vivo the activity-dependent plasticity of glutamatergic cortico-striatal synapses. Electrical stimuli were applied in the facial motor cortex and intracellular recordings were performed in the ipsilateral striatal projection field of this cortical area. Recorded cells exhibited the typical intrinsic membrane properties of striatal output neurons and were identified morphologically as medium spiny type I neurons. Subthreshold cortical tetanization produced either short-term posttetanic potentiation or short-term depression of cortically-evoked excitatory postsynaptic potentials. When coupled with a postsynaptic depolarization leading the membrane potential to a suprathreshold level, the tetanus induced long-term potentiation (LTP) of cortico-striatal synaptic transmission. Induction of striatal LTP was prevented by intracellular injection of a calcium chelator suggesting that this synaptic plasticity involves an increase of postsynaptic free calcium concentration. Contrasting with previous in vitro studies our findings demonstrate that LTP constitutes the normal form of use-dependent plasticity at cortico-striatal synapses. Since excitation of striatal neurons produces a disinhibition of premotor networks, LTP at excitatory striatal inputs should favor the initiation of movements and therefore could be critical for the functions of basal ganglia in motor learning.
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PMID:In vivo activity-dependent plasticity at cortico-striatal connections: evidence for physiological long-term potentiation. 919 87

The EL/Suz (EL) mouse is a strain that is highly susceptible to convulsive seizures after repeated sensory stimulation. Its control strain, DDY/Jc1 (DDY), is less susceptible under similar conditions. The seizure prone phenotype is the result of differences at several genetic loci. In vivo electrical recordings from the seizure prone EL mouse brain have shown that the appearance of abnormal discharges in the hippocampus are critical to the onset of generalized seizures, indicating that the hippocampus plays an important role in EL mouse seizure activity. In the present study, electrophysiological differences between EL and DDY mice (9-15 weeks of age) were examined by comparing field potentials recorded from the dentate granule cell layer of hippocampal brain slices from mice that had not been stimulated to induce seizures. In control physiological solution, no significant differences were observed in characteristics of perforant path evoked field potentials or in paired pulse depression of evoked field potentials using 20 to 300 ms interstimulus intervals. After 60 min of disinhibition following bicuculline (10 microM) exposure, however, prolonged large amplitude potentials, paroxysmal discharges, were evoked by perforant path stimulation in the dentate gyrus of EL mice but were absent in the DDY strain. Paroxysmal discharges were curtailed by APV and were similar to responses recorded from the dentate gyrus in hippocampal brain slices from temporal lobe epileptic patients. The field response to hilar stimulation was identical in both strains and was composed of a single population spike before and after bicuculline exposure. Mossy fiber terminals were not present in the molecular layer of either strain. We propose that the mechanisms leading to a greater likelihood of paroxysmal discharge generation in EL mouse may be important in the development and/or generation of epileptic seizures in this mouse strain and may be a significant phenotypic difference between the EL mouse and its parent strain.
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PMID:Paroxysmal discharges in the EL mouse, a genetic model of epilepsy. 923 45

The influence of serotonin (5-HT) depletion (5,7-dihydroxytryptamine, 5,7-DHT, 250.0 micrograms, ICV), on behavioral effects of non-competitive (MK-801) and competitive (CGP 37849) NMDA antagonists, was examined in rats. 5,7-DHT induced very potent and long lasting decrease in the 5-HT concentration in the brainstem and limbic forebrain. One week after 5,7-DHT administration, dopamine metabolism was found enhanced in the brainstem. The lesion did not change rat baseline motor and exploratory activity, but it significantly disinhibited animals' behavior suppressed by shock, in the Vogel test. Serotonin depletion revealed locomotor stimulating effect of MK-801, administered IP at the doses of 0.05 and 0.2 mg/kg. However, no change in striatal dopamine metabolism was detected in rats injected with the same dose of MK-801 (0.2 mg/kg), and examined one week after serotonergic denervation. Serotonergic lesions antagonized both enhancements of exploratory behavior, and motor suppression produced by the dose of 1.0 and 10.0 mg/kg of CGP 37849, respectively. Thus, 5,7-DHT-induced lesions influenced in a complex way the effects of NMDA antagonists. It is reasoned, that enhancement of motor stimulating effects of MK-801 in neurotoxin pretreated animals, reflects synergistic disinhibition of activity of dopaminergic neurons by MK-801 and serotonin depletion. On the other hand, antagonism of CGP 37849-caused motor depression can be explained by the lowering influence of 5,7-DHT on serotonin content. It is known that the release of serotonin is strongly stimulated by higher doses of CGP 37849, and takes part in the expression of some symptoms of the serotonin-like syndrome, including motor disturbances.
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PMID:The behavioral effects of NMDA antagonists in serotonin depleted rats. 926 85

Numerous studies in stroke patients suggest that the left frontal anterior region may be strategic for depression. However, these findings could not always be replicated. Some authors even deny any etiological contribution of lesion location to depression. The predominant role of the right hemisphere in secondary mania is well recognized. In disorders such as apathy, anxiety, catastrophe reactions and pathological laughing and crying, further studies are needed to determine the potential clinico-topographic correlations. Affective disorders are important to consider in stroke patients, since they may influence neurological recovery and may be responsive to treatment. Remarkable features of emotional behavior, such as disinhibition, denial, indifference, overt sadness and aggressiveness, are not rare during the acute phase of stroke and might be overlooked if not searched for systematically with appropriately designed scales. Some of these early behaviors, such as denial, may relate to the late development of depression, anxiety and other disorders. Systematic studies on large samples of patients may allow to establish which of these acute emotional behavioral changes are markers for the delayed development of mood disorders.
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PMID:Affective disorders following stroke. 928 28

Shortened REM latency and increased REM density are frequently observed in both narcolepsy and depression, suggesting a common mechanism of REM sleep disinhibition in these disorders. We compared night sleep recordings of 24 depressive and 24 narcoleptic patients. The amount of REM sleep and REM density did not differ between the patient groups; however, REM latency distributions differed significantly. Whereas in narcoleptic patients REM episodes started either immediately at sleep onset or following at least 60 min of non-REM sleep, in depressives two thirds of REM latencies were in the range from 1 to 60 min. In narcoleptic patients, short as compared to long REM latencies were associated with longer total sleep time, greater sleep efficiency, reduced amounts of wakefulness, and increased amounts of slow-wave sleep. In depressive subjects the reverse pattern was seen. We conclude that a common mechanism of REM sleep disinhibition in narcolepsy and depression is very unlikely.
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PMID:REM sleep disinhibition at sleep onset: a comparison between narcolepsy and depression. 932 65

A variety of neuropsychiatric symptoms occur in Alzheimer's disease (AD) including agitation, psychosis, depression, apathy, disinhibition, anxiety, purposeless behavior, and disorders of sleep and appetite. Neuropsychiatric symptoms have been related to cholinergic deficiency and improve after treatment with cholinomimetic agents. Cholinergic drugs are unique among psychotropic agents in exerting disease-specific and broad-spectrum effects. These observations provide the basis for the cholinergic hypothesis of the neuropsychiatric symptoms of AD, suggesting that the cholinergic deficit of AD contributes to the neuropsychiatric symptoms of AD and that cholinomimetic therapy ameliorates the behavioral disturbances accompanying AD.
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PMID:The cholinergic hypothesis of neuropsychiatric symptoms in Alzheimer's disease. 958 Dec 23

Set point theory suggests that successful maintenance of weight loss ("weight suppression") may be associated with psychological distress. This study examined the association between psychological symptoms and body weight suppression by using a registry of 629 women and 155 men who lost at least 13.6 kg (mean loss = 30 +/- 15 kg) and maintained the loss for at least 1 year (mean duration = 5.5 +/- 6.8 years). Participants completed measures of mood, distress, restraint, disinhibition, bingeing, and purging. Maintainers' levels of distress and depression were lower than those of psychiatric samples and resembled those of community-based samples. Binge-eating and purging rates were comparable to rates of community samples. Maintainers' levels of restraint and disinhibition were markedly different from those of eating-disordered samples, resembling levels found in patients recently treated for obesity. There was no evidence that long-term suppression of body weight is associated with psychological distress.
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PMID:Psychological symptoms in individuals successful at long-term maintenance of weight loss. 969 43


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