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

Pregnancy, parturition and lactation comprise a continuum of adaptive changes necessary for the development and maintenance of the offspring. The endocrine changes that are driven by the conceptus and are essential for the maintenance of pregnancy and are involved in the preparations for motherhood are outlined. These changes include large increases in the secretion of sex steroid hormones, and the secretion of peptide hormones that are unique to pregnancy. The ability of these pregnancy hormones to alter several aspects of brain function in pregnancy is considered, and the adaptive importance of some of these changes is discussed, for example in metabolic and body fluid adjustments, and the induction of maternal behavior. The importance of sex steroids in determining the timing of the various adaptive changes in preparing for parturition and maternal behavior is emphasized, and the concept that the actions of prolactin and oxytocin, quintessential mammalian motherhood neuropeptides, can serve to coordinate a spectrum of adaptive changes is discussed. The part played by oxytocin neurons and their regulatory mechanisms is reviewed to illustrate how neural systems involved in maternity are prepared in pregnancy via changes in phenotype, synaptic organization and in the relative importance of their different inputs, to function optimally when needed. For oxytocin neurons secreting from the posterior pituitary, important in parturition and essential in lactation, these changes include mechanisms to restrain their premature activation, and adaptations to support synchronized burst firing for pulsatile oxytocin secretion in response to stimulation via afferents from the birth canal, olfactory system or suckled nipples. Within the brain, expression of oxytocin receptors permits centrally released oxytocin to facilitate the expression of maternal behavior. Changes in other neuroendocrine systems are similarly extensive, leading to lactation, suppression of ovulation, reduced stress responses and increased appetite; these changes in lactation are driven by the suckling stimulus. The possible link between these adaptations and changes in cognition and mood in pregnancy and post partum are considered, as well as the dysfunctions that lead to common problems of depression and puerperal psychoses.
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PMID:Brain preparations for maternity--adaptive changes in behavioral and neuroendocrine systems during pregnancy and lactation. An overview. 1158 24

Previous data revealed that numerous neurons in the supraoptic nucleus degenerate after prolonged ethanol exposure, and that the surviving neurons increase their activity in order to prevent dramatic changes in water metabolism. Conversely, excess alcohol does not induce cell death in the suprachiasmatic nucleus, but leads to depression of neuropeptide synthesis that is further aggravated by withdrawal. The aim of the present study is to characterize the effects of prolonged ethanol exposure on the magnocellular neurons of the paraventricular nucleus (PVN) in order to establish whether or not magnocellular neurons display a common pattern of reaction to excess alcohol, irrespective of the hypothalamic cell group they belong. Using conventional histological techniques, immunohistochemistry and in situ hybridization, the structural organization and the synthesis and expression of vasopressin (VP) and oxytocin (OXT) in the magnocellular component of the PVN were studied under normal conditions and following chronic ethanol treatment (6 or 10 months) and withdrawal (4 months after 6 months of alcohol intake). After ethanol treatment, there was a marked decrease in the number of VP- and OXT-immunoreactive magnocellular neurons that was attributable to cell death. The surviving neurons were hypertrophied and the VP and OXT mRNA levels in the PVN unchanged. Withdrawal did not alter the number of VP- and OXT-producing neurons or the gene expression of these peptides. These results substantiate the view that after prolonged ethanol exposure numerous neurons of the hypothalamic magnocellular system degenerate, but the mRNA levels of VP and OXT are not decreased due to compensatory changes undergone by the surviving neurons.
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PMID:Prolonged alcohol intake leads to irreversible loss of vasopressin and oxytocin neurons in the paraventricular nucleus of the hypothalamus. 1175 2

We studied the effects of the neuropeptide oxytocin (OT) on the long-term potentiation (LTP) paradigm in the dentate gyrus (DG) of urethane anesthetized rats. Intracerebroventricular injection of 1 microg of the hormone in 1 microl of physiological solution 2min before tetanization produced a significant decrease in both components of the perforant path evoked potentials (EP) in the DG. The effects appeared right after the tetanization stimuli and were more pronounced in the excitatory postsynaptic components of the EPs. The decrements lasted for the 2h of recording time. We concluded that OT induced and maintained long-term depression on the DG. In contrast, injection of OT in the absence of tetanic stimulation did not significantly affect perforant path EP in the DG. The results are discussed taking particular consideration of the inhibitory effects the OT has on (Ca(2+)+Mg(2+)) ATPase at membrane levels and the potential interference that this action may have with phosphorylation processes via an ectoprotein kinase isolated from membranes of hippocampal pyramidal neurons. Blocking of this ectoprotein kinase in vitro significantly impairs establishment and maintenance of LTP.
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PMID:Oxytocin induces long-term depression on the rat dentate gyrus: possible ATPase and ectoprotein kinase mediation. 1212 11

Severe early stress and maltreatment produces a cascade of events that have the potential to alter brain development. The first stage of the cascade involves the stress-induced programming of the glucocorticoid, noradrenergic, and vasopressin-oxytocin stress response systems to augment stress responses. These neurohumors then produce effects on neurogenesis, synaptic overproduction and pruning, and myelination during specific sensitive periods. Major consequences include reduced size of the mid-portions of the corpus callosum; attenuated development of the left neocortex, hippocampus, and amygdala along with abnormal frontotemporal electrical activity; and reduced functional activity of the cerebellar vermis. These alterations, in turn, provide the neurobiological framework through which early abuse increases the risk of developing post-traumatic stress disorder (PTSD), depression, symptoms of attention-deficit/hyperactivity, borderline personality disorder, dissociative identity disorder, and substance abuse.
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PMID:Developmental neurobiology of childhood stress and trauma. 1213 7

From the author's direct involvement in clinical research, the conclusion has been drawn that clinically relevant long-term pain relieving effects of acupuncture (>6 months) can be seen in a proportion of patients with nociceptive pain. The mechanisms behind such effects are considered in this paper. From the existing experimental data some important conclusions can be drawn: 1. Much of the animal research only represents short-term hypoalgesia probably induced by the mechanisms behind stress-induced analgesia (SIA) and the activation of diffuse noxious inhibitory control (DNIC). 2. Almost all experimental acupuncture research has been performed with electro-acupuncture (EA) even though therapeutic acupuncture is mostly gentle manual acupuncture (MA). 3. Most of the experimental human acupuncture pain threshold (PT) research shows only fast and very short-term hypoalgesia, and, importantly, PT elevation in humans does not predict the clinical outcome. 4. The effects of acupuncture may be divided into two main components--acupuncture analgesia and therapeutic acupuncture. A hypothesis on the mechanisms of therapeutic acupuncture will include: 1. Peripheral events that might improve tissue healing and give rise to local pain relief through axon reflexes, the release of neuropeptides with trophic effects, dichotomising nerve fibres and local endorphins. 2. Spinal mechanisms, for example, gate-control, long-term depression, propriospinal inhibition and the balance between long-term depression and long-term potentiation. 3. Supraspinal mechanisms through the descending pain inhibitory system, DNIC, the sympathetic nervous system and the HPA-axis. Is oxytocin also involved in the long-term effects? 4. Cortical, psychological, "placebo" mechanisms from counselling, reassurance and anxiety reduction.
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PMID:Acupuncture mechanisms for clinically relevant long-term effects--reconsideration and a hypothesis. 1221 6

The mechanism by which dopamine induces or facilitates neurohypophysial hormone release is not completely understood. Because oxytocin- and vasopressin-secreting supraoptic neurons are under the control of a prominent GABAergic inhibition, we investigated the possibility that dopamine exerts its action by modulating GABA-mediated transmission. Whole cell voltage-clamp recordings of supraoptic neurons were carried out in acute hypothalamic slices to determine the action of dopamine on inhibitory postsynaptic currents. Application of dopamine caused a consistent and reversible reduction in the frequency, but not the amplitude, of miniature synaptic events, indicating that dopamine was acting presynaptically to reduce GABAergic transmission. The subtype of dopamine receptor involved in this response was characterized pharmacologically. Dopamine inhibitory action was greatly reduced by two highly selective D4 receptor antagonists L745,870 and L750,667 and to a lower extent by the antipsychotic drug clozapine but was unaffected by SCH 23390 and sulpiride, D1/D5 and D2/D3 receptor antagonists, respectively. In agreement with these results, the action of dopamine was mimicked by the potent D4 receptor agonist PD168077 but not by SKF81297 and bromocriptine, D1/D5 and D2/D3 receptor agonists, respectively. Dopamine and PD168077 also reduced the amplitude of evoked inhibitory postsynaptic currents, an effect that was accompanied by an increase in paired-pulse facilitation. These data clearly indicate that D4 receptors are located on GABA terminals in the supraoptic nucleus and that their activation reduces GABA release in the supraoptic nucleus. Therefore dopaminergic facilitation of neurohypophysial hormone release appears to result, at least in part, from disinhibition of magnocellular neurons caused by the depression of GABAergic transmission.
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PMID:Dopamine D4 receptor-mediated presynaptic inhibition of GABAergic transmission in the rat supraoptic nucleus. 1271 14

To model aspects of trait anxiety/depression, Wistar rats were bred for extremes in either hyper (HAB)- or hypo(LAB)-anxiety as measured on the elevated plus-maze and in a variety of additional behavioral tests. Similar to psychiatric patients, HAB rats prefer passive stress-coping strategies, indicative of depression-like behavior, show hyper-reactivity of the hypothalamo-pituitary-adrenal axis, and a pathological response to the dexamethasone/corticotropin-releasing hormone (CRH) challenge test. Here we tested central mRNA expression, release patterns, and receptor binding of neuropeptides critically involved in the regulation of both anxiety-related behavior and the HPA axis. Thus, CRH, arginine-8-vasopressin (AVP), and oxytocin (OXT) were studied in brains of HAB and LAB males both under basal conditions and after exposure to a mild emotional stressor. In HAB rats, CRH mRNA was decreased in the bed nucleus of the stria terminalis only. While no significant difference in CRH1-receptor binding was found in any brain area, CRH2-receptor binding was elevated in the hypothalamic paraventricular nucleus (PVN), the ventromedial hypothalamus, and the central amygdala of HABs compared to LABs. AVP, but not OXT, mRNA expression as well as release of the neuropeptide, were higher in the PVN of HABs, whereas AVP V1a-receptor binding failed to show significant differences in any brain region studied. Remarkably, intra-PVN treatment of HABs with the AVP V1-receptor antagonist d (CH(2))(5) Tyr (Me) AVP resulted in a decrease in anxiety/depression-related behavior. The elevated expression and release of AVP within the PVN of HAB rats together with the behavioral effects of the AVP V1-receptor antagonist suggest a critical involvement of this neuropeptide in neuroendocrine and behavioral phenomena associated with trait anxiety/depression.
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PMID:Alterations in central neuropeptide expression, release, and receptor binding in rats bred for high anxiety: critical role of vasopressin. 1294 43

Present experiments in rats were aimed to verify the hypothesis that glutamatergic neurotransmission and stress hormones play a role in impairment of hedonic behavior, a sign of depression-like state. On the basis of individual variability in sucrose preference, test rats were divided into anhedonic and hedonic groups. Anhedonic animals showed higher basal concentrations of adrenocorticotropin and corticosterone but reduced hormonal responses during novelty stress compared to hedonic animals. Acute administration of citalopram (10 mg/kg ip) induced similar effects in both groups. Corticotropin-releasing hormone (CRH) mRNA levels in hypothalamic paraventricular nucleus (PVN) were higher in anhedonic rats. Oxytocin (OT) and vasopressin gene expression in the PVN and proopiomelanocortin (POMC) expression in the anterior pituitary failed to show any significant differences. Gene expression of NR1 receptor subunit of N-methyl-D-aspartate (NMDA) glutamate receptor in the ventral tegmental area (VTA) was found to be lower in anhedonic rats. In the nucleus accumbens (NAc) and the hippocampus of anhedonic animals, higher mRNA levels of NR2A subunit compared to those of hedonic rats were detected. Thus, low sucrose preference is associated with altered HPA axis activity, NMDA receptor subunits and CRH gene expression in selected brain regions. These mechanisms may operate in the disposition to develop hedonic deficit in some mental disorders.
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PMID:Altered glutamate receptor and corticoliberin gene expression in brain regions related to hedonic behavior in rats. 1367 12

Carica papaya L. seeds extracted with 80% ethanol (EEPS) caused concentration-dependent tocolysis of uterine strips isolated from gravid and non-gravid rats. Prostaglandin F2alpha and oxytocin-induced contractions of the isolated rat uterus were also inhibited in a concentration-dependent fashion by EEPS. Recoveries of the uterine activity after EEPS-induced uterine quiescence were very weak. Higher concentration of EEPS caused prompt uterine quiescence, which was also significantly irreversible. Pre-incubation of the rat uterus in Ringer Locke solution containing 10 mg/ml of EEPS for 1 hour prior to suspension in tissue baths led to significant depression of the spontaneous and KCl (60 mM)-induced uterine contractions relative to the solvent control (P<0.05). Cross sections of EEPS-pretreated non-gravid rat uterus (stained with hematoxyline and eosin) examined under light microscope revealed degeneration of the endometrium and myometrium with obvious cytoplasmic vacuolation indicating that EEPS could have direct toxic effect on the uterine tissues. Previous workers have reported benzyl isothiocyanate (BITC) as the main bioactive and anthelmintic compound in different extracts of papaya seeds. Using electron impact ionization methods, the presence of BITC in EEPS was also shown in this study. Mass spectra of both EEPS and standard BITC showed a base peak of benzyl/tropylium ion at m/z 91 (indicative of an aromatic compound) and the molecular ion peak of BITC (m/z 149). Our earlier studies have demonstrated BITC-induced functional and morphological derangement of isolated uterus. We thus conclude that at high concentration, EEPS is capable of causing irreversible uterine tocolysis probably due to the damaging effect of BITC (its chief phytochemical) on the myometrium.
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PMID:Tocolytic and toxic activity of papaya seed extract on isolated rat uterus. 1462 29

This study was aimed to evaluate the reaction of the vasopressin (VP) and oxytocin (OT) neurons of the supraoptic nucleus (SON) in rats to single or repeated hypergravity (HG). Special attention was paid to the tyrosine hydroxylase (TH) expression in VP neurons as a marker of the neuron activation. Rats were revolved in a centrifuge with overloading 2G for 5 days or 34 days as well as for 34 days plus 5 days with an interval of 39 days between two rotations. Control rats were kept in a centrifuge room. Radioimmununoassay, quantitative and semi-quantitative immunocytochemistry and in situ hybridization were used to evaluate: a) VP concentration in the pituitary posterior lobe (PL) and in plasma; b) the number of VP-, OT- and TH-immunoreactive neurons in the SON; c) the optic density of VP-, OT- and TH-immunoreactive materials in cell bodies (SON) and distal axons (PL), d) the optic density of VP and OT mRNAs signals (S35) in the whole SON on microfilms. According to our data, VP neurons were strongly activated during HG (5 days or 34 days) that was manifested in the functional hypertrophy of the neurons, greatly increased concentrations of VP mRNA in the SON and VP in plasma, the onset of the TH expression. The neurons showed initially (5 days) the functional insufficiency (VP release > VP synthesis) followed by their adaptation (subsequent 29 days) to the increased need in VP (VP release < VP synthesis). No reaction of VP neurons was observed to repeated HG. In contrast to VP neurons, OT neurons did not react to short-term HG or showed functional depression after the long-term treatment.
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PMID:Influence of hypergravity on hypothalamic vasopressin and oxytocin neurons in rats. 1470 80


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