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Journal articles on the topic 'Guinea pig neurotransmission'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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1

Yang, Zhi-Jie, and David F. Biggs. "Muscarinic receptors and parasympathetic neurotransmission in guinea-pig trachea." European Journal of Pharmacology 193, no. 3 (February 1991): 301–8. http://dx.doi.org/10.1016/0014-2999(91)90143-e.

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2

Park, K. H., J. P. Long, and J. G. Cannon. "Effects of serotonin1-like receptor agonists on autonomic neurotransmission." Canadian Journal of Physiology and Pharmacology 69, no. 12 (December 1, 1991): 1855–60. http://dx.doi.org/10.1139/y91-274.

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Serotonin1A receptor agonists, 8-hydroxy-2-(di-n-propylamino)tetralin and 10-methyl-11-hydroxyaporphine, inhibited electrical stimulation-induced contraction of the guinea-pig ileum. These agonists also inhibited the pressor and tachycardiac responses to low frequency (0.25 Hz) but not to high frequency (2.0 Hz) electrical stimulation of the sympathetic nervous system in pithed rats. Serotonin1B receptor agonist RU 24969 inhibited pressor and tachycardiac responses to both low and high frequencies of stimulation in pithed rats. In the cat nictitating membrane, serotonin1A receptor agonists did not alter contractions elicited by electrical stimulation (0.1–3.0 Hz). Serotonin not only contracted the cat nicitating membrane but also facilitated contractile responses to low frequency (0.1 – 1.0 Hz) stimulation. The contractile effect of serotonin in the cat nictitating membrane was blunted by bretylium, methysergide, and ketanserin, but not by metoclopramide. The facilitatory effect of serotonin was antagonized by methysergide, but not by ketanserin, pindolol, propranolol, or metoclopramide. These results suggest that serotonin1A receptors modulate autonomic neurotransmission in the guinea-pig ileum and pithed rats, but not in the cat nictitating membrane. Serotonin contracts the cat nictitating membrane via serotonin2 subtypes, while facilitating stimulated contractile responses through the serotonin1-like receptors.Key words: guinea-pig ileum, pithed rats, nictitating membrane, serotonin receptors.

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3

Zhang, Lili, John C. Hancock, and Donald B. Hoover. "Tachykinin Agonists Modulate Cholinergic Neurotransmission at Guinea-Pig Intracardiac Ganglia." Journal of Pharmacological Sciences 99, no. 3 (2005): 228–38. http://dx.doi.org/10.1254/jphs.fp0050437.

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4

Ichinose, M., C. D. Stretton, J. C. Schwartz, and P. J. Barnes. "Histamine H3-receptors inhibit cholinergic neurotransmission in guinea-pig airways." British Journal of Pharmacology 97, no. 1 (May 1989): 13–15. http://dx.doi.org/10.1111/j.1476-5381.1989.tb11917.x.

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5

Belvisi, M. G., C. D. Stretton, and P. J. Barnes. "Modulation of cholinergic neurotransmission in guinea-pig airways by opioids." British Journal of Pharmacology 100, no. 1 (May 1990): 131–37. http://dx.doi.org/10.1111/j.1476-5381.1990.tb12064.x.

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6

Kortezova, N. I., L. I. Shikova, E. A. Milusheva, D. E. Itzev, V. A. Bagaev, and Z. N. Mizhorkova. "Muscarinic modulation of nitrergic neurotransmission in guinea-pig gastric fundus." Neurogastroenterology and Motility 16, no. 2 (April 2004): 155–65. http://dx.doi.org/10.1111/j.1365-2982.2004.00514.x.

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7

Ishikawa, Shiro, and Nicholas Sperelakis. "Cyclic Nucleotide Regulation of Neurotransmission in Guinea Pig Mesenteric Artery." Journal of Cardiovascular Pharmacology 13, no. 6 (June 1989): 836–45. http://dx.doi.org/10.1097/00005344-198906000-00005.

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8

Xiao-Xing, Luo, Tan Yue-Hua, and Sheng Bao-Hen. "Histamine H3-receptors inhibit sympathetic neurotransmission in guinea pig myocardium." European Journal of Pharmacology 204, no. 3 (November 1991): 311–14. http://dx.doi.org/10.1016/0014-2999(91)90857-m.

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9

Liu, Sumei, Hong-Zhen Hu, Na Gao, Chuanyun Gao, Guodu Wang, Xiyu Wang, Owen C. Peck, et al. "Neuroimmune interactions in guinea pig stomach and small intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 1 (January 1, 2003): G154—G164. http://dx.doi.org/10.1152/ajpgi.00241.2002.

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Enteric neuroimmune interactions in gastrointestinal hypersensitivity responses involve antigen detection by mast cells, mast cell degranulation, release of chemical mediators, and modulatory actions of the mediators on the enteric nervous system (ENS). Electrophysiological methods were used to investigate electrical and synaptic behavior of neurons in the stomach and small intestine during exposure to β-lactoglobulin in guinea pigs sensitized to cow's milk. Application of β-lactoglobulin to sensitized preparations depolarized the membrane potential and increased neuronal excitability in small intestinal neurons but not in gastric neurons. Effects on membrane potential and excitability in the small intestine were suppressed by the mast cell stabilizing drug ketotifen, the histamine H2 receptor antagonist cimetidine, the cyclooxygenase inhibitor piroxicam, and the 5-lipoxygenase inhibitor caffeic acid. Unlike small intestinal ganglion cells, gastric myenteric neurons did not respond to histamine applied exogenously. Antigenic exposure suppressed noradrenergic inhibitory neurotransmission in the small intestinal submucosal plexus. The histamine H3receptor antagonist thioperamide and piroxicam, but not caffeic acid, prevented the allergic suppression of noradrenergic inhibitory neurotransmission. Antigenic stimulation of neuronal excitability and suppression of synaptic transmission occurred only in milk-sensitized animals. Results suggest that signaling between mast cells and the ENS underlies intestinal, but not gastric, anaphylactic responses associated with food allergies. Histamine, prostaglandins, and leukotrienes are paracrine signals in the communication pathway from mast cells to the small intestinal ENS.

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10

Patra, Phani B., and David P. Westfall. "Potentiation of Purinergic Neurotransmission in Guinea Pig Urinary Bladder by Histamine." Journal of Urology 151, no. 3 (March 1994): 787–90. http://dx.doi.org/10.1016/s0022-5347(17)35088-7.

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11

Yamamoto, Ryuichi, Hideyuki Komidori, Chikako Nuki, and Koichiro Takasaki. "Prejunctional modulation of cholinergic neurotransmission in the isolated guinea pig ileum." Japanese Journal of Pharmacology 52 (1990): 211. http://dx.doi.org/10.1016/s0021-5198(19)55455-5.

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12

Stretton, C. D., and P. J. Barnes. "Modulation of cholinergic neurotransmission in guinea-pig trachea by neuropeptide Y." British Journal of Pharmacology 93, no. 3 (March 1988): 672–78. http://dx.doi.org/10.1111/j.1476-5381.1988.tb10325.x.

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13

Hall, Anthony K., Peter J. Barnes, Lorna A. Meldrum, and Jennifer Maclagan. "Facilitation by tachykinins of neurotransmission in guinea-pig pulmonary parasympathetic nerves." British Journal of Pharmacology 97, no. 1 (May 1989): 274–80. http://dx.doi.org/10.1111/j.1476-5381.1989.tb11951.x.

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14

Creed, Kate E., and Stephen M. Callahan. "Prostaglandins and neurotransmission at the guinea pig and rabbit urinary bladder." Pflügers Archiv - European Journal of Physiology 413, no. 3 (January 1989): 299–302. http://dx.doi.org/10.1007/bf00583544.

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15

Kimura, Yoshie, Yukihiro Yamada, and Yasuhiro Okada. "Excitatory effect of propentofylline on neurotransmission in guinea pig hippocampal slice." Neuroscience Letters 151, no. 1 (March 1993): 9–12. http://dx.doi.org/10.1016/0304-3940(93)90032-g.

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16

Canning, Brendan J., Sandra M. Reynolds, Linus U. Anukwu, Radhika Kajekar, and Allen C. Myers. "Endogenous neurokinins facilitate synaptic transmission in guinea pig airway parasympathetic ganglia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 2 (August 1, 2002): R320—R330. http://dx.doi.org/10.1152/ajpregu.00001.2002.

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Neurokinin-containing nerve fibers were localized to guinea pig airway parasympathetic ganglia in control tissues but not in tissues pretreated with capsaicin. The purpose of the present study was to determine whether neurokinins, released during axonal reflexes or after antidromic afferent nerve stimulation, modulate ganglionic synaptic neurotransmission. The neurokinin type 3 (NK3) receptor antagonists SB-223412 and SR-142801 inhibited vagally mediated cholinergic contractions of bronchi in vitro at stimulation voltages threshold for preganglionic nerve activation but had no effect on vagally mediated contractions evoked at optimal voltage or field stimulation-induced contractions. Intracellular recordings from the ganglia neurons revealed that capsaicin-sensitive nerve stimulation potentiated subsequent preganglionic nerve-evoked fast excitatory postsynaptic potentials. This effect was mimicked by the NK3 receptor agonist senktide analog and blocked by SB-223412. In situ, senktide analog markedly increased baseline tracheal cholinergic tone, an effect that was reversed by atropine and prevented by vagotomy or SB-223412. Comparable effects of intravenous senktide analog on pulmonary insufflation pressure were observed. These data highlight the important integrative role played by parasympathetic ganglia and indicate that activation of NK3 receptors in airway ganglia by endogenous neurokinins facilitates synaptic neurotransmission.

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17

YAMAMOTO, Ryuichi, Chikako NUKI, Hideyuki KOMIDORI, and Koichiro TAKASAKI. "Effect of /-Ephedrine on Cholinergic Neurotransmission in the Isolated Guinea Pig Ileum." Japanese Journal of Pharmacology 50, no. 4 (1989): 511–14. http://dx.doi.org/10.1016/s0021-5198(19)42438-4.

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18

Nishiyama, Mariko, Lihua Shan, Kayoko Moroi, Katsutoshi Goto, Tomoh Masaki, and Sadao Kimura. "ETBI receptor-mediated inhibition of autonomic neurotransmission in the guinea-pig ileum." Japanese Journal of Pharmacology 64 (1994): 134. http://dx.doi.org/10.1016/s0021-5198(19)50178-0.

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19

OHKAWA, Hiromichi. "Low-sodium resistant non-adrenergic inhibitory neurotransmission in the guinea-pig duodenum." Japanese Journal of Smooth Muscle Research 22, no. 1 (1986): 1–10. http://dx.doi.org/10.1540/jsmr1965.22.1.

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20

YAMAMOTO, Ryuichi, Chikako NUKI, Hideyuki KOMIDORI, and Koichiro TAKASAKI. "Effect of /-ephedrine on cholinergic neurotransmission in the isolated guinea pig ileum." Japanese Journal of Pharmacology 50, no. 4 (1989): 511–14. http://dx.doi.org/10.1254/jjp.50.511.

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21

Ren, Jun, Hong-Zhen Hu, Sumei Liu, Yun Xia, and Jackie D. Wood. "Glutamate modulates neurotransmission in the submucosal plexus of guinea-pig small intestine." NeuroReport 10, no. 14 (September 1999): 3045–48. http://dx.doi.org/10.1097/00001756-199909290-00031.

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22

Barthó, L., P. Holzer, S. Leander, and F. Lembeck. "Tachykinins may substitute for cholinergic nicotinic neurotransmission in the guinea-pig ileum." Regulatory Peptides 22, no. 1-2 (July 1988): 30. http://dx.doi.org/10.1016/0167-0115(88)90250-9.

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23

Fujiwara, H., N. Kurihara, K. Hirata, K. Ohta, S. Fujimoto, and T. Takeda. "Hypoxia modulates mediator responses and neurotransmission in guinea-pig trachea in vitro." Pulmonary Pharmacology 5, no. 1 (March 1992): 23–29. http://dx.doi.org/10.1016/0952-0600(92)90014-8.

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24

Wang, Jiang-ping, Guo-fu Ding, and Qin-zhang Wang. "Interstitial cells of Cajal mediate excitatory sympathetic neurotransmission in guinea pig prostate." Cell and Tissue Research 352, no. 3 (February 15, 2013): 479–86. http://dx.doi.org/10.1007/s00441-013-1572-3.

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25

Nishimura, Shunji, Yasuhiro Okada, and Mutsuo Amatsu. "Post-inhibitory excitation of adenosine on neurotransmission in guinea pig hippocampal slices." Neuroscience Letters 139, no. 1 (May 1992): 126–29. http://dx.doi.org/10.1016/0304-3940(92)90873-6.

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26

Vega, Teresa, Ricardo De Pascual, Oriol Bulbena, and Antonio G. García. "Effects of ω-toxins on noradrenergic neurotransmission in beating guinea pig atria." European Journal of Pharmacology 276, no. 3 (April 1995): 231–38. http://dx.doi.org/10.1016/0014-2999(95)00032-g.

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27

Hosokawa, Tomokazu, Hiroshi Suenaga, and Yutaka Kasuya. "Modulation of non-cholinergic neurotransmission by β1-adrenoceptors in guinea-pig hilus bronchi." Japanese Journal of Pharmacology 49 (1989): 138. http://dx.doi.org/10.1016/s0021-5198(19)56257-6.

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28

Barthó, L., G. Pethö, and Z. Rónai. "Theophylline-sensitive modulation of non-cholinergic excitatory neurotransmission in the guinea-pig ileum." British Journal of Pharmacology 86, no. 2 (October 1985): 315–17. http://dx.doi.org/10.1111/j.1476-5381.1985.tb08898.x.

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29

Semafuko, Wasswa E. B., Daniel L. Follett, and Walter R. Dixon. "Effect of Etorphine on Adrenergic Neurotransmission in the Rat and Guinea Pig Heart." Pharmacology 37, no. 3 (1988): 195–202. http://dx.doi.org/10.1159/000138463.

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30

Jiang, Fan, Chun Guang Li, and Michael J. Rand. "CHOLINERGIC PREJUNCTIONAL INHIBITION OF NITRERGIC NEUROTRANSMISSION IN THE GUINEA-PIG ISOLATED BASILAR ARTERY." Clinical and Experimental Pharmacology and Physiology 26, no. 4 (April 1999): 364–70. http://dx.doi.org/10.1046/j.1440-1681.1999.03041.x.

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31

Martin, C. A. E., D. Gully, E. Naline, and C. Advenier. "Neurotensin modulates cholinergic and noncholinergic neurotransmission in guinea-pig main bronchi in vitro." Neuropeptides 26, no. 3 (March 1994): 159–66. http://dx.doi.org/10.1016/0143-4179(94)90125-2.

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32

Belvisi, Maria G., David Stretton, and Peter J. Barnes. "Nitric oxide as an endogenous modulator of cholinergic neurotransmission in guinea-pig airways." European Journal of Pharmacology 198, no. 2-3 (June 1991): 219–21. http://dx.doi.org/10.1016/0014-2999(91)90626-2.

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33

Martin, Corinne A. E., Xavier Emonds-Alt, and Charles Advenier. "Inhibition of cholinergic neurotransmission in isolated guinea-pig main bronchi by SR 48968." European Journal of Pharmacology 243, no. 3 (October 1993): 309–12. http://dx.doi.org/10.1016/0014-2999(93)90192-k.

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34

López, Iván, Jang-Yen Wu, and Graciela Meza. "Immunocytochemical evidence for an afferent GABAergic neurotransmission in the guinea pig vestibular system." Brain Research 589, no. 2 (September 1992): 341–48. http://dx.doi.org/10.1016/0006-8993(92)91297-r.

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35

Creed, K. E., Y. Ito, and H. Katsuyama. "Neurotransmission in the urinary bladder of rabbits and guinea pigs." American Journal of Physiology-Cell Physiology 261, no. 2 (August 1, 1991): C271—C277. http://dx.doi.org/10.1152/ajpcell.1991.261.2.c271.

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Alpha, beta-Methyleneadenosine 5'-triphosphate (alpha, beta-mATP) produced transient contraction of strips of bladder taken from rabbits or guinea pigs, and mechanical responses to field stimulation at 5-100 Hz were reduced by this drug by 5-20%. Atropine reduced responses by approximately 50%, and both drugs together by 80-95%. In double sucrose gap experiments on the rabbit bladder, alpha, beta-mATP selectively reduced but did not abolish an initial excitatory junction potential (ejp), and atropine selectively abolished a late depolarization. In the guinea pig, a single ejp was partially inhibited by either alpha,beta-mATP or atropine. Residual responses were further reduced by tetrodotoxin in both species. The initial ejp and late depolarization in the rabbit were reduced in parallel by hemicholinium over 2 h, suggesting that release of acetylcholine (ACh) and the second transmitter by nerves may be coupled. ACh but not ATP produced an increase in intracellular concentration of inositol trisphosphate in dispersed smooth muscle cells from the rabbit bladder; ATP but not carbachol produced a small transient current across the cell membrane in this species. It is concluded that ACh mobilizes intracellular Ca2+ for contraction, whereas the effect of ATP is dependent on extracellular Ca2+.

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36

Undem, B. J., A. C. Myers, H. Barthlow, and D. Weinreich. "Vagal innervation of guinea pig bronchial smooth muscle." Journal of Applied Physiology 69, no. 4 (October 1, 1990): 1336–46. http://dx.doi.org/10.1152/jappl.1990.69.4.1336.

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We isolated the guinea pig right bronchus with the vagus nerves intact and evaluated the changes in isometric tension of the smooth muscle in response to nerve stimulation. Brief (10-s) trains of electrical field stimulation or vagus nerve stimulation caused a biphasic contraction: the "first phase" sensitive to atropine and the "second phase" sensitive to capsaicin. The two phases could be dissociated by adjusting the stimulus intensity; greater stimulus intensities (pulse durations or voltage) were required to evoke the capsaicin-sensitive phase. When stimulated at 30-min intervals, the magnitude of both phases of the contractions declined over a 2-h period of repeated stimulation; however, this was prevented by indomethacin. Stimulation of the left vagus nerve resulted in a monophasic contraction of the right bronchus, with little evidence of a capsaicin-sensitive phase. Blocking neurotransmission through the bronchial ganglion, as monitored by intracellular recording techniques, abolished the first-phase contraction but had no effect on the capsaicin-sensitive phase. Selective blockade of muscarinic M1 receptors had no effect on vagus nerve-mediated contractions. The results demonstrate that the left and right vagus nerves carry preganglionic fibers to the right bronchial ganglion. The right but not the left vagus nerve also carries capsaicin-sensitive afferent fibers that, when stimulated, result in a persistent contraction of the right bronchus. Finally, we provide functional and electrophysiological evidence supporting the hypothesis that capsaicin-sensitive afferent neurons communicate with postganglionic motoneurons within the bronchus.

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37

Herring, Neil, Junaid A. B. Zaman, and David J. Paterson. "Natriuretic peptides like NO facilitate cardiac vagal neurotransmission and bradycardia via a cGMP pathway." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 6 (December 1, 2001): H2318—H2327. http://dx.doi.org/10.1152/ajpheart.2001.281.6.h2318.

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We tested the hypothesis that natriuretic peptide receptors (NPRs) that are coupled to cGMP production act in a similar way to nitric oxide (NO) by enhancing acetylcholine release and vagal-induced bradycardia. The effects of enzyme inhibitors and channel blockers on the action of atrial natriuretic peptide (ANP), brain-derived natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) were evaluated in isolated guinea pig atrial-right vagal nerve preparations. RT-PCR confirmed the presence NPR B and A receptor mRNA in guinea pig sinoatrial node tissue. BNP and CNP significantly ( P < 0.05) enhanced the heart rate (HR) response to vagal nerve stimulation. CNP had no effect on the HR response to carbamylcholine and facilitated the release of [3H]acetylcholine during atrial field stimulation. The particulate guanylyl cyclase-coupled receptor antagonist HS-142–1, the phosphodiesterase 3 inhibitor milrinone, the protein kinase A inhibitor H89, and the N-type calcium channel blocker ω-conotoxin all blocked the effect of CNP on vagal-induced bradycardia. Like NO, BNP and CNP facilitate vagal neurotransmission and bradycardia. This may occur via a cGMP-PDE3-dependent pathway increasing cAMP-PKA-dependent phosphorylation of presynaptic N-type calcium channels.

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38

Kamikawa, Y., and Y. Shimo. "Adenosine selectively inhibits noncholinergic transmission in guinea pig bronchi." Journal of Applied Physiology 66, no. 5 (May 1, 1989): 2084–91. http://dx.doi.org/10.1152/jappl.1989.66.5.2084.

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The neuromodulatory action of adenosine and ATP was investigated in isolated guinea pig bronchial strip chain preparations contracted with electrical field stimulation. The tissues were placed in organ baths containing physiological salt solution and stimulated at 8-Hz frequency, 0.5-ms pulse duration, and 30 V (approximately 100 mA) for 5 s. Electrical field stimulation evoked a biphasic contraction of bronchial muscle, consisting of an initial contraction followed by a sustained contraction, which was mediated by intramural cholinergic and noncholinergic nerve stimulations, respectively. Adenosine, at concentrations greater than M, caused a concentration-dependent inhibition in the height of the noncholinergically mediated contraction, accompanied by a very weak inhibition on the cholinergically mediated response. ATP (10(-5) to 3 x 10(-3) M) also produced a similar inhibitory effect on the noncholinergically mediated contraction, but the inhibitory potency was less than that of adenosine. The inhibitory response to adenosine was enhanced by the pretreatment with dipyridamole (2 x 10(-6) M) but antagonized with aminophylline (10(-5) M). Contractions of bronchial muscle evoked by exogenous acetylcholine (2 x 10(-6) M) or substance P (2 x 10(-7) M) were significantly inhibited by the adenosine (3 x 10(-4) M) pretreatment. These data suggest that in isolated guinea pig bronchi adenosine selectively inhibits noncholinergic neurotransmission through prejunctional P1-purinoceptors.

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39

Liu, S. "Actions of galanin on neurotransmission in the submucous plexus of guinea pig small intestine." European Journal of Pharmacology 471, no. 1 (June 13, 2003): 49–58. http://dx.doi.org/10.1016/s0014-2999(03)01798-9.

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40

OHKAWA, Hiromichi. "Effects of neurotensin on the non-adrenergic inhibitory neurotransmission in the guinea-pig duodenum." Japanese Journal of Physiology 35, no. 6 (1985): 973–83. http://dx.doi.org/10.2170/jjphysiol.35.973.

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41

Morris, J. L., T. C. Cunnane, and G. D. S. Hirst. "Regional differences in sympathetic neurotransmission to cutaneous arteries in the guinea-pig isolated ear." Journal of the Autonomic Nervous System 73, no. 2-3 (November 1998): 115–24. http://dx.doi.org/10.1016/s0165-1838(98)00122-2.

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42

Tonini, M., J. J. Galligan, and R. A. North. "Effects of Cisapride on Cholinergic Neurotransmission and Propulsive Motility in the Guinea Pig Ileum." Gastroenterology 96, no. 5 (May 1989): 1257–64. http://dx.doi.org/10.1016/s0016-5085(89)80012-5.

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43

WIKLUND, N. P., and L. E. GUSTAFSSON. "On the nature of endogenous purines modulating cholinergic neurotransmission in the guinea-pig ileum." Acta Physiologica Scandinavica 131, no. 1 (September 1987): 11–18. http://dx.doi.org/10.1111/j.1748-1716.1987.tb08199.x.

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44

Lau, W. A. K., J. N. Pennefather, and F. J. Mitchelson. "Cholinergic facilitation of neurotransmission to the smooth muscle of the guinea-pig prostate gland." British Journal of Pharmacology 130, no. 5 (July 2000): 1013–20. http://dx.doi.org/10.1038/sj.bjp.0703409.

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45

Kocmalova, Michaela, Marian Kollarik, Brendan J. Canning, Fei Ru, R. Adam Herbstsomer, Sonya Meeker, Silvia Fonquerna, et al. "Control of Neurotransmission by NaV1.7 in Human, Guinea Pig, and Mouse Airway Parasympathetic Nerves." Journal of Pharmacology and Experimental Therapeutics 361, no. 1 (January 30, 2017): 172–80. http://dx.doi.org/10.1124/jpet.116.238469.

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46

Geber, Christian, Christian F. Mang, and Heinz Kilbinger. "Facilitation and inhibition by capsaicin of cholinergic neurotransmission in the guinea-pig small intestine." Naunyn-Schmiedeberg's Archives of Pharmacology 372, no. 4 (November 22, 2005): 277–83. http://dx.doi.org/10.1007/s00210-005-0021-6.

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47

Belvisi, Maria G., Miura Motohiko, David Stretton, and Peter J. Barnes. "Endogenous vasoactive intestinal peptide and nitric oxide modulate cholinergic neurotransmission in guinea-pig trachea." European Journal of Pharmacology 231, no. 1 (January 1993): 97–102. http://dx.doi.org/10.1016/0014-2999(93)90689-f.

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48

Rubino, A., L. Mantelli, S. Amerini, and F. Ledda. "Effect of adenosine on non-adrenergic non-cholinergic neurotransmission in isolated guinea-pig atria." Pharmacological Research 22 (September 1990): 436. http://dx.doi.org/10.1016/1043-6618(90)90471-o.

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49

Shih, Chung-Hung, Hsin-Te Hsu, Kuo-Hsien Wang, Chih-Hsieh Shih, and Wun-Chang Ko. "Calcium channel subtypes for cholinergic and nonadrenergic noncholinergic neurotransmission in isolated guinea pig trachea." Naunyn-Schmiedeberg's Archives of Pharmacology 382, no. 5-6 (September 5, 2010): 419–32. http://dx.doi.org/10.1007/s00210-010-0556-z.

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50

Skinner, Liam J., Véronique Enée, Maryline Beurg, Hak Hyun Jung, Allen F. Ryan, Aziz Hafidi, Jean-Marie Aran, and Didier Dulon. "Contribution of BK Ca2+-Activated K+ Channels to Auditory Neurotransmission in the Guinea Pig Cochlea." Journal of Neurophysiology 90, no. 1 (July 2003): 320–32. http://dx.doi.org/10.1152/jn.01155.2002.

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Abstract:

Large-conductance calcium-activated potassium (BK) channels are known to play a prominent role in the hair cell function of lower vertebrates where these channels determine electrical tuning and regulation of neurotransmitter release. Very little is known, by contrast, about the role of BK channels in the mammalian cochlea. In the current study, we perfused specific toxins in the guinea pig cochlea to characterize the role of BK channels in cochlear neurotransmission. Intracochlear perfusion of charybdotoxin (ChTX) or iberiotoxin (IbTX) reversibly reduced the compound action potential (CAP) of the auditory nerve within minutes. The cochlear microphonics (CM at f1 = 8 kHz and f2 = 9.68 kHz) and their distortion product (DPCM at 2f1–f2) were essentially not affected, suggesting that the BK specific toxins do not alter the active cochlear amplification at the outer hair cells (OHCs). We also tested the effects of these toxins on the whole cell voltage-dependent membrane current of isolated guinea pig inner hair cells (IHCs). ChTX and IbTX reversibly reduced a fast outward current (activating above –40 mV, peaking at 0 mV with a mean activation time constant τ ranging between 0.5 and 1 ms). A similar block of a fast outward current was also observed with the extracellular application of barium ions, which we believe permeate through Ca2+ channels and block BK channels. In situ hybridization of Slo antisense riboprobes and immunocytochemistry demonstrated a strong expression of BK channels in IHCs and spiral ganglion and to a lesser extent in OHCs. Overall, our results clearly revealed the importance of BK channels in mammalian cochlear neurotransmission and demonstrated that at the presynaptic level, fast BK channels are a significant component of the repolarizing current of IHCs.

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