scholarly journals Norepinephrine as a possible transmitter involved in synaptic transmission in frog taste organs and Ca dependence of its release.

1985 ◽  
Vol 85 (3) ◽  
pp. 431-442 ◽  
Author(s):  
S Nagahama ◽  
K Kurihara

In order to explore the role of catecholamine and Ca2+ in the synaptic transmission from taste cells to sensory nerve terminals, the effects of various agents added to an artificial solution perfusing the lingual artery on the frog taste nerve responses were examined. The injection of reserpine or guanetidine, which are catecholamine-depleting agents, led to a great reduction of the frog taste nerve responses. The addition of catecholamines to the perfusing solution did not practically enhance the spontaneous impulse discharges, but did recover the response to all the taste stimuli examined. Norepinephrine was most effective and is the most likely candidate for the transmitter. The enhancement of the responses by norepinephrine was suppressed by desipramine, cocaine, or imipramine, which suggests that the enhancement was brought about by incorporation of norepinephrine into taste cells. In a previous paper (Nagahama, S., Y. Kobatake, and K. Kurihara, 1982. J. Gen. Physiol. 80:785), we showed that the responses to the stimuli of one group depended on Ca2+, cGMP, and cAMP added to the perfusing solution and those to the stimuli of another group did not depend on these agents. After the injection or addition of reserpine to the lingual artery, which probably modified injection or addition of reserpine to the lingual artery, which probably modified the permeability of the artery, the responses to the stimuli of the latter group also came to exhibit dependences on these agents, which indicates that the responses to all the taste stimuli have dependences on Ca2+, cGMP, and cAMP.

2015 ◽  
Vol 8 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Shuang-Quan Yu ◽  
Louis S. Premkumar

Transient Receptor Potential Vanilloid 1 (TRPV1) expressed in peripheral terminals is responsible for transducing thermal and chemical nociception. Role of TRPV1 expressed in the central terminals is not clear, however, its activation modulates synaptic transmission and contributes to central sensitization. In this study, we have determined the role of TRPV1 expressed in the peripheral and central terminals using resiniferatoxin (RTX), a potent TRPV1 agonist. A single intraplantar injection of RTX, within two days induced loss of capsaicin-induced nocifensive behavior and enhanced response latency to hot plate, which recovered over a period of two months. RTX treatment resulted in the ablation of peripheral TRPV1 expressing fibers in paw skin, which regenerated over the same time period. On the other hand, a single dose of intrathecal administration of RTX, within two days caused thermal hypoalgesia. RTX treatment ablated TRPV1 expressing central sensory nerve terminals. Intriguingly, in contrast to peripheral nerve terminal regeneration that occurred within two months, the central TRPV1 expressing nerve terminals did not regenerate even after five months. The present study demonstrates that TRPV1 in the peripheral and central terminals play a role in nociception and the peripheral terminals have the ability to regenerate, whereas the central terminals do not regenerate even after five months.


2021 ◽  
Vol 22 (7) ◽  
pp. 3360
Author(s):  
Mee-Ra Rhyu ◽  
Yiseul Kim ◽  
Vijay Lyall

In addition to the sense of taste and olfaction, chemesthesis, the sensation of irritation, pungency, cooling, warmth, or burning elicited by spices and herbs, plays a central role in food consumption. Many plant-derived molecules demonstrate their chemesthetic properties via the opening of transient receptor potential ankyrin 1 (TRPA1) and transient receptor potential vanilloid 1 (TRPV1) channels. TRPA1 and TRPV1 are structurally related thermosensitive cation channels and are often co-expressed in sensory nerve endings. TRPA1 and TRPV1 can also indirectly influence some, but not all, primary taste qualities via the release of substance P and calcitonin gene-related peptide (CGRP) from trigeminal neurons and their subsequent effects on CGRP receptor expressed in Type III taste receptor cells. Here, we will review the effect of some chemesthetic agonists of TRPA1 and TRPV1 and their influence on bitter, sour, and salt taste qualities.


1989 ◽  
Vol 257 (4) ◽  
pp. R765-R770 ◽  
Author(s):  
K. T. Nakamura ◽  
J. M. Klinkefus ◽  
F. G. Smith ◽  
T. Sato ◽  
J. E. Robillard

The role of renal nerves and norepinephrine release on renin secretion during fetal and postnatal maturation has not been studied. Experiments were performed to determine the effect of veratridine, a substance known to promote norepinephrine release from nerve terminals, on active and inactive renin secretion from renal cortical slices of fetal (134-138 days gestation; term is 145 days), newborn (4-9 days of age), and adult nonpregnant sheep. Veratridine (10-300 microM) significantly increased active renin secretion and produced a small but nonsignificant rise in inactive renin secretion in all three groups of animals (P less than 0.05). The percent rise in active renin secretion during veratridine stimulation was similar among all groups. Veratridine-stimulated (300 microM) active renin secretion was antagonized by tetrodotoxin (0.5 and 5.0 microM) and DL-propranolol (1 microM) in fetal renal cortical slices. However, neither tetrodotoxin nor propranolol completely inhibited the stimulatory effect of veratridine on active renin secretion. These results suggest that 1) norepinephrine released from nerve terminals may regulate active renin secretion early during development; 2) the effect of veratridine on active renin secretion was similar in fetal, newborn, and adult sheep; 3) veratridine had no significant effect on inactive renin secretion; and 4) active renin secretion due to depolarization of nerve terminals in fetal sheep is dependent on activation of beta-adrenoceptors as it is in adults.


Synapse ◽  
2017 ◽  
Vol 71 (5) ◽  
pp. e21964 ◽  
Author(s):  
Filippo Weisz ◽  
Sonia Piccinin ◽  
Dalila Mango ◽  
Richard Teke Ngomba ◽  
Nicola B. Mercuri ◽  
...  

Synapse ◽  
2005 ◽  
Vol 58 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Maksim V. Storozhuk ◽  
Svetlana Y. Ivanova ◽  
Pavel M. Balaban ◽  
Platon G. Kostyuk

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Xinyan Gao ◽  
Yongfa Qiao ◽  
Baohui Jia ◽  
Xianghong Jing ◽  
Bin Cheng ◽  
...  

Previous studies have demonstrated the efficacy of electroacupuncture at ST36 for patients with gastrointestinal motility disorders. While several lines of evidence suggest that the effect may involve vagal reflex, the precise molecular mechanism underlying this process still remains unclear. Here we report that the intragastric pressure increase induced by low frequency electric stimulation at ST36 was blocked by AP-5, an antagonist of N-methyl-D-aspartate receptors (NMDARs). Indeed, stimulating ST36 enhanced NMDAR-mediated, but not 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl)propanoic-acid-(AMPA-) receptor-(AMPAR-) mediated synaptic transmission in gastric-projecting neurons of the dorsal motor nucleus of the vagus (DMV). We also identified that suppression of presynapticμ-opioid receptors may contribute to upregulation of NMDAR-mediated synaptic transmission induced by electroacupuncture at ST36. Furthermore, we determined that the glutamate-receptor-2a-(NR2A-) containing NMDARs are essential for NMDAR-mediated enhancement of gastric motility caused by stimulating ST36. Taken together, our results reveal an important role of NMDA receptors in mediating enhancement of gastric motility induced by stimulating ST36.


1996 ◽  
Vol 93 (1) ◽  
pp. 331-335 ◽  
Author(s):  
C. David ◽  
P. S. McPherson ◽  
O. Mundigl ◽  
P. de Camilli

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