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)

In order to receive a further understanding of stress-regulation in depressed suicide attempters, peptides that are supposed to be related to the stress system (the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system) were studied in plasma. When compared with healthy controls, cortisol was high (p<0.001) and corticotropin releasing hormone (CRH) and neuropeptide Y (NPY) appeared to be low (p<0.001) in patients who had recently attempted suicide. Patients who had repeatedly attempted suicide had the lowest NPY. A correlation between NPY and cortisol (p<0.05) was found in suicidal patients with depression NOS, whereas beta-endorphins correlated with cortisol (p<0.01) in suicidal patients with major depressive disorder. A postdexamethasone decrease of NPY was noted in the controls but not in the patients. These results suggest stress system alterations in suicidal patients with mood disorders.
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PMID:Alterations of corticotropin releasing hormone (CRH) and neuropeptide Y (NPY) plasma levels in mood disorder patients with a recent suicide attempt. 1020 89

Interleukin-1beta (IL-1beta) can be synthesized by macrophages, endothelial cells and vascular smooth muscle cells when stimulated by bacterial lipopolysaccharide (endotoxin) during septic shock. The IL-1beta levels in the blood vessel wall are also elevated in atherosclerosis. IL-1beta can cause induction of inducible nitric oxide synthase (iNOS) expression in vascular smooth muscle cells and produce vasorelaxation, hypotension and ultimately tissue damage. We studied the depressions of vascular smooth muscle contractions at 3 hours after exposure to IL-1beta in different positions of rat thoracic aorta. The data show that the aortic rings from the cranial end of rat thoracic aorta had little response to IL-1beta (0.5 and 1.0 ng/ml) while those from the caudal end of thoracic aorta had larger depressant response. S-methylisothiourea sulfate (SMT), an iNOS inhibitor, completely blocked the depression of contraction caused by IL-1beta in intact aortic rings. If the endothelium was removed from the aortic rings before exposure to IL-1beta, all rings from different parts of the thoracic aorta showed an equal amount of vasodepression. Thus, the difference in the depressant response of IL-1beta in different portions of thoracic aorta is endothelium-dependent and involves induction of NOS.
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PMID:Interleukin-1beta causes different levels of nitric oxide-mediated depression of contractility in different positions of rat thoracic aorta. 1032 17

The biological roles of nitric oxide (NO) and cGMP as inter- and intracellular messengers have been intensively investigated during the last decade. NO and cGMP both mediate physiological effects in the cardiovascular, endocrinological, and immunological systems as well as in central nervous system (CNS). In the CNS, activation of the N-methyl-D-aspartic acid (NMDA) type of glutamatergic receptor induces Ca(2+)-dependent NOS and NO release, which then activates soluble guanylate cyclase for the synthesis of cGMP. Both compounds appear to be important mediators in long-term potentiation and long-term depression, and thus may play important roles in the mechanisms of learning and memory. Aging and the accumulation of amyloid beta (A beta) peptides are important risk factors for the impairment of memory and development of dementia. In these studies, the mechanism of basal- and NMDA receptor-mediated cGMP formation in different parts of adult and aged brains was evaluated. The relative activity of the NO cascade was determined by assay of NOS and guanylate cyclase activities. In addition, the effect of the neurotoxic fragment 25-35 of A beta (A beta) peptide on basal and NMDA receptor-mediated NOS activity was investigated. The studies were carried out using slices of hippocampus, brain cortex, and cerebellum from 3- and 28-mo-old rats. Aging coincided with a decrease in the basal level of cGMP as a consequence of a more active degradation of cGMP by a phosphodiesterase in the aged brain as compared to the adult brain. Moreover, a loss of the NMDA receptor-stimulated enhancement of the cGMP level determined in the presence of cGMP-phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX) was observed in hippocampus and cerebellum of aged rats. However, this NMDA receptor response was preserved in aged brain cerebral cortex. A significant enhancement of the basal activity of NOS by about 175 and 160% in hippocampus and cerebellum, respectively, of aged brain may be involved in the alteration of the NMDA receptor response. The neurotoxic fragment of A beta, peptide 25-35, decreased significantly the NMDA receptor-mediated calcium, and calmodulim-dependent NO synthesis that may then be responsible for disturbances of the NO and cGMP signaling pathway. We concluded that cGMP-dependent signal transduction in hippocampus and cerebellum may become insufficient in senescent brain and may have functional consequences in disturbances of learning and memory processes. A beta peptide accumulated during brain aging and in Alzheimer disease may be an important factor in decreasing the NO-dependent signal transduction mediated by NMDA receptors.
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PMID:Aging modulates nitric oxide synthesis and cGMP levels in hippocampus and cerebellum. Effects of amyloid beta peptide. 1034 72

We examined characteristics of spreading depression (SD) induced on the rat cortex 1 day after transient focal ischemia. Male Wistar rats (n=21) were subjected to transient intraluminal thread occlusion of the right middle cerebral artery for 75 min. Twenty-four hours after the reperfusion, cerebral blood flow (CBF) was determined using laser Doppler flowmeter during multiple SDs elicited on both non-stroke (left) and stroke (right) cortex by the topical application of 2 M KCl. We also examined CBF responses before and after the intravenous administration of the nonspecific NOS inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg) in normal and stroke cortex. Animals were divided into two groups; Group 1 (n=12), animals with subcortical infarction and Group 2 (n=9), animals with subcortical plus cortical infarction. There were no differences between non-stroke and stroke sides in the duration or amplitude of the DC potential shifts in either group. The transient CBF hyperemia during SD was not different between non-stroke (372+/-23% of baseline, mean+/-S.E.) and stroke sides (383+/-30%) in Group 1. However, in Group 2, CBF was significantly restricted on the stroke side (192+/-15% vs. non-stroke side, 374+/-33%). In four normal animals without ischemia, there were no differences in CBF response between both sides. L-NAME had no effect on the transient CBF hyperemia during SD in any of the groups. These data suggest that the CBF responses during SD in the peri-infarction area is restricted 1 day after the transient focal ischemia, while CBF responses are intact in normal cortex overlapping a subcortical infarct. Further, our results indicate that nitric oxide does not promote CBF responses during SD in normal cortex or in tissue surrounding infarction.
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PMID:Characteristics of induced spreading depression after transient focal ischemia in the rat. 1076 Apr 93

Intrathecal administration(i.t.) of Dynorphin A1-17(Dyn) 1.25-20 nmol produced dose-dependent paralysis of hindlimbs and tail as well as inhibition of tail flick and foot flinch reflexes. The Dyn spinal neurotoxicity and antinociception involve two differential mechanisms: Enhancement of NMDA-Ca(2+)-NOS/NO pathway and c-fos over-expression in the ventral spinal cord for neurotoxicity, and depression of NMDA receptor and NOS activities in the dorsal spinal cord for antinociception. Both brain-derived constitutive NOS (predominant at early stage) and inducible NOS (at later stage) are detrimental, but endothelial constitutive NOS might be beneficial to Dyn spinal neurotoxicity. Dyn exerts a dualistic modulatory effect on [Ca2+]i of the cultured rat single spinal neurons, inducing sustained overload of intracellular free calcium via both NMDA and kappa receptor activation at higher concentrations, and producing significant inhibition of the depolarization-evoked calcium influx only via kappa receptor activation at lower concentrations. Dyn exposure for 1 h produced direct neurotoxicity in the cultured spinal neurons within an optimal range of concentrations.
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PMID:[Effects of dynorphin A1-17 on the activities, immunoreactivities and mRNA expression of cNOS and iNOS in rat spinal cord and their mechanisms]. 1092 Oct 77

Nitric oxide (NO) is implicated in the regulation of various endocrine functions, but the effect of NO on GABA(A) receptor transmission has never been reported in endocrine cells. In the present study, we have investigated the effects of various agents acting on the NO transduction pathway on GABA(A) receptor function in frog pituitary melanotrophs. Histochemical studies using the NADPH-diaphorase reaction and immunohistochemical labeling with antibodies against neuronal NO synthase (nNOS) revealed that nNOS is expressed in the intermediate lobe of the pituitary and in cultured melanotrophs. Whole-cell patch-clamp recordings showed that the specific substrate of NOS L-arginine (L-Arg, 10(-4) M) or the NO donor sodium nitroprusside (10(-5) M) provoked a long-lasting inhibition of the current evoked by GABA (5 x 10(-6) M). The NOS inhibitor L-nitroarginine (10(-5) M) produced a biphasic effect, i.e. a transient decrease followed by a delayed increase of the GABA-evoked current amplitude. Similarly, the specific nNOS inhibitor 7-nitroindazole and the specific inducible NOS (iNOS) inhibitor aminoguanidine (10(-5) M each) provoked a transient depression of the current followed by a sustained potentiation. Formation of cGMP in neurointermediate lobes was enhanced by L-Arg (10(-4) M) and by the calcium-releasing agent caffeine (10(-4) M), and inhibited by the calmodulin (CaM)/Ca2+ complex blocker W7 (10(-5) M). The GABA-evoked current was potentiated by the guanylyl cyclase inhibitor ODQ (10(-8)-10(-7) M) and inhibited by the protein kinase G (PKG) activator 8pCPT-cGMP (3 x 10(-7)-3 x 10(-5) M). The present data indicate that NO, produced by a CaM/Ca2+-dependent NOS in frog melanotrophs, exerts an autocrine inhibitory effect on the GABA-evoked current. The action of NO on the GABA(A) receptor function is mediated through activation of the cGMP/PKG pathway.
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PMID:Regulation of the GABA(A) receptor by nitric oxide in frog pituitary melanotrophs. 1096 18

A characteristic physiological property of the neuromuscular junction between giant motor neurones (MoGs) and fast flexor muscles in crayfish is synaptic depression, in which repetitive electrical stimulation of the MoG results in a progressive decrease in excitatory junction potential (EJP) amplitude in flexor muscle fibres. Previous studies have demonstrated that l-arginine (l-Arg) modulates neuromuscular transmission. Since l-Arg is a precursor of nitric oxide (NO), we examined the possibility that NO may be involved in modulating neuromuscular transmission from MoGs to abdominal fast flexor muscles. The effect of a NO-generating compound, NOC7, was similar to that of l-Arg, reversibly decreasing the EJP amplitude mediated by the MoG. While NOC7 reduced the amplitude of the EJP, it induced no significant change in synaptic depression. In contrast, a scavenger of free radical NO, carboxy-PTIO, and an inhibitor of nitric oxide synthase, l-NAME, reversibly increased the EJP amplitude mediated by MoGs. Synaptic depression mediated by repetitive stimulation of MoGs at 1 Hz was partially blocked by bath application of l-NAME. Bath application of a NO scavenger, a NOS inhibitor and NO-generating compounds had no significant effects on the depolarisation of the muscle fibres evoked by local application of l-glutamate. The opposing effects on EJP amplitude of NOC7 and of carboxy-PTIO and l-NAME suggest that endogenous NO presynaptically modulates neuromuscular transmission and that it could play a prominent role at nerve terminals in eliciting MoG-mediated synaptic depression in the crayfish Procambarus clarkii.
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PMID:Modulatory effects of nitric oxide on synaptic depression in the crayfish neuromuscular system. 1106 Feb 20

Nitric oxide (NO) has been shown to affect the behaviour in animal models of depression, anxiety and avoidance learning. Lithium has marked effect in avoidance learning, an effect that can be modulated via the 5-HT system. Experiments were carried out using the conditioned taste aversion (CTA) paradigm to investigate whether administration of NO-modifying drugs, serotonergic drugs and lithium, alone or in combination, induced or affected a CTA. The NO-precursor L-arginine (L-Arg), the non-specific inhibitor of NOS and guanylate cyclase, methylene blue (MB) and the specific NOS inhibitor 7-Nitroindazole (7-NI) all produced CTAs in a dose-dependent fashion. Furthermore, we found that L-Arg counteracted the CTAs induced by LiCl or MB but failed to modulate the CTA produced by 7-NI. The administration of the selective 5-HT1A agonist, 8-OH-DPAT, counteracted the CTAs produced by MB and 7-NI. In contrast, depletion of 5-HT by p-Chlorophenylalanine did not affect the aversions produced by MB and 7-NI, but counteracted the CTA produced by L-Arg. Our results suggest that NO plays a role in the acquisition of the CTA induced by LiCl. Furthermore, the results suggest that the 5-HT1A receptor plays an important role in the CTA induced by MB and 7-NI, thus indicating a possible interaction between the 5-HT and NO systems.
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PMID:Nitric oxide modulates lithium-induced conditioned taste aversion. 1116 17

In cerebellar slices conjunctive pairing of parallel fibre (PF) stimulation with depolarization of Purkinje cells (PCs) induces a long-term depression (LTD) of PF synaptic transmission that spreads to unpaired PF inputs to the same cell. Inhibitors of NO synthase (7-nitro-indazole), soluble guanylate cyclase (ODQ) and PKG (KT5823) all prevented depression at each of two independent PF pathways to a single PC. Inhibition of NOS also unmasked a platelet activating factor (PAF)-mediated synaptic potentiation of possible presynaptic origin. LTD was also prevented by the phospholipase A2 inhibitor OBAA but was rescued by co-perfusion with arachidonic acid. We conclude that NO and diffusible products of phospholipase A2 metabolism are potential mediators of the spread of cerebellar plasticity at the single cell level.
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PMID:Roles for nitric oxide and arachidonic acid in the induction of heterosynaptic cerebellar LTD. 1120 Oct 73

This study compared structured vs. unstructured interviews for making psychiatric diagnoses. Three clinicians independently diagnosed 56 inpatient-subjects, each using a different method: (1) the unstructured Traditional Diagnostic Assessment (TDA), the standard method of clinical practice; (2) the Structured Clinical Interview for DSM-Clinical Version (SCID-CV), a widely used structured method; and (3) the Computer Assisted Diagnostic Interview (CADI), a structured computer-based method. Once finished, the three clinicians developed a Consensus diagnosis, using Spitzer's LEAD Standard (L=Longitudinal evaluation of symptomatology, E=Evaluation by expert consensus, AD=All Data from multiple sources). Diagnoses were assigned to one of 10 groups (cognitive impairment, general medical condition-induced, alcohol-induced, drug-induced, mania, depression, schizophrenia, schizoaffective, psychosis NOS, and anxiety). Diagnostic accuracy for each method, measured against Consensus, was as follows: TDA-agreement=53.8%, kappa=0.4325 ('fair'); SCID-CV-agreement=85.7%, kappa=0.8189 ('excellent'); CADI -agreement=85.7%, kappa=0.8147 ('excellent'). All three methods reached acceptable levels of diagnostic accuracy. Structured methods (SCID-CV, CADI) were significantly better than the unstructured TDA.
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PMID:Inpatient diagnostic assessments: 1. Accuracy of structured vs. unstructured interviews. 1181 44


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