2,183 research outputs found
Expression of neuropeptides – galanin and Reg2 - in subcategories of nociceptors after nerve injury
No full textPhDNeuropeptides show dynamic changes in expression after nerve injury, and have been
implicated in chronic pain states. I sought to compare expression of two peptides which
are upregulated after nerve injury, galanin and Reg2, and to determine the subtypes of
dorsal root ganglion (DRG) cells in which they are expressed.
Rats underwent unilateral, L5 spinal nerve ligation (SNL) with recovery for 1 or
7 days. Galanin and Reg2 were expressed in 20% and 8% of DRG cells at 1 day, and
49% and 5% at 7 days, respectively. At 1 day, galanin was mainly expressed in CGRPpositive
DRG cells (62% of galanin cells); this expression was maintained at 7 days. At
1 day, galanin was expressed in few IB4-positive DRG cells (14% of galanin cells), but
expression in IB4 cells significantly increased by 7 days (30% of galanin cells). Galanin
was also coexpressed with TRPV2 (9%). Reg2 was coexpressed in 48% of galanin cells
(7 days) but not coexpressed with TRPV2 and sparsely with CGRP. Using isolated DRG
cultured in BSF2 supplemented with 2% foetal calf serum (FCS), galanin and Reg2 were
expressed in 36.5% and 23.3% after 72hrs. Addition of IL6 (40 ng/mL in FCSsupplemented
BSF2) increased galanin expression after 24 and 48hrs growth by 6.7%
and 13.1%, respectively. ED1-positive cells were shown infiltrating the spinal nerve and
associated with the ganglion by 7 days post-SNL.
These results show Reg2 is more selectively expressed after L5 SNL than
galanin. Both peptides show a complex temporal profile of expression. Galanin is
upregulated initially in CGRP-cells and then in IB4/P2X3-cells, whereas Reg2 is
expressed initially in IB4/P2X3-cells and then in larger cells. The factors that
differentially regulate galanin, and potentially Reg2, in these cell populations remain
unknown but it is hypothesized that IL6, or a related cytokine, drives-up galanin
expression in IB4/P2X3-cells by 7 days but that the early upregulation in CGRP-cells is
a direct consequence of axotomy
Plasma galanin concentrations in obese, normal weight and anorectic women
No full textObjective: Galanin is believed to play a role in the control of eating behavior. No information is available on its concentrations in the biological fluids in human obesity, and this study aimed to clarify this. Measurements: We measured plasma galanin and serum insulin levels in 30 obese, 35 normal weight and 11 anorectic women. Results: Mean galanin values were quite similar in obese and control subjects (76.8 ± 3.20 vs 76.1 ± 2.33 pg/ml) and only slightly reduced in anorectic patients (67.9 ± 2.30 pg/ml). Insulin levels were significantly increased and decreased in obese and anorectic patients, respectively, compared to controls. Insulin correlated positively with BMI in the whole group of subjects studied (r = 0.72, P < 0.0001) and in the obese subgroup (r = 0.56, P < 0.02). No correlations could be detected between WH ratio, insulin and galanin concentrations and between galanin and BMI. Conclusions: In conclusion, plasma galanin concentrations appear to be comparable in obese, normal weight and anorectic subjects. This does not exclude a role of galanin in the regulation of eating behavior since variations of the peptide in discrete brain areas may not be detectable in general circulation and peripheral sources of the peptide may contribute to its plasma levels. Also, our data suggest that galanin does not play a major role in the regulation of insulin secretion in humans
A comparative immunohistochemical study on a galanin-like peptide in the neuroendocrine system of the alimentary canal of three species of siluriform catfishes
No full textImmunohistochemical examination of the galaninergic and the diffuse endocrine systems of the alimentary canal of three catfish species, Ameiurus melas, Silurus glanis and Clarias gariepinus showed the presence of galanin-like immunoreactive endocrine cells in the stomachs and the proximal intestines and a galanin-like immunoreactivity within the enteric intramural neurons. The three species differed notably in the relative abundance of galaninergic neurons of the digestive system. A galanin-like peptide was detected in a high number of nerve bundles and nerve fibres running through the exocrine parenchyma and the endocrine islets of the pancreas of all three species. It is conceivable that the galaninergic system in these species plays a role in regulating gut muscle activity, in modulating mucosal secretive and absorptive processes, and in controlling pancreatic hormone secretion
Enhanced prolactin responsiveness to galanin in patients with Cushing's disease
No full textObjective: Galanin is believed to play a role in the control of prolactin (PRL) secretion in the rat. Such a role is uncertain in humans where the neuropeptide is expressed by the corticotrophs. However, in clinical conditions of enhanced ACTH secretion, increased PRL levels are often observed. Therefore, we evaluated the effect of galanin infusion on serum PRL levels in patients with Cushing's disease and in control subjects. For comparison, the PRL responses to TRH and metoclopramide were also investigated in the same patients. Design - Four tests were performed: (a) 40-minute infusion of 0.3 μg/kg/min of galanin; (b) infusion of normal saline only; (c) metoclopramide test (10 mg as i.v. bolus); (d) TRH test (200 mg as i.v. bolus). Patients: Twenty-four normal subjects and nine patients suffering from active Cushing's disease were investigated. Measurements: Serum concentrations of PRL were measured by radioimmunoassay on blood samples collected before and for 90 minutes after drug or saline administration. Results: Serum baseline PRL levels were superimposable in normal subjects and in patients with Cushing's disease. In normal subjects, infusion of galanin induced a distinct PRL increase compared to saline (mean ±SEM incremental areas 6514 ± 2572 vs 540 ± 571 mU/l/90 min, P = 0.05, respectively). In patients with Cushing's disease, galanin evoked a remarkable PRL rise with hormone levels which were significantly greater (p < 0.001) than those observed in the same patients after infusion of saline (21908 ± 4180 vs 534 ± 1556 mU/l/90 min) or after galanin administration in controls (P < 0.01). The PRL response to TRH, and, much more so, to metoclopramine was significantly lower in patients with Cushing's disease than in normal subjects (42125 ± 8000 vs 73181 ± 7246 mU/l/90 min, P < 0.01 after TRH and 79095 ± 27265 vs 229049 ± 10602 mU/l/90 min, P < 0.01 after metoclopramide). Conclusions: Galanin appears to be a specific, though weak, PRL secretagogue in normal subjects. The galanin-induced PRL release was significantly increased in patients with Cushing's disease. A number of hypothetical mechanisms may underlie the enhanced PRL reactivity to galanin in Cushing's disease. This finding together with the impaired PRL responsiveness to TRH and metoclopramide, also observed in this study, is a further example of a dysregulation of PRL secretion in patients with Cushing's disease
Aging impairs galanin expression in luteinizing hormone-releasing hormone neurons: effect of ovariectomy and /or estradiol treatment
No full textIn the medial preoptic area and the diagonal band of Broca, a subset of LHRH neurons coexpresses galanin at 4- to 5-fold higher rate in female than male rats, suggesting that estradiol (E2) plays a key role in galanin gene expression within LHRH neurons. In the present studies we investigated the incidence of colocalization of these paptides in different age groups, i.e., 2-, 10-, 18-, and 24-month-old intact female Fisher rats; 24-month-old E2-treated rats; 24-month-old ovariectomized (OVX) rats; and 24-month-old OVX E2-treated rats with single or double labeling immunocytochemistry. For cell counting, we took advantage of the typical fusiform morphology of galanin-immunoreactive neurons that colocalize LHRH. The presence of both peptides in the same perikaryon was substantiated by double staining representative sections from each brain. Our observations indicate that the number of galanin/LHRH-coexpressing perikarya dramatically decreased with age. Although in 18-month-old rats a moderate decline was observed, in 24-month-old female rats no, or only a few, faintly stained, fusiform galanin-immunopositive perikarya were present. Although galanin was absent from LHRH neurons of aged rats, their LHRH content was not altered. E2 treatment of intact 24-month-old rats had no effect on the low incidence of colocalization. However, when OVX 24-month-old rats were E2 treated, the incidence of colocalization increased to the level seen in 2- or 10-month-old estrous animals. Our observations on the presence of colocalizing pericarya in intact and E2-treated aged animals provide further evidence for the key role of E2 in galanin gene expression within LHRH neurons and emphasize that some ovarian factor(s) may blunt this effect. (Endocrinology 134:324-330, 1994
Effects of endogenous galanin on the growth of regenerating rat adrenal gland as investigated by the metaphase-arrest and the PCNA-immunostaining techniques
No full textWe have investigated the effects of three subcutaneous injections of 2 nmol/100 g body weight of galanin and its receptor antagonist (galanin-A) [D-Thr 6,D-Trp 8,9,-15-ol]-galanin 1-15 on the proliferative activity of regenerating rat adrenal cortex. The metaphase-arrest and the proliferating-cell nuclear antigen (PCNA)-immunostaining techniques were used to estimate the number of M phase (metaphase index) and S phase cells (PCNA index), respectively. Galanin-A raised the metaphase index at both day 5 and day 8 of regeneration. Galanin was per se ineffective, but reversed the galanin-A effect at day 8. Neither galanin nor galanin-A changed PCNA index at day 5. Galanin evoked a moderate increase in PCNA index at day 8. Taken together, these findings indicate that endogenous galanin exerts a tonic maximal inhibitory effect on adrenal regeneration in the rat
Galanin hatása a vazopresszin kiválasztásra patkányba
Get PDFThe 29 amino acid-containing galanin isolated from the porcine intestine is known to play a significant role in the regulation of the function of the hypothalamo-neurohypophyseal system. The basal vasopressin concentration was examined, and also those vasopressin levels following osmotic and non-osmotic stimuli after centrally administered galanin. The effects of rat, porcine and human galanin and the human galanin 1-16 fragment on vasopressin release were studied. Finally, the question was investigated of whether the galanin receptor antagonist galantid (M15) was able to prevent the vasopressin level changes induced by galanin. Galanin administered intravenously did not influence the vasopressin excretion. After the intracerebroventricular (i.c.v.) injection of galanin, the vasopressin level decreased and the enhancement of the plasma vasopressin concentration following intraperitoneal 2.5% NaCI solution or histamine administration was significantly moderated. There was no essential difference in the vasopressin release effects of rat, porcine and human galanins. The human galanin 1-16 fragment proved to be active as concerns vasopressin regulation. Galantid administered i.c.v. before the galanin injection prevented all of the vasopressin- responsive effects of galanin. The results indicate that galaninergic control is of great importance in the regulation of vasopressin secretion
The co-expression of galanin and nestin in human carotid body differentiating the neuronal-like cell - the hypoxia sensor
No full textThe carotid body is a highly specialized chemoreceptive organ of neural crest origin whose role is to detect changes in arterial oxygen content. The sensory units are the chemoreceptor cells, which are neuronal-like cells, surrounded by sustentacular or glial-like cells. It is suggested that the carotid body contains self-renewing multipotent stem cells, which are putatively represented by glial-like sustentacular cells. The mechanisms of renewal of neuronal-like cells are unclear. Recently, we have demonstrated the expression of galanin, a peptide promoting neurogenesis, in chemoreceptor cells in the human CB. Thus, in the present study we seek to determine whether galanin expression in chemoreceptor cells could be matched with that of nestin, a peptide that is a marker of multipotent neural stem cells, or rather with the glial fibrillary acidic protein (GFAP), a marker for glial cells. The latter would underscore the pluasibly essential role of sustentacular cells in the self-renewal capability of chemorecetors. We found that galanin expression is matched with nestin in chemoreceptor cells of the human carotid body, but not with that of GFAP. Thus, galanin expression in chemoreceptor cells could provide a signal for neurogenesis and chemoreceptor cell differentiation in the carotid body
Evidence for a paracrine role of endogenous adrenomedullary galanin in the regulation of glucocorticoid secretion in the rat adrenal gland
No full textPrevious investigations have shown that rat adrenocortical cells are provided with galanin receptors, and galanin stimulates glucocorticoid secretion from dispersed cells. The present study aimed to clarify the possible role of galanin in the physiological regulation of rat adrenal secretory activity. Reverse transcription-polymerase chain reaction detected galanin mRNA expression in the adrenal medulla, but not in the cortex. Sizeable concentrations of galanin-immunoreactivity were measured by radioimmune assay only in the adrenomedullary tissue. Galanin raised norepinephrine, but not epinephrine, release from adrenomedullary tissue. Galanin immunoneutralization (obtained with concentrations of anti-galanin antibody able to block the galanin glucocorticoid secretagogue effect on dispersed adrenocortical cells) decreased basal corticosterone production from adrenal slices containing adrenomedullary tissue, without affecting that from dispersed adrenocortical cells. The beta-adrenoceptor antagonist l-alprenolol partially prevented galanin-stimulated corticosterone secretion from adrenal slices, without per se altering basal secretion. Taken together, our findings allow us to conclude that endogenous galanin, produced in adrenal medulla, is involved in the regulation of adrenocortical glucocorticoid secretion acting via a two-fold paracrine mechanism: i) direct activation of adrenocortical galanin receptors; and ii) stimulation of adrenomedullary release of catecholamines, which in turn activate beta-adrenoceptors located on adrenocortical cells
Internalization of intracerebrally administered porcine galanin (1-29) by a discrete nerve cell population in the hippocampus of the rat
No full textIn spite of numerous studies utilizing intraventricular administration of porcine galanin (1-29), little is known about the spread and cellular distribution of exogenous galanin following intraventricular administration. In this study a discrete nerve cell body population with their dendrites became strongly galanin immunoreactive (IR) in the dorsal hippocampus following intraventricular porcine galanin (1.5 nmol/rat), Time course experiments showed that after time intervals of 10 and 20 min, but not at 60 min, scattered small-to medium-sized galanin-IR nerve cell bodies and their dendrites were present in all layers of the dorsal and ventral hippocampus. In double-immunolabeling experiments most of these nerve cells were identified as putative GABA interneurons costoring NPY-IR or somatostatin-IR in some cases. Twenty minutes after intraventricular injection of artificial cerebrospinal fluid (aCSF), only endogenous punctate and coarse galanin-IR terminals were found, but no galanin-IR cell bodies. Intrahippocampal injection of fluorophore-labeled galanin resulted in the appearance of fluorescent nerve cell bodies with the same morphology and localization as in the above experiments. Coadministration of the putative galanin antagonist M35 (0.5 nmol) and galanin (1.5 nmol) resulted in a reduced number of galanin-IR nerve cell bodies in the hippocampus of half of the rats. These findings support the existence of a population of putative hippocampal GABA interneurons with the ability to internalize and concentrate galanin and/or its fragments present in the extracellular fluid, possibly mediated by galanin receptors
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