Anti-neural-inhibition: a conserved mechanism for neural induction.
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Animals↗
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[Relationship between trace excitation and inhibition neural processes during a brief action of conditioned stimuli].
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Conditioning, Classical↗
Nitric oxide affects mammalian distal colonic smooth muscle by tonic neural inhibition.
1 The role of the L-arginine-nitric oxide (NO) pathway in tonic neural inhibition of spontaneous mechanical activity of distal colonic circular smooth muscle (DCCSM) was investigated in male Wistar rats. 2 Muscle strips were mounted in organ baths and spontaneous contractions recorded with isometric force transducers. They were characterized as low frequency (LFCs) 0.41 +/- 0.03 N cm-2 or high frequency contractions (HFCs) 0.22 +/- 0.04 N cm-2. The latter occurred intermittently to produce summation contractions (SCs) range 0.5-12 N cm-2. 3 Tetrodotoxin (100 nM) increased the forces of LFCs and SCs. Increase in force to tetrodotoxin did not occur after incubation of the muscle with NG-monomethyl-L-arginine (L-NMMA) 500 microM, an inhibitor of NO biosynthesis. 4 L-NMMA but not its enantiomer D-NMMA increased the force of LFCs (EC50: 200 microM) and SCS (EC50:175 microM) in a concentration-dependent manner which was reversed by L-arginine but not by D-arginine. 5 Muscle, precontracted by acetylcholine, relaxed to sodium nitroprusside (EC50:1.8 microM) NO gas (EV50:70 microliters) and NO solutions (EC50:4 microM) in a concentration-dependent manner. Guanosine 3':5'-cyclic monophosphate tissue concentrations (pmol mg-1 protein) were elevated in muscle after relaxation by sodium nitroprusside (500 microM) from 0.32 +/- 0.06 to 1.2 +/- 0.37 and by 1 ml of NO gas from 0.49 +/- 0.05 to 1.54 +/- 0.14. 6 These data suggest that DCCSM is under tonic neural inhibition mediated by NO biosynthesis.
Acetylcholine↗
Neural inhibition of gastrointestinal smooth muscle motility in guinea-pigs.
The neural inhibition of the gastrointestinal (GI) smooth muscle motility was studied by means of electrical transmural nerve stimulation (ETNS) in guinea-pigs. In untreated muscle strips, ETNS induced four types of response, consisting of three basic components, i.e., contraction and relaxation during ETNS, and after-contraction. Following atropinization, all the responses changed to only one type, i.e., relaxation during ETNS followed by after-contraction. The relaxation of the muscle strips induced by ETNS after atropinization was not significantly reduced under superimposing guanethidine treatment in any site of the GI tract. The maximal relaxation of the muscle strips induced by ETNS after atropine and guanethidine treatments was not uniform throughout the GI tract. The relaxation of the gastric body and colon was greater than that of the jejunum and ileum. The extent of the relaxation was significantly different even in the colon. Theophylline and phentolamine did not reduce the ETNS-induced relaxation following atropine and guanethidine treatments in the distal colon and taenia coli. The findings suggest the following: the non-adrenergic inhibitory (NAI) nerve is the main postganglionic nerve to inhibit the GI smooth muscle motility; and the role of adrenergic nerve is of little importance in respect to postganglionic inhibition. The innervation of the NAI nerve seems not to be uniform throughout the GI tract. Theophylline and phentolamine are not the specific antagonists of the NAI nerve.
Adrenergic Fibers↗
Neural inhibition sharpens auditory spatial selectivity of bat inferior collicular neurons.
This study examines the role of neural inhibition in auditory spatial selectivity of inferior collicular neurons of the big brown bat, Eptesicus fuscus, using a two-tone inhibition paradigm. Two-tone inhibition decreases auditory spatial response areas but increases the slopes of directional sensitivity curves of inferior collicular neurons. Inferior collicular neurons have either directionally-selective or hemifield directional sensitivity curves. A directionally-selective curve always has a peak which is at least 50% larger than the minimum. A hemifield directional sensitivity curve rises from an ipsilateral angle by more than 50% and either reaches a plateau or declines by less than 50% over a range of contralateral angles. Two-tone inhibition does not change directionally-selective curves but changes most hemifield directional sensitivity curves into directionally-selective curves. Auditory spatial selectivity determined both with and without two-tone inhibition increases with increasing best-excitatory frequency. Sharpening of auditory spatial selectivity by two-tone inhibition is larger for neurons with smaller differences between excitatory and inhibitory best frequencies. The effect of two-tone inhibition on auditory spatial selectivity increases with increasing inhibitory tone intensity but decreases with increasing intertone interval. The implications of these findings in bat echolocation are discussed.
Animals↗
Evidence for neural inhibition in bittersweet taste mixtures.
Three lines of evidence from psychophysical experiments implied that mutual suppression of bitter and sweet tastes is due to neural inhibition rather than chemical interactions in solution or competition of molecules for common receptor sites. Removal of sweetness from bittersweet mixtures caused the bitterness to increase. This was accomplished by adaptation to sucrose or by treatment with Gymnema sylvestre, neither of which affect the concentration of sucrose on the tongue. Such increases in the bitterness of mixtures, independent of the concentration of the sweet masking substance, are difficult to reconcile with suppression by means of chemical interactions. Similar dependence of suppression on perceived intensity (and independence from concentration) was observed with mixtures of phyenylthiocarbamide and sucrose. Tasters of phenylthiocarbamide showed stronger suppression of sweetness than nontasters. This result was also inconsistent with molecular interactions causing suppression, which would have resulted in the same degree of suppression for the two groups. Instead, these findings support neural explanations of mixture suppression, such as antidromic inhibition or occlusion.
Adaptation, Physiological↗
Propranolol and lidocaine inhibit neural norepinephrine release in hearts with increased extracellular potassium and ischemia.
BACKGROUND: Propranolol and lidocaine are effective antiarrhythmic drugs in myocardial ischemia and infarction. As sympathetic nerve activation and norepinephrine release in ischemic hearts are arrhythmogenic, we tested the possibility that both agents inhibit neural norepinephrine release following sympathetic activation in the ischemic environment. METHODS AND RESULTS: The model used was an in situ perfused innervated rat heart. Norepinephrine release was induced by electrical stimulation of the left cervicothoracic stellate ganglion and analyzed using radioenzymatic assay or high-performance liquid chromatography. In normoxically perfused hearts, evoked norepinephrine release was not affected by either of the two agents at doses of 1 to 10 mumol/L when extracellular K+ concentration was 4 mmol/L but dose-dependently reduced at 10 mmol/L K+ (D,L-propranolol: -53 +/- 4% at 1 mumol/L and -64 +/- 6% at 10 mumol/L K+, lidocaine: -37 +/- 11% at 0.1 mumol/L, -67 +/- 5% at 1 mumol/L, and -75 +/- 6% at 10 mumol/L). At 10 mmol/L K+, norepinephrine release was not affected by timolol or atenolol (both 10 mumol/L but was equally inhibited by D- or L-propranolol at 10 mumol/L (-56 +/- 5% and -53 +/- 9%, respectively), indicating a beta-blocking-independent mechanism. In hearts with metabolic acidosis (pH 6.85) at K+ of 4 mmol/L, neural norepinephrine release was also reduced by propranolol at 10 mumol/L (-37%). Finally, in hearts perfused with 4 mmol/L K+ and subjected to 6-minute periods of ischemia, neural norepinephrine release was similarly suppressed by D,L-propranolol (-38 +/- 6% at 0.1 mumol/L, -44 +/- 5% at 1 mumol/L, and -78 +/- 3% at 10 mumol/L) or lidocaine (-39 +/- 7% at 0.1 mumol/L, -58 +/- 9% at 1 mumol/L, and -91 +/- 3% at 10 mumol/L). CONCLUSIONS: These data indicate that propranolol and lidocaine inhibit neural norepinephrine release via a Na+ channel-blocking mechanism that is synergistic with changes induced by ischemia, primarily raised extracellular K+. This mechanism may contribute to the anti-ischemic and antiarrhythmic properties of both agents in acute myocardial ischemia, which induces increased extracellular K+ and sympathetic activation.
Animals↗
Neural inhibition of the corpus allatum in the last larval instar differs from that in adults in the blood-feeding insect, Rhodnius prolixus.
An active corpus allatum (CA) in the blood feeding insect, Rhodnius prolixus, releases a substance that inhibits metamorphosis in larvae, and activates egg production in adults. In adults, transecting the nervus corporis cardiacum II's (NCCII), which are attached posteriorly to each protocerebral lobe, greatly increases egg production indicating that the adult CA is activated and receives neural inhibition from cells associated with the NCCII [Chiang, Arch. Insect. Biochem. Physiol. 39:126-131 (1998)]. In the present study, the NCCII's in fifth instar larvae were transected immediately before or after feeding to determine if these nerves normally inhibit CA activity in the last larval instar. Approximately 20 to 25 days following ingestion of a blood meal, L5's with transected NCCII's emerged as fully-formed adults with no larval characteristics. Examination of the brain in these recently emerged adults revealed that the NCCII's were absent. Since fifth instar larvae with transected NCCII's emerged with no juvenile characteristics, cutting the NCCII's did not activate the CA, indicating that the mechanism for inhibition of the CA differs in the last larval instar and adult animals.
Animals↗
Assessment of neural inhibition of the lower esophageal sphincter in cats with esophagitis.
BACKGROUND: The aim of this study was to investigate the inhibitory innervation of the lower esophageal sphincter in the presence of esophagitis. METHODS: Esophagitis was produced in five anesthetized cats with intraesophageal perfusion of HCl. Sphincter pressure responses were assessed with a sleeve catheter after administration of bethanechol, cholecystokinin octapeptide, and McNeil-A343 and with intraesophageal balloon distension. RESULTS: In the presence of esophagitis (1) resting lower esophageal sphincter pressure decreased; (2) the excitatory response to bethanechol was maintained; (3) there was a reduction in the excitatory response to McNeil-A343 and cholecystokinin at the highest dosages; (4) there was an increase in the potency of cholecystokinin and McNeil-A343 to produce an inhibitory response; (5) the inhibitory response to intraesophageal balloon distension was maintained; and (6) increased inhibitory responses took longer to normalize than the reduced excitatory responses. CONCLUSIONS: Esophagitis decreases cholinergic excitation, but neural inhibition to the LES remains intact. These findings suggest that blocking intact inhibition may be a new therapeutic approach for esophagitis caused by gastroesophageal reflux.
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
Tumorhead, a Xenopus gene product that inhibits neural differentiation through regulation of proliferation.
Tumorhead (TH) is a novel maternal gene product from Xenopus laevis containing several basic domains and a weak coiled-coil. Overexpression of wild-type TH resulted in increased proliferation of neural plate cells, causing expansion of the neural field followed by neural tube and craniofacial abnormalities. Overexpressed TH protein repressed neural differentiation and neural crest markers, but did not inhibit the neural inducers, pan-neural markers or mesodermal markers. Loss of function by injection of anti-TH antibody inhibited cell proliferation. Our data are consistent with a model in which tumorhead functions in regulating differentiation of the neural tissues but not neural induction or determination through its effect on cell proliferation.
Amino Acid Sequence↗
Galanin inhibits neural activity in the subfornical organ in rat slice preparation.
The activation of the subfornical organ (SFO), a circumventricular organ, induces water intake and vasopressin release. Since central administrations of galanin (GAL) suppress water intake and vasopressin release, GAL may inhibit the neural activity of SFO neurons. In the present study, we investigated effects of GAL on the SFO using molecular biological, electrophysiological and anatomical techniques. Reverse transcription-polymerase chain reaction analysis demonstrated the presence in the SFO of rats of the mRNAs for each of the three known GAL receptor subtypes (GalR1, GalR2 and GalR3). In extracellular recordings in SFO slice preparations, GAL dose-dependently inhibited the neural activity of cells from a number of recording sites. Many GAL-sensitive SFO neurons showed excitatory responses to angiotensin II (ANGII). The GalR1 agonist M617 inhibited the activity of SFO neurons, whereas the GalR2 and GalR3 agonist GAL(2-11) had almost no effect. In patch-clamp recordings, GAL induced an outward current in SFO neurons without influencing synaptic currents. An immunoelectron microscopic study revealed the existence of GAL-containing synaptic vesicles in the SFO. These results suggest that the SFO has neural inputs involving GAL. The response to GAL is inhibitory, mediated at least in part by GalR1 and provides a plausible explanation for the opposite effects of ANGII and GAL seen in vivo on water intake and vasopressin release.
Action Potentials↗
Melatonin inhibits neural apoptosis induced by homocysteine in hippocampus of rats via inhibition of cytochrome c translocation and caspase-3 activation and by regulating pro- and anti-apoptotic protein levels.
In the present study, we examined the molecular mechanism by which homocysteine causes neuronal cell apoptosis. We further investigated the mechanisms of melatonin's ability to reduce homocysteine-induced apoptosis. Consistent with its antioxidant properties, melatonin reduced homocysteine-induced lipid peroxidation and stimulated glutathione peroxidase enzyme activity in hippocampus of rats with hyperhomocysteinemia. Furthermore, melatonin treatment diminished cytochrome c release from mitochondria and reduced caspase 3 and caspase 9 activation induced by hyperhomocysteinemia. Chronic hyperhomocysteinemia also led to poly(ADP-ribose) polymerase cleavage and subsequently DNA fragmentation. Treatment with melatonin markedly inhibited poly(ADP-ribose) polymerase cleavage and reduced DNA damage. Hyperhomocysteinemia caused an elevation of pro-apoptotic Bax levels while reducing anti-apoptotic protein, Bcl-2, levels. Daily administration of melatonin up-regulated Bcl-2 and down-regulated Bax levels. We propose that, in addition to its antioxidant properties, melatonin has the ability to protect neuronal cells against apoptosis mediated homocysteine neurotoxicity by modulating apoptosis-regulatory proteins in the hippocampus of rats.
Animals↗
Neural inhibition by c-Jun as a synergizing factor in bone morphogenetic protein 4 signaling.
The transcription factor, activator protein 1 (AP-1) complexes (c-Jun and c-Fos heterodimers) has been shown to interact with transforming growth factor beta signaling in mammalian cells and Drosophila embryo. Here we show that c-Jun alone is involved in the anti-neuralizing activity of bone morphogenetic protein 4, a transforming growth factor beta superfamily member, in Xenopus neurogenesis. Co-injection of mRNAs encoding c-jun and a dominant negative bone morphogenetic protein receptor completely inhibits dominant negative bone morphogenetic protein receptor-induced neuralization and reverses the epidermal fate in the animal cap. Surprisingly, a dominant negative c-Jun does not induce neural tissue in the animal cap, but it synergizes with dominant negative bone morphogenetic protein receptor for neural induction. Temporal analysis using a dexamethasone-inducible c-Jun shows that exogenous c-Jun activity must be turned on before or at stage 11 to fulfill the anti-neuralizing effect. Neural inhibition by c-Jun does not occur until stage 13 suggesting that c-Jun probably acts by suppressing neural maintenance rather than neural initiation. This is also supported by the fact that c-Jun does not inhibit expression of the neural-initializing gene Zic-r1 but the neural cofactor Sox2, and that ectopic expression of Sox2 attenuates the anti-neuralizing effect of c-Jun. Finally, we display that the c-Jun effect is enhanced by an auto-regulatory loop between c-Jun and bone morphogenetic protein. These studies suggest that c-Jun/AP-1 is a converging point in both the fibroblast growth factor and transforming growth factor beta signaling pathways. Based on our findings, we propose that c-Jun synergizes with bone morphogenetic protein 4 signaling to inhibit neural development in Xenopus ectoderm.
Animals↗
Neural inhibition of insulin secretion from the isolated canine pancreas.
UNLABELLED: By using an isolated in situ, cross-perfused pancreas preparation, direct neural effects on the immunoreactive insulin secretion rate (ISR) were separated from blood-borne influences. Blood from a large, anesthetized "support" dog was perfused through the pancreas of a small, anesthetized "pancreas" dog. Both splanchnic nerves of the pancreas dog were cut above the diaphragm and stimulated simultaneously (10 Hz, 0.1-ms pulses, 5-15 mA) for three 10-min periods, twice before and once during a pancreatic arterial phentolamine infusion (10 or 20 mug/min). Splanchnic nerve section caused a transient increase whereas stimulation caused a decrease in ISR. Phentolamine infusion blocked this decrease. In control experiments, an epinephrine infusion (25 or 50 mug/kg per min) was made into the systemic circulation of the pancreas dog instead of the first and second neural stimulations. No decrease in ISR occurred. Later neural stimulation (in the absence of phentolamine) was accompanied by a decrease in the ISR in three of four dogs. CONCLUSIONS: the ISR can be inhibited by direct neural imput to the pancreas, and this inhibition is mediated by alpha-adrenergic receptors.
Adrenalectomy↗
Human esophageal response to rapid swallowing: muscle refractory period or neural inhibition?
The peristaltic response of the normal human esophagus to 10 repeated water swallows separated by varying time intervals (5, 10, 15, 20, and 30 s) between swallows was studied. Pressures measured during the shorter time intervals were of lower amplitude than those at 30-s swallowing intervals throughout the esophagus, with the distal esophagus showing the greatest effect. Frequency of peristalsis was decreased throughout the esophagus with rapid swallowing, especially distally at the 5- and 10-s time intervals. There was no significant change in wave velocity or duration at these time intervals. These data suggest that there is a refractory period in the distal (smooth muscle) esophagus. A series of paired swallows separated by 5 s resulted in a significant decrease in amplitude of the first swallow, and this was more marked in the distal esophagus. These data indicate that there is an inhibition of the progression of peristalsis by a subsequent swallow, probably through a neural mechanism. These studies show that repeated liquid swallows may effect peristalsis by two mechanisms: refractoriness of esophageal smooth muscle and a neural inhibitory discharge.
Adult↗
[Comparative effects of vitamin B12, 5, 6-dimethyl-benzyimidazole and dibazole on certain types of neural inhibition].
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Benzimidazoles↗
[Generalized neural inhibition evoked by photogenic convulsive electric activity].
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Animals↗