Selective mechanical stimulation of an identified proprioceptor in freely moving locusts: role of resistance reflexes in active posture

1987 ◽  
Vol 417 (1) ◽  
pp. 195-198 ◽  
Author(s):  
Sasha N. Zill
1987 ◽  
Vol 88 (1) ◽  
pp. 121-127
Author(s):  
R. D. BUTLER ◽  
C. R. McCROHAN

Experiments were carried out to determine the role of the plasma membrane in the control of tentacle contraction in Heliophrya erhardi. Intracellular recordings gave membrane potentials between −20 and −30 mV. In a Ca2+-containing medium mechanical stimulation induced tentacle contraction but no associated electrical events were recorded. Intracellular stimulation with 50 nA, 100 ms hyperpolarizing current induced contraction, but no significant changes in membrane potential, whereas up to 100 nA, 100 ms depolarizing current had no effect. In a Ca2+-free medium neither mechanical stimulation nor electrical stimulation induced contraction. Extracellular stimulation of 15 V, 100 ms induced a Ca2+-dependent, unilateral (anodal) contraction response with a threshold of 5x10−9M-Ca2+. At concentrations above this neither latency to contraction nor contraction time showed significant variation. In a standard concentration of 10−4M-Ca2+ the sensitivity to extracellular stimulation was increased and latency to contraction was reduced in the presence of a phorbol ester (TPA), which mimics the second messenger diacylglycerol in stimulating the activity of protein kinase C. It is suggested that control of tentacle contraction is unlikely to be mediated by stimulus-activated ion channels in the plasma membrane, and the possibility that the polyphosphoinositide signalling pathway is involved is discussed.


1988 ◽  
Vol 35 (2-3) ◽  
pp. 201-207 ◽  
Author(s):  
Dennis M Freeman ◽  
Thomas F Weiss

1976 ◽  
Vol 85 (1) ◽  
pp. 65-70 ◽  
Author(s):  
Richard T. Jackson

A brief review of the literature from otorhinolaryngology and the basic sciences shows the existence and role of nasal-cardiopulmonary reflexes in animals and man There is ample evidence that odors, fluids and mechanical stimulation of the nasal mucosa will induce changes in the lungs and cardiovascular system. The proposition that nasal obstruction also produces cardiopulmonary changes is briefly reviewed. The suggestion is made that one of the functions of the nose is to act as an expiratory brake. The removal of this brake could result in changes in laryngeal resistance that lead to poor ventilation.


1994 ◽  
Vol 72 (4) ◽  
pp. 1464-1475 ◽  
Author(s):  
P. M. Dougherty ◽  
J. Palecek ◽  
V. Paleckova ◽  
W. D. Willis

1. Activation of neurokinin receptors contributes to the excitation of many dorsal horn neurons by cutaneous sensory stimuli, particularly noxious stimuli. In the present study we investigate the role of neurokinin receptors in the activation of primate spinothalamic tract (STT) neurons by cutaneous mechanical stimuli and by intradermal injection of capsaicin. This was done by testing the responses of these neurons to a battery of cutaneous stimuli before and during infusion by microdialysis of antagonists selective for NK1 and NK2 receptors. 2. The NK1 receptor antagonists cis-3-(2-methoxybenzyl-amino-2-benzhydrylquinuclidine (CP96345) and D-Pro9-[Spiro-y-lactam]-Leu10,Trp11)-Physalaemin(1-11) (GR82334) did not significantly reduce the responses of STT cells to mechanical stimulation of the skin. Both NK1 antagonists did, however, produce a significant reduction in the responses of STT neurons to an intradermal injection of capsaicin. Finally, despite having no effects on responses to mechanical stimuli, both NK1 antagonists prevented the sensitization of the responses to cutaneous stimuli that is usually observed after intradermal injections of capsaicin. 3. The NK2 selective antagonists PhCO-Ala-Ala-D-Trp-Phe-D-Pro-Pro-Nle-NH2 (GR98400) and [Tyr5,D-Trp6,8,9,Lys10]-NKA (4–10) (MEN10376) had effects very similar to those of the NK1 antagonists, but with an important difference. Neither NK2 antagonist affected the responses of STT neurons to noxious or innocuous mechanical stimulation of the skin, but they did reduce the responses to intradermal capsaicin injections. These compounds failed to prevent capsaicin-induced sensitization. In fact, cells exposed to GR98400 or MEN10376 showed unusually sustained increases in the responses to mechanical stimuli after the first capsaicin injection, suggesting that these compounds actually induced sensitization. 4. These results support the contention that both neurokinin receptors participate in the processing of nociceptive information in the dorsal horn, especially responses to strong stimuli such as intradermal injection of capsaicin. NK1 receptors are also involved in the sensitization of STT neurons after peripheral injury. A clearer understanding of the role of NK2 receptors in sensitization requires further studies with improved antagonists.


2001 ◽  
Vol 120 (5) ◽  
pp. A83-A83
Author(s):  
M KIM ◽  
N JAVED ◽  
F CHRISTOFI ◽  
H COOKE

Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.


2003 ◽  
Vol 773 ◽  
Author(s):  
James D. Kubicek ◽  
Stephanie Brelsford ◽  
Philip R. LeDuc

AbstractMechanical stimulation of single cells has been shown to affect cellular behavior from the molecular scale to ultimate cell fate including apoptosis and proliferation. In this, the ability to control the spatiotemporal application of force on cells through their extracellular matrix connections is critical to understand the cellular response of mechanotransduction. Here, we develop and utilize a novel pressure-driven equibiaxial cell stretching device (PECS) combined with an elastomeric material to control specifically the mechanical stimulation on single cells. Cells were cultured on silicone membranes coated with molecular matrices and then a uniform pressure was introduced to the opposite surface of the membrane to stretch single cells equibiaxially. This allowed us to apply mechanical deformation to investigate the complex nature of cell shape and structure. These results will enhance our knowledge of cellular and molecular function as well as provide insights into fields including biomechanics, tissue engineering, and drug discovery.


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