scholarly journals TSH Elicits Cell-Autonomous, Biphasic Responses: A Mechanism Inhibiting Hyperstimulation

Endocrinology ◽  
2020 ◽  
Vol 161 (8) ◽  
Author(s):  
Alisa Boutin ◽  
Susanne Neumann ◽  
Marvin C Gershengorn
Keyword(s):  
Author(s):  
R. Chen

ABSTRACT:Cutaneous reflexes in the upper limb were elicited by stimulating digital nerves and recorded by averaging rectified EMG from proximal and distal upper limb muscles during voluntary contraction. Distal muscles often showed a triphasic response: an inhibition with onset about 50 ms (Il) followed by a facilitation with onset about 60 ms (E2) followed by another inhibition with onset about 80 ms (12). Proximal muscles generally showed biphasic responses beginning with facilitation or inhibition with onset at about 40 ms. Normal ranges for the amplitude of these components were established from recordings on 22 arms of 11 healthy subjects. An attempt was made to determine the alterent fibers responsible for the various components by varying the stimulus intensity, by causing ischemic block of larger fibers and by estimating the afferent conduction velocities. The central pathways mediating these reflexes were examined by estimating central delays and by studying patients with focal lesions


2008 ◽  
Vol 294 (1) ◽  
pp. F120-F129 ◽  
Author(s):  
Frédéric Michel ◽  
Serge Simonet ◽  
Christine Vayssettes-Courchay ◽  
Florence Bertin ◽  
Patricia Sansilvestri-Morel ◽  
...  

Early manifestations of kidney disease occur in atherosclerosis and activation of TP (thromboxane A2) receptors is implicated in atherosclerotic, diabetes, and renal diseases. The purpose of the present study was to analyze, in isolated, perfused mouse kidneys, the participation of TP receptors in renal vasoconstrictions and vasodilatations. In kidneys, taken from wild-type C57BL6, apolipoprotein E-deficient (ApoE-KO) and diabetic ApoE-KO mice, changes in perfusion pressure were recorded. Constrictions to TP receptor ligands U 46619, arachidonic acid, PGH2, and 8-iso-PGF2α, but not those to angiotensin II, endothelin, or norepinephrine, were inhibited by the selective TP receptor antagonist Triplion (S 18886; 10 nM). Acetylcholine and prostacyclin evoked biphasic responses during methoxamine constrictions; the constrictor part was blocked by Triplion. In ApoE-KO mouse kidneys, compared with C57BL6, a specific decrease in norepinephrine response and no modification in dilator responses were observed. In diabetic ApoE-KO mouse kidneys, constrictions to U 46619 and those to 8-iso-PGF2α were significantly and selectively augmented, without modification in the expression of the TP receptor, and again without any significant change in vasodilator activity. Thus TP receptors are functional, and their activation is not involved in norepinephrine, endothelin, and angiotensin II vasoconstrictions but is implicated in the unusual vasoconstrictions to acetylcholine and prostacyclin. Increased responsiveness of TP receptors occurs in diabetic ApoE-KO mouse kidneys. Thus early changes in TP receptor-mediated vasoconstrictor activity may participate in the development of kidney disease in atherosclerosis and diabetes.


2009 ◽  
Vol 106 (3) ◽  
pp. 893-903 ◽  
Author(s):  
Z. Ghanim ◽  
J. C. Lamy ◽  
A. Lackmy ◽  
V. Achache ◽  
N. Roche ◽  
...  

The vestibular responses evoked by transmastoid galvanic stimulation (GS) in the rectified soleus electromyogram (EMG) in freely standing human subjects disappear when seated. However, a GS-induced facilitation of the soleus monosynaptic (H and tendon jerk) reflex has been described in few experiments in subjects lying prone or seated. This study addresses the issue of whether this reflex facilitation while seated is of vestibulospinal origin. GS-induced responses in the soleus (modulation of the rectified ongoing EMG and of the monosynaptic reflexes) were compared in the same normal subjects while freely standing and sitting with back and head support. The polarity-dependent biphasic responses in the free-standing position were replaced by a non-polarity-dependent twofold facilitation while seated. The effects of GS were hardly detectable in the rectified ongoing voluntary EMG activity, weak for the H reflex, but large and constant for the tendon jerk. They were subject to habituation. Anesthesia of the skin beneath the GS electrodes markedly reduced the reflex facilitation, while a similar, although weaker, facilitation of the tendon jerk was observed when GS was replaced with purely cutaneous stimulation, a tap to the tendon of the sternomastoid muscle, or an auditory click. The stimulation polarity independence of the GS-induced reflex facilitation argues strongly against a vestibular response. However, the vestibular afferent volley, insufficient to produce a vestibular reflex response while seated, could summate with the GS-induced tactile or proprioceptive volley to produce a startle-like response responsible for the reflex facilitation.


1999 ◽  
Vol 31 (Supplement) ◽  
pp. S330
Author(s):  
M. J. Danduran ◽  
S. R. Boas ◽  
A. L. McBride
Keyword(s):  

1997 ◽  
Vol 14 (3) ◽  
pp. 533-544 ◽  
Author(s):  
Donald C. Hood ◽  
William Seiple ◽  
Karen Holopigian ◽  
Vivienne Greenstein

AbstractThe multi-input technique of Sutter and Tran (1992) yields multiple focal ERGs. The purpose here was to compare the components of this multifocal ERG to the components of the standard, full-field ERG. To record multifocal ERGs, an array of 103 hexagons was displayed on a monitor. Full-field (Ganzfeld) ERGs were elicited by flashes presented upon steady background fields. The latencies of two prominent subcomponents of the full-field ERG were altered by varying the intensity of the incremental flash or the intensity of the background field. By showing that similar manipulations of the multi-input parameters produce similar changes in latency, we were able to relate the components of the multifocal ERG to the components of the full-field ERG. The biphasic responses of the multifocal ERG appear to be generated by the same cells generating the a-wave and positive peaks of the full-field cone ERG.


1998 ◽  
Vol 80 (3) ◽  
pp. 1033-1041 ◽  
Author(s):  
L. L. Hwang ◽  
N. J. Dun

Hwang, L. L. and N. J. Dun. 5-Hydroxytryptamine responses in immature rat rostral ventrolateral medulla neurons in vitro. J. Neurophysiol. 80: 1033–1041, 1998. Whole cell patch recordings were made from rostral ventrolateral medulla (RVLM) neurons of brainstem slices from 8- to 12-day-old rats. By superfusion or pressure ejection to RVLM neurons, 5-hydroxytryptamine (5-HT) elicited three types of membrane potential changes: a slow hyperpolarization (5-HTH), a slow depolarization (5-HTD) and a biphasic response, which persisted in a tetrodotoxin (TTX, 0.3 μM)-containing solution. 5-HTH were accompanied by a decrease of input resistance in the majority of responsive neurons. Hyperpolarization reduced and depolarization increased the 5-HTH; the mean reversal potential was −92.3 mV in 3.1 mM and shifted to −69.3 mV in 7 mM [K+]o. Barium (Ba2+, 0.1 mM) but not tetraethylammonium (TEA, 10 mM) suppressed 5-HTH. The 5-HT1A receptor agonist (±)-8-hydroxy-dipropylamino-tetralin (8-OH-DPAT; 5–50 μM) hyperpolarized RVLM neurons. The 5-HT1A antagonist pindobind-5-HT1A (PBD; 1–3 μM) and the 5-HT2/5-HT1 receptor antagonist spiperone (1–10 μM) suppressed 5-HTH and the hyperpolarizing phase of biphasic responses; the 5-HT2 receptor antagonist ketanserin (3 μM) was without significant effect. 5-HTD were associated with an increase or no apparent change of input resistance in RVLM neurons. Hyperpolarization of the membrane decreased or caused no apparent change in 5-HTD. 5-HTD were reduced in an elevated [K+]o (7.0 mM) solution and >60% in a low Na+ (26 mM) solution and were not significantly changed in a low Cl− (6.7 mM) or Ca2+-free/high Mg2+ (10.9 mM) solution. The 5-HT2 receptor agonist α-methyl-5-HT (50 μM) depolarized RVLM neurons, and the 5-HT2 antagonist ketanserin (1–10 μM) attenuated the 5-HTD and the depolarizing phase of biphasic responses, whereas the 5-HT1A receptor antagonist PBD (2 μM) was without effect. Inclusion of the hydrolysis resistant guanine nucleotide GDP-β-S in patch solution significantly reduced the 5-HTH as well as the 5-HTD. The present study shows that, in the immature rat RVLM neurons, 5-HT causes a slow hyperpolarization and depolarization probably by interacting with 5-HT1A and 5-HT2 receptors, which are G-proteins coupled. 5-HTH may involve an increase of an inwardly rectifying K+ conductance, and 5-HTD appear to be caused by a decrease of K+ conductance and/or increase of nonselective cation conductance.


1992 ◽  
Vol 262 (1) ◽  
pp. H31-H37 ◽  
Author(s):  
A. M. Low ◽  
C. Y. Kwan ◽  
E. E. Daniel

Novel transient biphasic responses of the dog mesenteric artery to phenylephrine hydrochloride (PE, 10 microM) in Ca(2+)-free medium containing 50 microM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) have been analyzed. The initial component was significantly inhibited by ryanodine (30-100 microM), an agonist enhancing Ca2+ release from the sarcoplasmic reticulum, whereas the second was significantly inhibited by nifedipine (1 microM), and L-type Ca2+ channel antagonist, or EGTA, to chelate Ca2+, and was potentiated by BAY K 8644 (1 microM), an L-type Ca2+ channel agonist. After repletion of Ca2+ stores in normal Krebs solution or in high KCl (60 mM) Krebs, the first component was inhibited by cyclopiazonic acid (CPA, 30 microM), a putative, reversible, and selective microsomal Ca2+ pump adenosinetriphosphatase inhibitor. BAY K 8644 potentiated the second component in the presence of CPA. The inhibition of the first component by CPA suggests that the refilling ultimately requires the CPA-sensitive Ca2+ pump for Ca2+ resequestration. However, the second component may refill by a CPA-independent route opened by BAY K 8644. These results, taken as a whole, indicate that the biphasic PE response in Ca(2+)-free medium may reflect compartmentalization of Ca2+ storage related to the different routes of refilling.


1990 ◽  
Vol 69 (5) ◽  
pp. 1594-1598 ◽  
Author(s):  
T. Aikawa ◽  
K. Sekizawa ◽  
S. Itabashi ◽  
H. Sasaki ◽  
T. Takishima

Effects of nonadrenergic and noncholinergic (NANC) inhibitory nerves on cholinergic neurotransmission were examined in isolated bronchial segments from cats in the presence of propranolol (10(-6) M) and indomethacin (10(-6) M) by use of electrical field stimulation (EFS) techniques. EFS caused contraction alone in tissues at the baseline tension and biphasic responses (contraction and relaxation) in tissues precontracted with 5-hydroxytryptamine. Contraction was abolished by atropine (10(-6) M), and relaxation was abolished by tetrodotoxin (10(-6) M). At the baseline tension, EFS at frequencies greater than 10 Hz inhibited the subsequent (4 min later) contraction induced by EFS at 1-5 Hz. EFS-induced inhibition was stimulus frequency dependent and reached maximum at 20 Hz. However, EFS at 20 Hz did not inhibit the subsequent contractile response to acetylcholine (10(-7) to 10(-3) M). Exogenously applied vasoactive intestinal peptide mimicked EFS-induced inhibitory effects, but substance P and calcitonin gene-related peptide did not. The inhibitory effect of EFS at 20 Hz was not altered by pyrilamine, cimetidine, naloxone, methysergide, phentolamine, BW755C, AF-DX 116, or removal of epithelium. These results imply that the NANC transmitter acts via presynaptic cholinergic receptors.


2012 ◽  
Vol 112 (11) ◽  
pp. 1906-1914 ◽  
Author(s):  
Robyn Laube ◽  
Sendhil Govender ◽  
James G. Colebatch

An impulsive acceleration stimulus, previously shown to activate vestibular afferents, was applied to the mastoid. Evoked EMG responses from the soleus muscles in healthy subjects ( n = 10) and patients with bilateral vestibular dysfunction ( n = 3) were recorded and compared with the effects of galvanic stimulation (GVS). Subjects were stimulated while having their eyes closed, head rotated, and while tonically activating their soleus muscles. Rectified EMG responses were recorded from the leg contralateral to the direction of head rotation. Responses were characterized by triphasic potentials that consisted of short-latency (SL), medium-latency (ML), and long-latency (LL) components beginning at (mean ± SD) 54.2 ± 4.8, 88.4 ± 4.7, and 121 ± 7.1 ms, respectively. Mean amplitudes for the optimum stimulus rise times were 9.05 ± 3.44% for the SL interval, 16.70 ± 4.41% for the ML interval, and 9.75 ± 4.89% for the LL interval compared with prestimulus values. Stimulus rise times of 14 and 20 ms evoked the largest ML amplitudes. GVS evoked biphasic responses (SL and ML) with similar latencies. Like GVS, the polarity of the initial interval was determined by the polarity of the stimulus and the evoked EMG response was attenuated when subjects were seated. There was no significant EMG response evoked when subjects were stimulated using 500-Hz vibration or in patients with bilateral vestibular dysfunction. Our study demonstrates that a brief lateral acceleration, likely to activate the utricle, can evoke spinal responses with properties similar to those previously shown for vestibular activation by GVS. The triphasic nature of the responses may allow the nervous system to respond differently to short compared with long-duration linear accelerations, consistent with their differing significance.


2016 ◽  
Vol 115 (3) ◽  
pp. 1289-1297 ◽  
Author(s):  
Christopher J. Dakin ◽  
Martin E. Héroux ◽  
Billy L. Luu ◽  
John Timothy Inglis ◽  
Jean-Sébastien Blouin

The soleus (Sol) and medial gastrocnemius (mGas) muscles have different patterns of activity during standing balance and may have distinct functional roles. Using surface electromyography we previously observed larger responses to galvanic vestibular stimulation (GVS) in the mGas compared with the Sol muscle. However, it is unclear whether this difference is an artifact that reflects limitations associated with surface electromyography recordings or whether a compensatory balance response to a vestibular error signal activates the mGas to a greater extent than the Sol. In the present study, we compared the effect of GVS on the discharge behavior of 9 Sol and 21 mGas motor units from freely standing subjects. In both Sol and mGas motor units, vestibular stimulation induced biphasic responses in measures of discharge timing [11 ± 5.0 (mGas) and 5.6 ± 3.8 (Sol) counts relative to the sham (mean ± SD)], and frequency [0.86 ± 0.6 Hz (mGas), 0.34 ± 0.2 Hz (Sol) change relative to the sham]. Peak-to-trough response amplitudes were significantly larger in the mGas (62% in the probability-based measure and 160% in the frequency-based measure) compared with the Sol (multiple P < 0.05). Our results provide direct evidence that vestibular signals have a larger influence on the discharge activity of motor units in the mGas compared with the Sol. More tentatively, these results indicate the mGas plays a greater role in vestibular-driven balance corrections during standing balance.


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