scholarly journals Respiratory responses to thyrotropin-releasing hormone microinjected into the rabbit medulla oblongata

1999 ◽  
Vol 277 (5) ◽  
pp. R1331-R1338 ◽  
Author(s):  
Donatella Mutolo ◽  
Fulvia Bongianni ◽  
Marco Carfì ◽  
Tito Pantaleo
Keyword(s):  
Area Postrema ◽  
Thyrotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Dorsal Respiratory Group ◽  
Bötzinger Complex ◽  
Expiratory Neurons ◽  
Inspiratory Activity ◽  
First Time ◽  
Respiratory Responses

We investigated the respiratory role of thyrotropin-releasing hormone (TRH) input to medullary structures involved in the control of breathing in anesthetized, vagotomized, paralyzed, and artificially ventilated rabbits. Microinjections (10–20 nl) of 1 or 10 mM TRH were performed in different regions of the ventral respiratory group (VRG), namely the rostral expiratory portion or Bötzinger complex (Böt. c.), the inspiratory portion, the transition zone between these two neuronal pools, and the caudal expiratory component. TRH microinjections were also performed in the dorsal respiratory group (DRG) and the area postrema (AP). Injection sites were localized by using stereotaxic coordinates and extracellular recordings of neuronal activity; their locations were confirmed by subsequent histological control. TRH microinjections in the Böt. c. and the directly caudally located region where a mix of inspiratory and expiratory neurons were encountered elicited depressant respiratory responses. TRH microinjections were completely ineffective at sites within the inspiratory and the caudal expiratory components of the VRG. TRH microinjections in either the DRG or the AP induced excitatory effects on inspiratory activity. The results show for the first time that TRH may exert inhibitory influences on respiration at medullary levels by acting on rostral expiratory neurons and that not only the DRG, as previously suggested, but also the AP may mediate TRH-induced excitatory effects on respiration.

Substitution of extracellular Ca2+ by Sr2+ prolongs inspiratory burst in pre-Bötzinger complex inspiratory neurons

2015 ◽  
Vol 113 (4) ◽  
pp. 1175-1183 ◽  
Author(s):  
Consuelo Morgado-Valle ◽  
Juan Fernandez-Ruiz ◽  
Leonor Lopez-Meraz ◽  
Luis Beltran-Parrazal
Keyword(s):  
Neurotransmitter Release ◽  
Action Potentials ◽  
Hypoglossal Nerve ◽  
Glutamate Release ◽  
Established Method ◽  
Bötzinger Complex ◽  
Inspiratory Activity ◽  
First Time ◽  
Intense Debate

The pre-Bötzinger complex (preBötC) underlies inspiratory rhythm generation. As a result of network interactions, preBötC neurons burst synchronously to produce rhythmic premotor inspiratory activity. Each inspiratory burst consists of action potentials (APs) on top of a 10- to 20-mV synchronous depolarization lasting 0.3–0.8 s known as inspiratory drive potential. The mechanisms underlying the initiation and termination of the inspiratory burst are unclear, and the role of Ca2+ is a matter of intense debate. To investigate the role of extracellular Ca2+ in inspiratory burst initiation and termination, we substituted extracellular Ca2+ with Sr2+. We found for the first time an ionic manipulation that significantly interferes with burst termination. In a rhythmically active slice, we current-clamped preBötC neurons ( Vm ≅ −60 mV) while recording integrated hypoglossal nerve (∫XIIn) activity as motor output. Substitution of extracellular Ca2+ with either 1.5 or 2.5 mM Sr2+ significantly prolonged the duration of inspiratory bursts from 653.4 ± 30.7 ms in control conditions to 981.6 ± 78.5 ms in 1.5 mM Sr2+ and 2,048.2 ± 448.5 ms in 2.5 mM Sr2+, with a concomitant increase in decay time and area. Substitution of extracellular Ca2+ by Sr2+ is a well-established method to desynchronize neurotransmitter release. Our findings suggest that the increase in inspiratory burst duration is determined by a presynaptic mechanism involving desynchronization of glutamate release within the network.

scholarly journals The Physiological Role of Thyrotropin-Releasing Hormone in the Regulation of Thyroid-Stimulating Hormone and Prolactin Secretion in the Rat

1978 ◽  
Vol 61 (2) ◽  
pp. 441-448 ◽  
Author(s):  
Arthur R. C. Harris ◽  
Dana Christianson ◽  
M. Susan Smith ◽  
Shih-Lieh Fang ◽  
Lewis E. Braverman ◽  
...  
Keyword(s):  
Physiological Role ◽  
Thyroid Stimulating Hormone ◽  
Prolactin Secretion ◽  
Thyrotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Stimulating Hormone

Thyrotropin-Releasing Hormone Gene Expression in Cultured Anterior Pituitary Cells: Role of Gender

1995 ◽  
Vol 61 (1) ◽  
pp. 77-84 ◽  
Author(s):  
Thomas O. Bruhn ◽  
Jan M.M. Rondeel ◽  
Thomas G. Bolduc ◽  
Ivor M.D. Jackson
Keyword(s):  
Gene Expression ◽  
Anterior Pituitary ◽  
Thyrotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Releasing Hormone ◽  
Anterior Pituitary Cells

Preferential Role of Calcium in the Regulation of Prolactin Gene Transcription by Thyrotropin-Releasing Hormone in GH3Pituitary Cells*

Endocrinology ◽  
1988 ◽  
Vol 122 (1) ◽  
pp. 333-340 ◽  
Author(s):  
JEAN-NOËL LAVERRIERE ◽  
ANDRÉE TIXIER-VIDAL ◽  
NICOLE BUISSON ◽  
ANNIE MORIN ◽  
JOSEPH A. MARTIAL ◽  
...  
Keyword(s):  
Gene Transcription ◽  
Thyrotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Prolactin Gene

scholarly journals Dominant Role of Thyrotropin-releasing Hormone in the Hypothalamic-Pituitary-Thyroid Axis

2005 ◽  
Vol 281 (8) ◽  
pp. 5000-5007 ◽  
Author(s):  
Amisra A. Nikrodhanond ◽  
Tania M. Ortiga-Carvalho ◽  
Nobuyuki Shibusawa ◽  
Koshi Hashimoto ◽  
Xiao Hui Liao ◽  
...  
Keyword(s):  
Dominant Role ◽  
Thyrotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis

Role of guanine nucleotide-binding proteins, Giα3 and Gsα, in dopamine and thyrotropin-releasing hormone signal transduction: evidence for competition and commonality

1996 ◽  
Vol 148 (3) ◽  
pp. 447-455 ◽  
Author(s):  
R D Kineman ◽  
T W Gettys ◽  
L S Frawley
Keyword(s):  
Signal Transduction ◽  
G Proteins ◽  
Cell Cultures ◽  
Intracellular Signaling ◽  
Receptor Activation ◽  
Pituitary Cell ◽  
Thyrotropin Releasing Hormone ◽  
Female Rats ◽  
Releasing Hormone

Abstract It is clear that dopamine (DA) at high concentrations (>100 nmol/l) inhibits the release of prolactin (PRL). Paradoxically, this monoamine at low concentrations (<10 nmol/l) has also been shown to augment PRL secretion. One possible explanation for these divergent effects is that DA binds receptors capable of interacting with multiple G protein subtypes that recruit opposing intracellular signaling pathways within lactotropes. To identify G proteins which couple DA receptor activation to PRL secretion, we have selectively immunoneutralized the activity of Giα3 and Gsα in primary cultures of rat pituitaries and subsequently tested the ability of these cultures to respond to high and low dose DA. Specifically, permeabilized pituitary cell cultures from random-cycling female rats were treated with control immunoglobulins (IgGs; 50 μg/ml) purified from preimmune serum (PII) or IgGs directed against the C-terminal portion of Giα3 or Gsα. After immunoneutralization of these G proteins, cells were challenged with 10 or 1000 nmol Da/l and the relative amount of PRL released was assessed by reverse hemolytic plaque assay. Results were expressed as % of basal values and compared. Under control conditions (PII), 1000 nmol DA/l inhibited (61·4 ±7·6% of basal values; mean ± s.e.m.) while 10 nmol DA/l augmented (120·0 ± 7·0%) PRL release in five separate experiments. Treatment of cells with anti-Giα3 attenuated the inhibitory effect of high dose DA (87·3 ± 14·5%). However, elimination of Giα3 activity did not significantly alter the PRL stimulatory effect of 10 nmol DA/l (121·0 ± 5·2%). Interestingly, immunoneutralization of Gsα resulted in a reciprocal shift in the activity of the lower dose of DA from stimulatory to inhibitory (69·7 ± 7·3%) while combined treatment of anti-Giα3 and anti-Gsα abrogated the responsiveness of pituitary cell cultures to either DA treatment (1000 nmol/l, 70·7 ± 12·5% and 10 nmol/l, 87·5 ± 21·4%). These data reveal that ligand-activated DA receptors can interact with both Giα3 and Gsα. Elimination of the stimulatory component (Gsα) favors the DA receptor activation of the inhibitory pathway (Giα3) suggesting a competition between negative and positive intracellular signaling mechanisms in normal lactotropes. In addition to DA treatment, we also challenged permeabilized pituitary cells with 100 nmol thyrotropin-releasing hormone (TRH)/1 as a positive control for secretory integrity. As anticipated, TRH stimulated PRL release to 188·0±31·0% of basal values under control conditions. Unexpectedly, immunoneutralization of Gsα completely blocked the ability of TRH to induce PRL release (101·8 ± 12·0% This neutralizing effect was specific to Gsα in that blockade of Giα3 activity had no significant effect on TRH-stimulated PRL release (166·2 ± 13·1%). These data are the first to support a direct role of Gsα in TRH signal transduction within PRL-secreting cells. Journal of Endocrinology (1996) 148, 447–455

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