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

Unilateral olfactory deprivation in the rat profoundly modifies olfactory bulb anatomy, chemistry and function. The present report examined the time-course of the functional effects of unilateral deprivation on inhibition in the olfactory bulb using paired-pulse stimulation of the lateral olfactory tract and olfactory nerve. In addition, an attempt was made to correlate these physiological measures with olfactory bulb dopamine and norepinephrine levels and tyrosine hydroxylase immunoreactivity. Deprivation from postnatal day 1 to postnatal day 20 or postnatal day 40 significantly enhanced lateral olfactory tract paired-pulse depression, while late onset deprivation (postnatal day 20) had no effect. Olfactory nerve paired-pulse depression was enhanced by 40 days of deprivation regardless of the age at onset. The time-course of these deprivation-induced physiological changes did not correlate well with reductions in dopamine. Dopamine levels were reduced in all deprivation conditions by 70-80% compared with control bulbs. Norepinephrine content was slightly elevated in deprived bulbs. These results suggest that early olfactory deprivation modifies olfactory bulb synaptic activity and further, as with other sensory systems, these effects are age and duration dependent.
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PMID:Functional consequences of unilateral olfactory deprivation: time-course and age sensitivity. 135 86

Dopamine autoreceptor agonists reduce the firing rate, synthesis, and release of dopamine in dopaminergic neurons by means of a negative feedback mechanism via stimulation of autoreceptors. Moreover, dopamine autoreceptor agonists are able to stimulate supersensitive but not normosensitive postsynaptic receptors. For dopamine autoreceptor agonists, therapeutic effects by readjustment of excessive or deficient dopaminergic function have been postulated for positive and negative schizophrenic symptomatology as well as for subtypes of depressive disorders. Investigations on the therapeutic effects of autoreceptor-nonselective dopamine agonists in schizophrenia or depression have yielded inconsistent results. In order to reduce the excess of central dopaminergic activity postulated by the dopamine hypothesis of schizophrenia, dopamine autoreceptor agonists have been tested in open clinical trials in positive schizophrenic symptomatology. However, administration of selective dopamine autoreceptor agonists like talipexole or roxindole did not result in a significant improvement of positive psychotic symptoms. In negative schizophrenic symptomatology, a dopamine deficit rather than an excess has been hypothesized. Current evidence from pilot studies suggests that dopamine autoreceptor agonists like roxindole may produce a minor to moderate improvement of symptoms like affective flattening, depressed mood, alogia, and avolition, possibly by stimulation of supersensitive postsynaptic dopamine receptors. For certain subgroups of depression, a reduction of functional dopamine activity has been postulated. In an open pilot study in patients with a major depression, roxindole demonstrated antidepressive properties comparable to those of standard antidepressants, justifying further double-blind controlled trials against reference drugs.
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PMID:Dopamine autoreceptor agonists in the treatment of schizophrenia and major depression. 136 97

A hypothesis implicating dopamine in depression was proposed over 15 years ago (Randrup et al 1975). The identification of multiple new subtypes of dopamine receptors and evolving views regarding the function of the dopamine systems in the brain require a reexamination of this hypothesis. Results from studies in depression, Parkinson's disease, and animal models of depression suggest a deficiency of dopamine in depression. Dopamine precursors, dopamine agonists, and dopamine reuptake inhibitors show therapeutic efficacy in depression. Electroconvulsive therapy (ECT) and standard pharmacological antidepressants enhance dopamine function. Studies using receptor-specific drugs in clinical trials and neuroimaging studies are needed to further clarify the role of dopamine in depression.
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PMID:Role of the dopaminergic system in depression. 139 Dec 89

Dopamine (DA) causes a dose-dependent increase in the frequency of motor neuron bursts [virtual ventilation (fR)] produced by deafferented crab ventilatory pattern generators (CPGv). Domperidone, a D2-specific DA antagonist, by itself reversibly depresses fR and also blocks the stimulatory effects of DA. Serotonin (5HT) has no direct effects on this CPGv. Nicotine also causes dramatic dose-dependent increases in the frequency of motor bursts from the CPGv. The action is triphasic, beginning with an initial reversal of burst pattern typical of reversed-mode ventilation, followed by a 2- to 3-min period of depression and then a long period of elevated burst rate. Acetylcholine chloride (ACh) alone is ineffective, but in the presence of eserine is moderately stimulatory. The inhibitory effects of nicotine are only partially blocked by curare. The excitatory action of nicotine is blocked by prior perfusion of domperidone, but not by SKF-83566.HCl, a D1-specific DA antagonist. SKF-83566 had no effects on the ongoing pattern of firing. These observations support the hypothesis that dopaminergic pathways are involved in the maintenance of the CPGv rhythm and that the acceleratory effects of nicotine may involve release of DA either directly or via stimulation of atypical ACh receptors at intraganglionic sites.
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PMID:Dopamine and nicotine, but not serotonin, modulate the crustacean ventilatory pattern generator. 143 39

In the present study, we replicated and extended our previous findings of increased 24-hour urinary catecholamine excretion in posttraumatic stress disorder (PTSD). Dopamine, norepinephrine, and epinephrine concentrations were measured in 22 male patients with PTSD (14 inpatients and eight outpatients) and in 16 nonpsychiatric normal males. The PTSD inpatients showed significantly higher excretion of all three catecholamines compared with both outpatients with PTSD and normal controls. Dopamine and norepinephrine, but not epinephrine, levels were significantly correlated with severity of PTSD symptoms in the PTSD group as a whole. In particular, these catecholamines seemed related to intrusive symptoms. None of the catecholamines were correlated with severity of depression. The findings support the hypothesis of an enhanced sympathetic nervous system activation in PTSD, and suggest that increased sympathetic arousal may be closely linked to severity of certain PTSD symptom clusters.
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PMID:Urinary catecholamine excretion and severity of PTSD symptoms in Vietnam combat veterans. 158 75

The purpose of this article is to give the clinician not proficient in biochemistry an understanding of the biochemical research data on neurotransmitters and suicide. This literature review reports the current findings on serotonin (5-HT), dopamine (DA), and norepinephrine (NE) as possible biochemical markers of depression and suicide. In conjunction with known environmental and behavioral indicators of suicide, neurotransmitter balance could be a factor in determining the severity of depression and the possible suicidal ideation in patients. Numerous studies have been performed on the monoamines: Serotonin, Dopamine and Norepinephrine, neurotransmitters that innervate parts of the spinal cord and all areas of the brain. Studies appear to suggest a relationship among monoamine levels, depression, and suicide. Significantly low levels of serotonin and the neurotransmitter metabolite (5-HIAA) may be correlated with suicidal behavior.
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PMID:Monoamines: biochemical markers of suicide? 168 24

The influence of digoxin (0.01 mg/kg) given as an intravenous bolus followed by dopamine at different infusion rates (1.25, 2.5 and 5.0 micrograms/kg/min) on the cardiovascular depression during a standard halothane anaesthesia was studied in dorsally recumbent ventilated ponies. Preanaesthetic digitalization induced no clear positive cardiovascular effects over 30 minutes, except for non-significant increases in mean pulmonary artery pressure and total pulmonary resistance. These changes were probably time-related. No specific side-effects related to the fast intravenous digitalization were noticed. Dopamine at lower infusion rates (1.25 and 2.5 micrograms/kg/min) given minimally 30 minutes after the digitalization did not induce further changes (only minor non-significant increases in cardiac output and systemic blood pressure). Dopamine infusions at a higher infusion rate (5.0 micrograms/kg/min) improved the cardiovascular depression (significant increases in cardiac output and systemic blood pressure while total peripheral resistance tended to decrease). Heart rate, blood gases and total pulmonary resistance remained constant. The combination of a fast acting inotropic agent, dopamine, and a slow acting inotropic drug, digoxin, induced positive effects in reversing the cardiovascular depression and might therefore be useful during clinical anaesthesia in the horse.
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PMID:Influence of digoxin followed by dopamine on the cardiovascular depression during a standard halothane anaesthesia in dorsally recumbent, ventilated ponies. 177 80

The influence of different rates of dopamine and dobutamine on the cardiovascular depression during a standard halothane anesthesia was studied in dorsally recumbent ventilated ponies. Haemodynamic and respiratory responses were investigated by means of cardiac output (CO) determination (thermodilution technique), mean systemic (MAP) and pulmonary artery pressure (MPAP) (direct intravascular method) and arterial blood analysis (blood gases and packed cell volume). An important cardiopulmonary depression characterized by decreases (55% of the standing values) in CO, cardiac index (CI), MAP, MPAP and other cardiovascular related parameters occurred in the dorsally recumbent anaesthetized ponies after a stabilization period of 30 minutes. Dopamine at 2 different infusion rates (2.5 and 5.0 micrograms/kg/min) induced few changes of the cardiopulmonary parameters (non-significant increases in MAP, CI, left ventricular work [LVW], stroke volume [SV]; non-significant decrease in total peripheral resistance [TPR]). Several minor time related influences were also observed (increases in MPAP and total pulmonary resistance [TpR]). Arterial blood gases did not change during the different dopamine infusions. Low doses of dobutamine (1.25 micrograms/kg/min) were efficient to counteract the cardiovascular depression. Significant increases in CO, CI, MAP, MPAP and SV were observed. TPR and TpR tended to decrease but non-significantly. Heart rate and blood gases remained constant. The higher doses of dobutamine (2.5 and 5.0 micrograms/kg/min) accentuated these changes but a significant increase in heart rate with even periods of severe tachycardia and an increase of the packed cell volume were also observed. Apparently, low doses of dobutamine were indicated for the management of the cardiovascular depression during anaesthesia in the dorsally recumbent ventilated horse.
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PMID:Influence of dopamine and dobutamine on the cardiovascular depression during a standard halothane anaesthesia in dorsally recumbent, ventilated ponies. 195 Feb 40

In hippocampal pyramidal cells (HPCs), Dopamine (DA) application (1 microM) produced, in 50% of recorded cells, an hyperpolarization of the resting membrane potential (r.m.p.) and an increase of the afterhyperpolarization (AHP) amplitude and duration in 79% of recorded cells. DA-induced effects on both the r.m.p. and AHP were mimicked by bath application of a D-1 selective agonist, SKF 38393 (20 microM). In addition, we have observed that a D-1 selective antagonist such as SCH 23390 (1 microM) abolished the action of both DA and SKF 38393. In contrast, the activation of D-2 receptors through LY 171555 (10 microns) produced, in 50% of cells, a depolarization of the r.m.p. and a depression of the AHP in 67% of recorded cells. These results suggest that the effects observed in hippocampal pyramidal neurons after DA application of micromolar concentration are mediated by D-1 subtype of receptors.
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PMID:Effects of dopamine, D-1 and D-2 dopaminergic agonists on the excitability of hippocampal CA1 pyramidal cells in guinea pig. 198 61

Dopamine-3-O-sulfate (DA-3-O-S) and dopamine-4-O-sulfate (DA-4-O-S) are important end products of L-dopa metabolism. Therefore they may give indications of disturbances in the peripheral metabolism of catecholamines, when measured in urine samples of patients with Parkinson's disease (PD). In addition, information about the reliability of DA sulfatation after L-dopa therapy may be of significance for its role in the elimination of DA from the peripheral nervous system. Although DA-3-O-S appears to be the predominant sulfo-conjugate in urine, there are no changes in PD nor in depression syndrome compared to controls with or without other neurological disorders. By contrast, DA-4-O-S is significantly decreased in de novo PD subjects. However, a similar reduction is notable in patients with other neurological disorders. In depressed persons the loss of this compound was less pronounced as compared to de novo PD. Treatment with combined L-dopa therapy caused increased excretion of DA-3-O-S, while changes in DA-4-O-S were only marginal. It is concluded that urinary DA-3-O-S cannot be used as marker for PD, while DA-4-O-S is significantly reduced in a variety of neurological disorders and in particular in de novo PD. Further studies are necessary to elucidate its role as possible peripheral marker to distinguish preclinical PD and depression syndrome.
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PMID:Urinary dopamine sulfate: regulations and significance in neurological disorders. 208 10


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