scholarly journals Behavioral variation correlates with differences in single neuron serotonin receptor subtype expression within and across species

2017 ◽  
Author(s):  
A.N. Tamvacakis ◽  
A. Senatore ◽  
P.S. Katz
Keyword(s):  
Serotonin Receptor ◽  
Single Neuron ◽  
Receptor Gene ◽  
Motor Pattern ◽  
Receptor Expression ◽  
Receptor Subtype ◽  
Marine Mollusc ◽  
Pleurobranchaea Californica ◽  
Receptor Gene Expression ◽  
Daily Changes

AbstractThe marine mollusc, Pleurobranchaea californica varies daily in whether it swims and this correlates with whether serotonin (5-HT) enhances the strength of synapses made by the swim central pattern generator neuron, C2. Another species, Tritonia diomedea, reliably swims and does not vary in serotonergic neuromodulation. A third species, Hermissenda crassicornis, never produces this behavior and lacks the neuromodulation. We found that expression of particular 5-HT receptor genes in C2 correlates with swimming. Seven 5-HT receptor subtype genes were identified from whole-brain transcriptomes. We isolated individual C2 neurons and sequenced their RNA or measured 5-HT receptor gene expression using quantitative PCR. C2 neurons isolated from Pleurobranchaea individuals that produced a swim motor pattern just prior to isolation expressed the 5-HT2a and 5-HT7 receptor genes, as did the Tritonia samples. These subtypes were absent from C2 neurons isolated from Pleurobranchaea individuals that did not swim that day and from Hermissenda C2 neurons. Expression of other receptors did not correlate with swimming. This suggests that 5-HT2a and 5-HT7 receptors mediate the modulation of C2 synaptic strength and play an important role in swimming. Furthermore, the results suggest that regulation of receptor expression might underlie daily changes in behavior as well as behavioral evolution.

scholarly journals Single neuron serotonin receptor subtype gene expression correlates with behaviour within and across three molluscan species

2018 ◽  
Vol 285 (1885) ◽  
pp. 20180791 ◽  
Author(s):  
A. N. Tamvacakis ◽  
A. Senatore ◽  
P. S. Katz
Keyword(s):  
Gene Expression ◽  
Serotonin Receptor ◽  
Single Neuron ◽  
Motor Pattern ◽  
Receptor Expression ◽  
Receptor Subtype ◽  
Marine Mollusc ◽  
Pleurobranchaea Californica ◽  
Molluscan Species ◽  
Daily Changes

The marine mollusc, Pleurobranchaea californica varies daily in whether it swims and this correlates with whether serotonin (5-HT) enhances the strength of synapses made by the swim central pattern generator neuron, A1/C2. Another species, Tritonia diomedea , reliably swims and does not vary in serotonergic neuromodulation. A third species, Hermissenda crassicornis , never produces this behaviour and lacks the neuromodulation. We found that expression of particular 5-HT receptor subtype (5-HTR) genes in single neurons correlates with swimming. Orthologues to seven 5-HTR genes were identified from whole-brain transcriptomes. We isolated individual A1/C2 neurons and sequenced their RNA or measured 5-HTR gene expression using absolute quantitative PCR. A1/C2 neurons isolated from Pleurobranchaea that produced a swim motor pattern just prior to isolation expressed 5-HT2a and 5-HT7 receptor genes, as did all Tritonia samples. These subtypes were absent from A1/C2 isolated from Pleurobranchaea that did not s wim on that day and from Hermissenda A1/C2 neurons. Expression of other receptors was not correlated with swimming. This suggests that these 5-HTRs may mediate the modulation of A1/C2 synaptic strength and play an important role in swimming. Furthermore, it suggests that regulation of receptor expression could underlie daily changes in behaviour as well as evolution of behaviour.

Hypothalamic GH receptor gene expression in the rat: effects of altered GH status

1995 ◽  
Vol 147 (2) ◽  
pp. 225-234 ◽  
Author(s):  
P A Bennett ◽  
A Levy ◽  
S Sophokleous ◽  
I C A F Robinson ◽  
S L Lightman
Keyword(s):  
Gene Expression ◽  
Receptor Gene ◽  
Feedback Regulation ◽  
Receptor Expression ◽  
Physiological Regulation ◽  
Background Strain ◽  
Gh Receptor ◽  
The Central Nervous System ◽  
Receptor Gene Expression

Abstract GH synthesis and release from the anterior pituitary is governed by the opposing actions of somatostatin (SS) and GH-releasing factor (GRF), derived from the periventricular and arcuate nucleus (ARC) of the hypothalamus respectively. GH is known to regulate its own release by hypothalamic autofeedback mechanisms, but the extent to which this is a direct effect rather than indirectly via the generation of IGFs is still a subject of debate. GH receptors are known to be present in the hypothalamus, but their physiological regulation is poorly understood. We therefore used in situ hybridization histochemistry to investigate the effects of GH status on hypothalamic GH receptor gene expression, using hypophysectomized normal and dw/dw dwarf rats as models of acquired and congenital GH deficiency. Hypophysectomy resulted in a timedependent reduction in GH receptor gene expression. ARC GH receptor transcripts in untreated dw/dw dwarf rats were half those found in normal animals of the same background strain (16·8±1·7 vs 9·3± 1·9 d.p.m./mg, P<0·05). Increasing circulating GH by peripheral infusion of 200 μg human GH (hGH)/day for 6 days increased ARC GH receptor expression in dw/dw rats to normal. In contrast, central infusions of hGH at 26·4 and 79·2 μg/day for 6 days in normal rats lowered ARC GH receptor gene expression. The sensitivity of GH receptor gene expression within the central nervous system to peripheral and central GH levels suggests that feedback regulation of GRF and/or SS may be mediated directly by these receptors, and that the sensitivity to GH feedback is also subject to autoregulation by GH altering its own receptor expression. Journal of Endocrinology (1995) 147, 225–234

scholarly journals Modulation of glomerular endothelin and endothelin receptor gene expression in aminonucleoside-induced nephrosis.

1995 ◽  
Vol 5 (8) ◽  
pp. 1585-1590
Author(s):  
T Nakamura ◽  
I Ebihara ◽  
M Fukui ◽  
S Osada ◽  
Y Tomino ◽  
...  
Keyword(s):  
Gene Expression ◽  
Receptor Gene ◽  
Mrna Level ◽  
Experimental Period ◽  
Receptor Expression ◽  
Mrna Levels ◽  
Puromycin Aminonucleoside ◽  
Receptor Mrna ◽  
Etb Receptor ◽  
Receptor Gene Expression

This study assessed glomerular endothelin (ET)-1, ET-3, and ET-receptor A and B mRNA levels in puromycin aminonucleoside (PAN)-induced nephrosis. During the nephrotic stage, 8 days after PAN injection, ET-1 and ETB receptor mRNA were elevated by 2.8 +/- 0.8-fold (P < 0.01) and 2.4 +/- 0.9-fold (P < 0.01), respectively, as compared with controls. These mRNA levels decreased to control levels by Day 20, when the nephrosis was in remission. In contrast, glomerular ETA receptor mRNA levels did not change in PAN nephrosis or control rats during the experimental period. ET-3 mRNA was not detected in the glomeruli of PAN nephrosis or control rats. Additionally, plasma ET concentration and glomerular ET production were measured in PAN nephrosis and control rats by radio-immunoassay. Eight days after PAN injection, ET-1 levels in plasma and glomeruli were not significantly altered in rats with PAN-induced nephrosis (glomeruli, 104.68 +/- 16.46 pg/mg of protein versus 98.24 +/- 13.68 pg/mg of protein; plasma, 2.68 +/- 1.10 versus 2.52 +/- 0.98 pg/mL). The administration of methylprednisolone to PAN rats resulted in the rapid disappearance of proteinuria and partially attenuated the increased ET-1 and ETB receptor gene expression in the glomeruli. These data indicate that glomerular ET-1 and ETB receptor expression in PAN nephrosis in increased at the mRNA level and that methylprednisolone treatment results in an attenuated increase.

Parathyroid hormone receptor stimulation induces human adipocyte lipolysis and browning

2021 ◽  
Vol 184 (5) ◽  
pp. 687-697
Author(s):  
Peter Breining ◽  
Steen B Pedersen ◽  
Mads Kjolby ◽  
Jacob B Hansen ◽  
Niels Jessen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Parathyroid Hormone ◽  
Receptor Gene ◽  
Receptor Expression ◽  
Whole Body ◽  
Brown Adipocyte ◽  
Cell Models ◽  
Receptor Stimulation ◽  
Receptor Gene Expression

Objective Activation of brown adipose tissue is a promising strategy to treat and prevent obesity and obesity-related disorders. Activation of uncoupling protein 1 (UCP1) leads to uncoupled respiration and dissipation of stored energy as heat. Induction of UCP1-rich adipocytes in white adipose tissue, a process known as ‘browning’, serves as an alternative strategy to increase whole body uncoupling capacity. Here, we aim to assess the association between parathyroid hormone (PTH) receptor expression and UCP1 expression in human adipose tissues and to study PTH effects on human white and brown adipocyte lipolysis and UCP1 expression. Design A descriptive study of human neck adipose tissue biopsies substantiated by an interventional study on human neck-derived adipose tissue cell models. Methods Thermogenic markers and PTH receptor gene expression are assessed in human neck adipose tissue biopsies and are related to individual health records. PTH-initiated lipolysis and thermogenic gene induction are assessed in cultured human white and brown adipocyte cell models. PTH receptor involvement is investigated by PTH receptor silencing. Results PTH receptor gene expression correlates with UCP1 gene expression in the deep-neck adipose tissue in humans. In cell models, PTH receptor stimulation increases lipolysis and stimulates gene transcription of multiple thermogenic markers. Silencing of the PTH receptor attenuates the effects of PTH indicating a direct PTH effect via this receptor. Conclusion PTH 1 receptor stimulation by PTH may play a role in human adipose tissue metabolism by affecting lipolysis and thermogenic capacity.

Serotonin receptor gene expression in the pathology of schizophrenia

2002 ◽  
Vol 17 ◽  
pp. 24
Author(s):  
P.W.J. Burnet ◽  
S. Eastwood ◽  
S. East ◽  
N. Crossland ◽  
P. Harrison
Keyword(s):  
Gene Expression ◽  
Serotonin Receptor ◽  
Receptor Gene ◽  
Receptor Gene Expression

scholarly journals PDGF ligand and receptor gene expression during repair of arterial injury.

1990 ◽  
Vol 111 (5) ◽  
pp. 2149-2158 ◽  
Author(s):  
M W Majesky ◽  
M A Reidy ◽  
D F Bowen-Pope ◽  
C E Hart ◽  
J N Wilcox ◽  
...  
Keyword(s):  
Gene Expression ◽  
Carotid Artery ◽  
Receptor Gene ◽  
Receptor Expression ◽  
Quiescent State ◽  
Mrna Levels ◽  
Luminal Surface ◽  
Receptor Mrna ◽  
Beta Receptor ◽  
Receptor Gene Expression

Smooth muscle cells (SMC) in rat carotid artery leave the quiescent state and proliferate after balloon catheter injury, but the signals for mitogenesis are not known. In this study, the possibility that cells within damaged arteries produce a growth factor that could act locally to stimulate SMC replication and repair was examined. We found that the genes for PDGF-A and -B (ligand) and PDGF receptor (alpha and beta subunits) were expressed in normal and injured carotid arteries and were independently regulated during repair of carotid injury. Two phases of PDGF ligand and receptor gene expression were observed: (a) In the early stage, a large decrease in PDGF beta-receptor mRNA levels preceded 10- to 12-fold increases in PDGF-A transcript abundance in the first 6 h after wounding. No change in PDGF alpha-receptor or PDGF-B gene expression was found at these times. (b) In the chronic phase, 2 wk after injury, neointimal tissue had lower levels of PDGF alpha-receptor mRNA (threefold) and higher levels of PDGF beta-receptor mRNA (three- to fivefold) than did restored media. Moreover, in situ hybridization studies identified a subpopulation of neointimal SMC localized at or near the luminal surface with a different pattern of gene expression than the underlying carotid SMC. Luminal SMC were strongly positive for PDGF-A and PDGF beta-receptor transcripts, while showing little or no hybridization for PDGF-B or PDGF alpha-receptor. Immunohistochemical studies showed strongly positive staining for PDGF-A in SMC along the luminal surface. These data show that changes in PDGF ligand and receptor expression occur at specific times and locations in injured carotid artery and suggest that these changes may play a role in regulating arterial wound repair.

scholarly journals Regulation of angiotensin II type 2 receptor gene expression in the adrenal medulla by acute and repeated immobilization stress

2012 ◽  
Vol 215 (2) ◽  
pp. 291-301 ◽  
Author(s):  
Regina Nostramo ◽  
Andrej Tillinger ◽  
Juan M Saavedra ◽  
Ashok Kumar ◽  
Varunkumar Pandey ◽  
...  
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Receptor Gene ◽  
Receptor Expression ◽  
Mrna Levels ◽  
Ang Ii ◽  
Catecholamine Biosynthesis ◽  
Receptor Mrna ◽  
Receptor Gene Expression

While the renin–angiotensin system is important for adrenomedullary responses to stress, the involvement of specific angiotensin II (Ang II) receptor subtypes is unclear. We examined gene expression changes of angiotensin II type 1A (AT1A) and type 2 (AT2) receptors in rat adrenal medulla in response to immobilization stress (IMO). AT2 receptor mRNA levels decreased immediately after a single 2-h IMO. Repeated IMO also decreased AT2 receptor mRNA levels, but the decline was more transient. AT1A receptor mRNA levels were unaltered with either single or repeated IMO, although binding was increased following repeated IMO. These effects of stress on Ang II receptor expression may alter catecholamine biosynthesis, as tyrosine hydroxylase and dopamine β-hydroxylase mRNA levels in PC12 cells are decreased with Ang II treatment in the presence of ZD7155 (AT1 receptor antagonist) or with CGP42112 (AT2 receptor agonist) treatment. Involvement of stress-triggered activation of the hypothalamic–pituitary–adrenocortical or sympathoadrenal axis in AT2 receptor downregulation was examined. Cultured cells treated with the synthetic glucocorticoid dexamethasone displayed a transcriptionally mediated decrease in AT2 receptor mRNA levels. However, glucocorticoids are not required for the immediate stress-triggered decrease in AT2 receptor gene expression, as demonstrated in corticotropin-releasing hormone knockout (Crh KO) mice and hypophysectomized rats, although they can regulate basal gene expression. cAMP and pituitary adenylate cyclase-activating polypeptide also reduced AT2 receptor gene expression and may mediate this response. Overall, the effects of stress on adrenomedullary AT1A and AT2 receptor expression may contribute to allostatic changes, such as regulation of catecholamine biosynthesis.

Bombesin-like peptide receptor gene expression, regulation, and function in fetal murine lung

2004 ◽  
Vol 286 (1) ◽  
pp. L165-L173 ◽  
Author(s):  
Lin Shan ◽  
Rodica L. Emanuel ◽  
Denise Dewald ◽  
John S. Torday ◽  
Nithiananthan Asokanathan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Development ◽  
Gene Expression Regulation ◽  
Receptor Gene ◽  
Fetal Lung ◽  
Mouse Lung ◽  
Receptor Subtype ◽  
Fetal Lung Development ◽  
And Function ◽  
Receptor Gene Expression

Bombesin-peptide (BLP) immunoreactivity occurs at high levels in fetal lung. Previous studies showed that bombesin promotes fetal lung development. To test the hypothesis that such effects are mediated by known mammalian bombesin receptors [gastrin-releasing peptide (GRP)/bombesin-preferring receptor (GRPR), neuromedin B (NMB) receptor (NMBR), and the orphan bombesin receptor subtype-3 (BRS-3)], we analyzed the ontogeny of GRPR, NMBR, and BRS-3 gene expression in mouse lung. We examined the regulation of these three genes by dexamethasone and bombesin, which modulate lung development. Using incorporation of [3H]thymidine and [3H]choline, we then assessed whether GRP, NMB, and Leu8-phyllolitorin modulate lung growth and maturation in fetal lung explants. GRPR gene expression was detected predominantly in utero, whereas NMBR and BRS-3 genes were expressed from embryonic days 13–16 and on multiple postnatal days. All three mRNAs are present in airway epithelium and mesenchymal cells but occur in different relative patterns. These genes were regulated differently. Dexamethasone and bombesin increased GRPR mRNA, bombesin downregulated NMBR, and neither agent affected BRS-3. GRP increased incorporation of [3H]thymidine and [3H]choline in explants, whereas NMB induced cell proliferation and Leu8-phyllolitorin yielded variable results. Cumulative data suggest the involvement of multiple BLP receptors, including novel molecules, and argue against simple functional redundancy within this gene family during lung development.

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