scholarly journals Functional Studies on Blockade by Neosurugatoxin of Nicotinic Receptors in Nitroxidergic and Sensory Nerve Terminals and Intramural Ganglionic Cells

1998 ◽  
Vol 78 (2) ◽  
pp. 217-223 ◽  
Author(s):  
Ayajiki Kazuhide ◽  
Okamura Tomio ◽  
Fujioka Hideyuki ◽  
Nakayama Koichi ◽  
Tsuji Kuniro ◽  
...  
Keyword(s):  
Nicotinic Receptors ◽  
Sensory Nerve ◽  
Nerve Terminals ◽  
Functional Studies

Regulation of neuropeptide release

1980 ◽  
Vol 210 (1178) ◽  
pp. 91-111 ◽  
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Gaba Receptors ◽  
Opiate Receptors ◽  
Sensory Nerve ◽  
Substantia Gelatinosa ◽  
Nerve Terminals ◽  
Analgesic Effects ◽  
Spinal Cord Level

The demonstration of depolarization-induced release of substance P, Met- and Leu-enkephalin, somatostatin, neurotensin, vasoactive intestinal polypeptide and cholecystokinin-like material from various regions of rat brain in vitro supports the hypothesis that these and other neuropeptides may act as neurotransmitters. In each case the stimulusevoked release, but not the basal release, of peptide was dependent on the presence of calcium ions in the external medium. The stimulus-evoked release of substance P from nerve terminals in rat substantia nigra may be regulated by presynaptic γ -aminobutyric acid (GABA) receptors. The possible existence of presynaptic opiate receptors on substance P-containing sensory nerve terminals may offer an explanation for the analgesic effects of opiates at spinal cord level, and for the existence of enkephalin neurons in substantia gelatinosa. Capsaicin releases substance P from spinal cord nerve terminals and may impair their function, while having no effect on substance P neurons in supraspinal regions. The possibility of cosecretion of peptide and amine products from the same cells is discussed.

The sensory nerve terminals of the mesentery

1973 ◽  
Vol 85 (4) ◽  
pp. 514-532
Author(s):  
J. Vajda ◽  
Elisabeth Fehér ◽  
K. Csányi
Keyword(s):  
Sensory Nerve ◽  
Nerve Terminals

scholarly journals The Effects of Polarizing Current on Nerve Terminal Impulses Recorded from Polymodal and Cold Receptors in the Guinea-pig Cornea

2002 ◽  
Vol 120 (3) ◽  
pp. 395-405 ◽  
Author(s):  
Richard W. Carr ◽  
Svetlana Pianova ◽  
James A. Brock
Keyword(s):  
Guinea Pig ◽  
Nerve Terminal ◽  
Sensory Nerve ◽  
Outward Current ◽  
Nerve Terminals ◽  
Functional Difference ◽  
Inward Current ◽  
Cold Receptor ◽  
Cold Receptors

It was reported recently that action potentials actively invade the sensory nerve terminals of corneal polymodal receptors, whereas corneal cold receptor nerve terminals are passively invaded (Brock, J.A., S. Pianova, and C. Belmonte. 2001. J. Physiol. 533:493–501). The present study investigated whether this functional difference between these two types of receptor was due to an absence of voltage-activated Na+ conductances in cold receptor nerve terminals. To address this question, the study examined the effects of polarizing current on the configuration of nerve terminal impulses recorded extracellularly from single polymodal and cold receptors in guinea-pig cornea isolated in vitro. Polarizing currents were applied through the recording electrode. In both receptor types, hyperpolarizing current (+ve) increased the negative amplitude of nerve terminal impulses. In contrast, depolarizing current (−ve) was without effect on polymodal receptor nerve terminal impulses but increased the positive amplitude of cold receptor nerve terminal impulses. The hyperpolarization-induced increase in the negative amplitude of nerve terminal impulses represents a net increase in inward current. In both types of receptor, this increase in inward current was reduced by local application of low Na+ solution and blocked by lidocaine (10 mM). In addition, tetrodotoxin (1 μM) slowed but did not reduce the hyperpolarization-induced increase in the negative amplitude of polymodal and cold nerve terminal impulses. The depolarization-induced increase in the positive amplitude of cold receptor nerve terminal impulses represents a net increase in outward current. This change was reduced both by lidocaine (10 mM) and the combined application of tetraethylammomium (20 mM) and 4-aminopyridine (1 mM). The interpretation is that both polymodal and cold receptor nerve terminals possess high densities of tetrodotoxin-resistant Na+ channels. This finding suggests that in cold receptors, under normal conditions, the Na+ conductances are rendered inactive because the nerve terminal region is relatively depolarized.

scholarly journals Ca2+ changes induced by different presynaptic nicotinic receptors in separate populations of individual striatal nerve terminals

2001 ◽  
Vol 76 (6) ◽  
pp. 1860-1870 ◽  
Author(s):  
Sanjay V. Nayak ◽  
John J. Dougherty ◽  
J. Michael McIntosh ◽  
Robert A. Nichols
Keyword(s):  
Nicotinic Receptors ◽  
Nerve Terminals

TRPA1 in bradykinin-induced mechanical hypersensitivity of vagal C fibers in guinea pig esophagus

2009 ◽  
Vol 296 (2) ◽  
pp. G255-G265 ◽  
Author(s):  
Shaoyong Yu ◽  
Ann Ouyang
Keyword(s):  
Guinea Pig ◽  
Action Potentials ◽  
Transient Receptor Potential ◽  
Ex Vivo ◽  
Sensory Nerve ◽  
Sensory Nerves ◽  
Peripheral Sensitization ◽  
Nerve Terminals ◽  
Mechanical Hypersensitivity ◽  
C Fibers

Bradykinin (BK) activates sensory nerves and causes hyperalgesia. Transient receptor potential A1 (TRPA1) is expressed in sensory nerves and mediates cold, mechanical, and chemical nociception. TRPA1 can be activated by BK. TRPA1 knockout mice show impaired responses to BK and mechanical nociception. However, direct evidence from sensory nerve terminals is lacking. This study aims to determine the role of TRPA1 in BK-induced visceral mechanical hypersensitivity. Extracellular recordings of action potentials from vagal nodose and jugular neurons are performed in an ex vivo guinea pig esophageal-vagal preparation. Peak frequencies of action potentials of afferent nerves evoked by esophageal distension and chemical perfusion are recorded and compared. BK activates most nodose and all jugular C fibers. This activation is repeatable and associated with a significant increase in response to esophageal distension, which can be prevented by the B2 receptor antagonist WIN64338. TRPA1 agonist allyl isothiocyanate (AITC) activates most BK-positive nodose and jugular C fibers. This is associated with a transient loss of response to mechanical distensions and desensitization to a second AITC perfusion. Desensitization with AITC and pretreatment with TRPA1 inhibitor HC-030031 both inhibit BK-induced mechanical hypersensitivity but do not affect BK-evoked activation in nodose and jugular C fibers. In contrast, esophageal vagal afferent Aδ fibers do not respond to BK or AITC and fail to show mechanical hypersensitivity after BK perfusion. This provides the first evidence directly from visceral sensory afferent nerve terminals that TRPA1 mediates BK-induced mechanical hypersensitivity. This reveals a novel mechanism of visceral peripheral sensitization.

Nicotinic Receptors on Vagal Nerve Terminals in the Atrium

1987 ◽  
pp. 239-244 ◽  
Author(s):  
S. Nishi ◽  
H. Higashi ◽  
K. Odawara ◽  
K. Ikeda
Keyword(s):  
Nicotinic Receptors ◽  
Vagal Nerve ◽  
Nerve Terminals
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