Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

McN-A-343 (McN), a non nicotinic ganglionic stimulant, induced slow contractile responses of the toad rectus abdominis. A relaxation was also observed when large doses were added in the presence of a contraction caused by acetylcholine (Ach). The relaxation induced by McN could not be overcome by increasing Ach concentration. Bell-shaped log dose-response curves were obtained for McN. d-Tubocurarine caused an unusual change on these curves, suggesting an indirect action of the agonist. This possibility was corroborated by the fact that hemicholinium, procaine, and cold storage of the muscle caused a marked decrease of the organ sensitivity to McN but not to ACh.
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PMID:A comparative study of the effects induced by MCN-A-343 and acetylcholine on the isolated toad rectus abdominis. 6 2

The principal cells of the mudpuppy cardiac ganglion receive synapses from three sources: vagal axons, interneurons and axon collaterals from other principal cells. The simplicity of the structural organization and the visual clarity in the living preparation provide favorable conditions for examining the function of these synapses and how different classes of synapses on the same cell influence its function. We have studied the sensitivity of the principal cells to iontophoretically applied acetylcholine--the transmitter at synapses made by the vagal axons and by postganglionic axon collaterals from other principal cells. In normal ganglia, the ACh sensitivity on the cell surface is highest at the region of synapses. Partial denervation, produced by severing the vagus nerves, results in an increased ACh sensitivity in nonsynaptic areas but does not appear to affect synaptic transmission at the remaining synapses.
Cold Spring Harb Symp Quant Biol 1976
PMID:Synaptic organization and acetylcholine sensitivity of multiply innervated autonomic ganglion cells. 18 Nov 98

ACh response in the isolated duodenum from SART stressed (repeated cold stressed) mice was remarkably decreased in comparison to normal mice 5 days after onset of loading SART stress, and maximal contraction in SART stress mice duodenum was about 37% of that in non-stressed mice. Pilocarpine and KCl responses were also considerably decreased, but BaCl2 response was much the same as in the controls. Thus, the contraction system of the muscle is apparently not damaged by SART stress. Though body weights decreased, the daily intake of food incressed in SART stressed mice. Length of small intestine from SART stressed mice was much the same as in controls, but wet weights of small intestines were larger than in controls. Autonomic agonists, antagonists, tranquilizers and other drugs were given intraperitoneally to mice once daily during SART stress, and the ACh responses in the isolated duodenum were investigated. Pretreatment with adrenergic and anticholinergic drugs inhibited the decrease of ACh response, but antiadrenergic and cholinergic drugs had no effects. Pretreatment with tranquilizers such as reserpine, chlorpromazine, carpipramine and imipramine inhibited the decrease of ACh response in the isolated duodenum, but diazepam, meprobamate and benadryl had no influence. Pretreatment of neurotropin, a neurosedative had good inhibitory effects. Our results suggest that SART stressed mice may be in a state of unbalance regarding sympathetic and parasympathetic nerves, particularly with regard to abnormal tension in the parasympathetic nervous system, in part of duodenum. Pretreatment with most of the above drugs had no influence on loss of body weight in SART stressed mice while pretreatment with neurotropin inhibited body weight to a considerable extent.
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PMID:[Decrease of ACh response in isolated duodenum from SART stressed (repeated cold stressed) mice (author's transl)]. 43 83

The effects of ACh on the smooth muscle cell membrane and mechanical property of the guinea-pig main coronary artery were observed by micro-electrode and isometric tension recording methods. 1. The membrane potential was low (--44 mV) and the membrane was electrically quiescent. Application of outward current pulse generated only a small graded response. The current--voltage relationship was linear for application of inward current pulses. 2. In low external Na or Cl solution the membrane was hyperpolarized. In external K solution of the 1.2--17.8 mM the membrane potential remained nearly the same; however increasing it to more than 29.5 mM depolarized the membrane. The maximum slope of depolarization was 42 mV per tenfold increase in external K. These results indicate that both Na and Cl equilibrium potentials were positive to the resting membrane potential. 3. ACh (greater than 10(-8) g/ml.) hyperpolarized the membrane, to a maximum of --67 mV with 10(-6) g ACh/ml. The dose--response relationship was sigmoidal, and the hyperpolarization was suppressed by atropine (10(-7) g/ml.). In external K of 1.2--29.5 mM, the application of 10(-6) g/ml. ACh hyperpolarized the membrane; this ACh-induced hyperpolarization was maximal in 1.2 mM-K (from --42.4 to --82.4 mV). When the hyperpolarization produced by 10(-6) g ACh/ml. was plotted against the external K concentration on a log scale, the relationship was linear above 1.2 mM-K and similar to that observed between the membrane potential and external K concentration between 29.5 and 118 mM in the absence of ACh. However, in a solution containing less than 1.2 mM-K, the amplitudes of ACh-induced hyperpolarization were reduced. 4. In Na- or Cl-deficient solution the membrane was hyperpolarized. The peak hyperpolarization to ACh was not modified by these changes in the ionic environments. It is concluded that ACh increases K permeability selectively in this muscle membrane. 5. To observe the reversal potential level of ACh-induced hyperpolarization, the effects of ACh were observed during the hyperpolarization and subsequent recovery of the membrane on rewarming the tissue following cold storage. When the membrane potential was high (less than --70 mV) ACh produced depolarization, but when it was low (greater than --70 mV) ACh produced hyperpolarization. The reversal potential level for ACh-induced potential change was about --70 mV. 6. Application of ACh (greater than 10(-8) g/ml.) evoked a mechanical response. The hyperpolarization of the membrane produced by ACh appeared coincidently with tension development. ACh also enhanced the amplitude of contracture produced by excess external K concentration. 7. It is concluded that ACh might increase K and Ca permeabilities of the membrane and release Ca from the intracellular store, thus causing hyperpolarization of the membrane and contraction.
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PMID:Effects of acetylcholine on the smooth muscle cell of isolated main coronary artery of the guinea-pig. 50 78

The effects of hypothermia (4 degrees C) on the components of the cholinergic system of the ileal longitudinal muscle and the adherent Auerbach's plexus of the guinea pig ileum have been investigated. Acetylcholine (ACh) content of the muscle was determined by pyrolysis-gas chromatography. It decreased from 119 to a fairly steady level of 16 nmol/g of wet tissue during the first 72 h of cold storage at 4 degrees C under anoxic conditions. Concomitantly, responsiveness to intramural electrical stimulation decreased by 72%. Cholinesterase (ChE) and choline acetyltransferase (ChA) activities each dropped by 40% during this period. However, the de novo synthesis of ACh over the period of study did not change significantly. The response of the preparation to the exogenously applied ACh remained fairly constant suggesting that the changes in the cholinergic receptor are not accountable for the decrease in responsiveness to intramural stimulation. From the results of this study, it has been concluded that cold storage for 5 days leads to: (1) a significant decline in ACh content within 72 h of storage; (2) a decrease in ChE and ChA activities; (3) no significant effect on the cholinergic receptor; and (4) a decrease in responsiveness to intramural electrical stimulation which is probably due to a malfunction of the ACh-releasing mechanism.
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PMID:Effects of cooling on the levels of acetylcholine, cholinesterase, choline acetyltransferase and the intramural electrical stimulation on the guinea pig ileum. 62 70

Single unit activity was recorded by means of five-barrel micropipettes from temperature-sensitive neurons in the reticular formation of the medulla oblongata in urethanized cats. Acetylcholine (ACh), norepinephrine (NE) and 5-hydroxytryptamine (5-HT) were applied microiontophoretically to the immediate vicinity of the neurons. Both thermally sensitive and insensitive units responded to ACh (82.0%) and 5-HT (93.0%) by increasing discharge rate. Iontophoretically applied atropine, but not hexamethonium, antagonized the excitatory responses to ACh. NE was shown to have different effects on the medullary neurons. Most temperature-insensitive units were either nonresponsive (52.4%) or excited (28.6%) by NE, while a majority of warm-sensitive (61.8%) and cold-sensitive (55.6%) neurons were inhibited by NE. Iontophoretically application of the alpha-adrenergic blocking agent, phentolamine, or the beta-antagonists, propranolol, or sotalol, produced no effect on the inhibitory responses to NE. These results tend to support the current concept of the transmitter role of monoamines in thermoregulation.
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PMID:Response of temperature-sensitive medullary neurons to acetylcholine, norepinephrine, and 5-hydroxytryptamine. 92 15

1. Postsynaptic responses to acetylcholine released from nerve terminals and from iontophoretic micropipettes were investigated in skeletal twitch-muscle fibers of the snake. The preparation consists of thin sheets of muscle fibers in which details of the end plate, including the outlines of individual synaptic boutons, are clearly seen in the living state. After treatment with collagenase, the motor nerve and its terminal boutons can be removed to expose the intact subsynaptic membrane to direct application of ACh by iontophoretic pipettes. 2. The number of ACh molecules in a quanta was estimated to be fewer than 10,000. This was done by developing a sensitive bioassay to measure the output of ACh from iontophoretic pipettes needed to produce synaptic responses closely resembling nerve-released miniature postsynaptic potentials. 3. Postsynaptic receptors are not saturated by the ACh in a quantum, since the peak of the quantal response produced by an appropriate background concentration of ACh from a pipette. 4. When acetylcholine esterase is inhibited, two or more quanta can act upon partially overlapping postsynaptic membrane areas and potentiate each other's effects. This potentiation reveals itself as a prolongation of the synaptic current. Postsynaptic potentiation is a consequence of the nonlinear dose-response characteristics of ACh receptors and can also be demonstrated in a model system in which ACh micropipettes substitute for quantal release from the nerve. 5. With AChE fully active, however, each quantum is functionally isolated from its neighbors and no postsynaptic potentiation is seen. 6. It is suggested that postsynaptic potentiation between quantum may play a role in signaling at synapses which have nonlinear dose-response characteristics and where transmitter is not so rapidly inactivated as at the neuromuscular synapse.
Cold Spring Harb Symp Quant Biol 1976
PMID:The number of acetylcholine molecules in a quantum and the interaction between quanta at the subsynaptic membrane of the skeletal neuromuscular synapse. 106 24

The relative number of acetylcholine receptors at normal and denervated end plates in rat soleus muscles was studied using the binding of 125I-alpha-bungarotoxin as a quantitative assay. After short-term denervation (up to 2.4 weeks), the extrajunctional binding increased, but there was no change in specific binding to the motor end plate. Denervation for longer periods (up to 7 weeks) reduced binding sites at the end plate by as much as 60-70%. Direct electrical stimulation of these muscles for the entire period of denervation did not prevent the slow loss of junctional binding sites, even though it was adequate to abolish the increase in extrajunctional binding. Cross-innervation by a foreign nerve at a site distant from the original end plates was more effective than stimulation in preserving the old end plates; in cross-innervated muscles, many denervated end plates continued to bind normal amounts of toxin for over 4 months. In comparison with the rapid rate of appearance or disappearance of extrajunctional ACh receptors, however, the number of junctional receptors at all denervated end plates was quite stable, suggesting that the persistence of these receptors is not immediately dependent on the presence of a motor nerve terminal.
Cold Spring Harb Symp Quant Biol 1976
PMID:Persistence of junctional acetylcholine receptors following denervation. 106 30

To develop an animal model for experimental nasal hypersensitivity and hyperreactivity, guinea pigs were subjected to intermittent exposure to cold temperature (intermittent cold stress, SART stress) for 5 consecutive days. In SART-stressed guinea pigs, nasal mucosal hypersensitivity to histamine evoking sneeze response and nasal hypersecretion in response to methacholine were observed. The hypersensitivity remained for further 7 days after being released from SART stress. On the other hand, such nasal mucosal hypersensitivity was not caused by a continuous cold stress alone, suggesting that intermittent exposure to cold may be of importance for the appearance of nasal mucosal hypersensitivity. In passively sensitized SART-stressed guinea pigs, the quantity of nasal secretion induced by an allergen was significantly increased compared with that of a group of normal animals. The expression of muscarinic acetylcholine receptor (m-ACh.R) became higher in SART-stressed guinea pigs. Thus, hypersensitivity and hyperreactivity in this system were found to be associated with an increase in density of m-ACh.R. SART-stressed guinea pigs will serve as an animal model for hypersensitivity in nasal mucosa, which would be useful for the study of nasal allergy.
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PMID:Nasal mucosal hypersensitivity in guinea pigs intermittently exposed to cold. 166 87

The in vivo rabbit cornea was used to investigate the effect of acetylcholine on "free" nerve endings from A-delta and C-fibers in the long-ciliary (corneal) nerve. Extracellular electrophysiologic recordings were obtained from 67 corneal nerve fibers. Acetylcholine in concentrations of 10(-5) to 10(-3) M stimulated a specific population of these corneal afferents that were not activated by mechanical or thermal stimuli. Their conduction velocity was determined to be 1.14 +/- 0.34 m/s (mean +/- SD). The other three previously characterized corneal nerve populations (mechanical, mechano-heat, and cold) were not stimulated by the cholinergic agonists or antagonists. Acetylcholine sensitive afferents were also stimulated by carbachol (10(-5) to 10(-3) M) and nicotine (10(-6) to 10(-4) M) but not by bethanecol (10(-5) to 10(-3) M). Acetylcholine-induced activity was abolished by d-tubocurare (10(-4) M) and kappa-bungarotoxin (10(-6) M). The cAMP analog 8-bromoadenosine 3'5'-cyclic monophosphate activated the same population of chemosensitive C-fibers as acetylcholine. It is concluded that a specific population of C-fiber afferents exist in the rabbit cornea which are stimulated by acetylcholine possibly acting via a neuronal nicotinic receptor. Physiologically, these nerves may be involved in the production of pain following tissue injury or ischemia.
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PMID:Cholinergic activation of a population of corneal afferent nerves. 175 14


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