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)

Locomotor activity and behaviour in the forced swimming test were examined in rats which had received neurotensin (0.5-5.0 micrograms) in the ventral tegmental area. Doses of 5 micrograms neurotensin but not lower increased the locomotor activity for at least 2 h. At 0.5 and 1.0 microgram neurotensin significantly increased the time the animals spent in struggling with no changes in general motor activity (swimming). The effect of 1.0 microgram neurotensin on struggling was completely antagonized by 0.5 microgram (-)-sulpiride administered in the posterior nucleus accumbens. The results suggest that activation of the mesolimbic dopamine system through administration of neurotensin in the ventral tegmental area produces antidepressant-like effects. The significance of these findings for a role of endogenous neurotensin in depression remains to be clarified.
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PMID:Antidepressant-like effect of neurotensin administered in the ventral tegmental area in the forced swimming test. 136 37

1. The effects of neurotensin (NT) on membrane potential and membrane current of the longitudinal smooth muscle of chicken rectum were investigated by intracellular recording and whole-cell voltage clamp. 2. NT (3 nM-1.2 microM), when applied via the bathing medium, produced a concentration-dependent membrane depolarization with an EC50 of 18 +/- 2 nM (n = 7) which was accompanied by an increase in the membrane conductance. The effect was biphasic: an initial, rapid depolarization reached a peak within 2-3 min and then declined to a lower but still elevated level which was sustained until washout. 3. Excitatory junction potentials (e.j.ps), which were non-adrenergic non-cholinergic (NANC) in nature, were decreased in amplitude and total duration in the presence of NT (0.6 microM). The depression of the e.j.p. was due mainly to the reduction of the membrane resistance. 4. When NT was applied locally by means of pressure ejection from a micropipette containing NT, some cells responded with a membrane depolarization and some failed to respond, whereas e.j.ps could invariably be elicited from all of them. 5. In single muscle cells enzymatically isolated from the muscle and dialyzed under voltage clamp at -50 mV with a CsCl-rich solution, NT (5 or 10 microM) produced an inward current. NT-induced inward currents were obtained with inclusion of 10 mM EGTA in the pipette solution and their reversal potential was around 0 mV. In cells dialyzed under voltage clamp at 0 mV with a KCl-rich solution, NT (5 microM) produced a brief outward current followed by abolition of spontaneous transient outward currents.6. The present results suggest that the membrane depolarization, which may arise from activation of non-selective cation channels, and release of calcium from internal stores produced by neurotensin are responsible for its contractile activity in the longitudinal smooth muscle of chicken rectum. Further, the depolarizing effect may provide support for the involvement of NT in the NANC transmission in this preparation.
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PMID:Membrane potential and current responses to neurotensin in the longitudinal muscle of the rectum of the fowl. 147 75

A 7-day infusion with neurotensin (NT) (10 micrograms.kg-1.day-1) stimulated adrenal growth in intact female rats, and raised ACTH blood concentration, without altering corticosterone (B) plasma level and output by adrenal homogenates. For a week dexamethasone (Dx) administration (125 micrograms.kg-1.day-1) caused a notable adrenal atrophy, a marked lowering of ACTH and B blood concentrations, and a profound depression of B output by adrenal homogenates. NT infusion reversed Dx-induced adrenal atrophy and plasma ACTH-level drop, but not the impairment in adrenal-cortex secretory activity. In vitro studies showed that NT (10(-6) mol/l) significantly reduced basal, but not ACTH-stimulated B release by isolated rat inner adrenocortical cells. These findings suggest that NT exerts a direct inhibitory effect on B production by rat adrenals, while it is able to enhance ACTH secretion and consequently adrenal growth. Moreover, they indicate that NT evokes a striking, and at present unexplained dissociation between structure and function in the adrenal cortex of Dx-suppressed rats.
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PMID:Effects of neurotensin on the pituitary-adrenocortical axis of intact and dexamethasone-suppressed rats. 166 3

The responsiveness of functionally identified cat spinal dorsal horn neurons to iontophoretically applied substance P (SP) and 5-hydroxytryptamine (5-HT) has been investigated by means of extracellular recording after 5-HT depletion with p-chlorophenylalanine (p-CPA). In addition, the spinal levels of 5-HT, SP, cholecystokinin octapeptide, neurotensin, and vasoactive intestinal polypeptide have been measured in intact and p-CPA-pretreated cats. In the present study we have demonstrated an altered responsiveness of dorsal horn neurons to locally applied SP and 5-HT. We found in p-CPA-pretreated cats that the proportion of neurons responding with excitation to SP and 5-HT was significantly increased. At the same time, depression induced by 5-HT in the dorsal horn cells was virtually absent in p-CPA-pretreated animals. Our finding that spinal level of 5-HT was significantly decreased in p-CPA-treated animals is consistent with previous studies. No convincing alteration in the spinal levels of 4 analyzed peptides was found in p-CPA-treated animals. The present study has shown that pharmacological depletion of 5-HT has two major effects: (1) it increases significantly the proportion of dorsal horn neurons excited by SP and 5-HT; and (2) it is ineffective in inducing 5-HT supersensitivity. Further work is needed to explain mechanisms involved in these effects.
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PMID:Altered responsiveness to substance P and 5-hydroxytryptamine in cat dorsal horn neurons after 5-HT depletion with p-chlorophenylalanine. 242 Apr 13

Neurotensin (NT) concentrations in cerebrospinal fluid (CSF) were measured by a sensitive and specific radioimmunoassay in psychiatric patients and age- and sex-matched normal controls. No increase in CSF NT concentrations was observed after antipsychotic drug treatment. CSF NT concentrations were significantly lower in one group of schizophrenic subjects. NT concentrations were unaltered in patients with depression, anorexia/bulimia, or premenstrual syndrome, and no rostral-caudal gradient for NT in CSF was evident. NT concentrations were not related to age or sex, and probenecid treatment did not alter CSF NT concentrations. Finally CSF NT concentrations were unaltered in paranoid schizophrenic subjects. These findings confirm and extend previous studies of CSF NT that showed certain patients with schizophrenia, nonparanoid type, have reduced CSF concentrations of this tridecapeptide.
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PMID:Neurotensin-like immunoreactivity in cerebrospinal fluid of patients with schizophrenia, depression, anorexia nervosa-bulimia, and premenstrual syndrome. 257 18

The effects of a number of vasoactive and neurotransmitter substances on lymphocyte traffic were studied by assessing their effects on the release of lymphocytes into primary peripheral (popliteal) nodal efferent lymph of sheep following acute infusion into cannulated afferent nodal lymphatics. In a total of 23 experiments, the output of lymphocytes, small and blast, was increased by serotonin, substance P, bombesin, [met]enkephalin, isoprenaline and phenylephrine and was decreased by vasoactive intestinal peptide (VIP), neurotensin and carbachol. Substances whose actions are modulated by prostaglandins and enhanced by prostaglandin synthesis inhibitors and which elevate blood monocyte and nervous tissue levels of cyclic GMP tended to increase lymphocyte traffic through peripheral lymph nodes in sheep in vivo. The opposite effect tended to be produced by substances whose actions require or are associated with prostaglandins or histamine, and which affect blood monocytic cyclic nucleotide levels by elevation of cyclic AMP or depression of cyclic GMP. Pain and inflammation tended to increase lymphocyte traffic, while analgesics and immunomodulators tended to decrease it.
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PMID:Modification of lymphocyte traffic by vasoactive neurotransmitter substances. 614 65

The levels of neurotensin and thyrotropin-releasing hormone (TRH) in normal post mortem human amygdala have been compared with those in cases of schizophrenia, Alzheimer's disease and depression. Amongst various factors which can influence post mortem human brain biochemistry (including age, sex, post mortem delay, time of death, disease status and severity), sex difference appeared to be responsible for the most extensive variation. The levels of both peptides were nearly doubled in males compared with females and this increase was significant in the case of neurotensin. There was also a positive correlation between neurotensin and TRH levels. Although levels of neurotensin and TRH tended to be lower in the disease groups these trends did not reach significance.
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PMID:Post mortem levels of thyrotropin-releasing hormone and neurotensin in the amygdala in Alzheimer's disease, schizophrenia and depression. 640 15

The tridecapeptide neurotensin (NT), injected intracerebroventricularly in rats, induced a naloxone-insensitive and dose-dependent analgesia (tail-flick test), the ED50 being 3.22 nmol/animal. Higher doses induced a dose-dependent respiratory depression, mostly accounted for by a reduction of frequency; the ED50 for this action was 144.6 nmol/animal. In contrast to analgesia, the respiratory depression was antagonized by naloxone, suggesting the possibility that NT and opioid systems might interact at the level of respiration-related nuclei.
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PMID:Different mechanisms are involved in the respiratory depression and analgesia induced by neurotensin in rats. 671 97

Morphine, met-enkephalin, beta-endorphin, tetrodotoxin (TTX), and atropine antagonized the gut-contracting effects of the peptides neurotensin and bombesin. The opioids and TTX shifted the concentration-response curves to the right and mostly depressed the maximum response to the agonists; atropine caused only depression of the maximum. Morphine was more potent than the opioid peptides. Naloxone did not modify the effects of neurotensin and bombesin. However, it completely abolished the antagonistic effects of the opioids, but not that of atropine. In conclusion, neurotensin and bombesin stimulate the intramural neurons via a process that is inhibited by the activation of opioid receptors.
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PMID:Antagonism of the gut-contracting effects of bombesin and neurotensin by opioid peptides, morphine, atropine or tetrodotoxin. 743 14

Cholecystokinin and neurotensin are present in fibres innervating the parabrachial nucleus and have previously been shown to modulate the flow of visceral afferent information through the parabrachial nucleus to the cortex in the rat. This study examined the effects of cholecystokinin and neurotensin on synaptic transmission in the parabrachial nucleus using a pontine slice preparation and the nystatin perforated-patch recording technique. Stimulation of the ventral, external lateral portion of the parabrachial nucleus elicited glutamate-mediated, excitatory postsynaptic currents in cells recorded in the parabrachial nucleus. Bath application of neurotensin dose-dependently and reversibly enhanced, while cholecystokinin attenuated, the evoked excitatory postsynaptic current. In addition, the frequency of spontaneous, miniature excitatory postsynaptic currents recorded in parabrachial nucleus cells was significantly increased by neurotensin and decreased by cholecystokinin application. Paired-pulse depression was also enhanced and decreased by neurotensin and cholecystokinin, respectively. These synaptic changes induced by neurotensin and cholecystokinin were not accompanied by changes in input resistance of parabrachial nucleus cells over a wide voltage range (although neurotensin reduced an outwardly rectifying conductance at potentials positive to -20 mV), nor did these peptides alter the inward current induced by a brief bath application of the glutamate agonist, alpha-amino-3-hydroxy-methylisoxazole-4-propionate. The neurotensin antagonist, SR48692 (100 microM), completely and reversibly blocked the neurotensin-induced enhancement of the excitatory postsynaptic current. The non-selective cholecystokinin receptor antagonist, proglumide (100 microM), completely and reversibly blocked the cholecystokinin-induced attenuation of the excitatory postsynaptic current. In addition, the selective cholecystokinin-A receptor antagonist, L-364,718 (10 microM), but not the selective cholecystokinin-B receptor antagonist, L-365,260 (100 microM), blocked the effect of cholecystokinin on synaptic transmission. These results suggest that neurotensin and cholecystokinin act at presynaptic neurotensin and cholecystokinin-A receptors, respectively, to modulate excitatory synaptic transmission in the parabrachial nucleus.
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PMID:Cholecystokinin and neurotensin inversely modulate excitatory synaptic transmission in the parabrachial nucleus in vitro. 904 71


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