On neural inhibition, contrast effects and visual sensitivity.
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Color Perception↗
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Capsazepine partially inhibits neurally mediated gastric mucus secretion following activation of protease-activated receptor 2.
1. Protease-activated receptor 2 (PAR2), present in capsaicin-sensitive sensory neurons, induces gastric mucus secretion and mucosal cytoprotection. 2. We studied the possible cross-talk between PAR2 and vanilloid receptor 1 (VR1). The VR1 antagonist capsazepine partially inhibited the PAR2-mediated increase in gastric mucus secretion. 3. Thus, activation of VR1 is responsible, at least in part, for the neurally mediated mucosal cytoprotection following activation of PAR2.
Animals↗
Spinal clonidine inhibits neural firing in locus coeruleus.
Intrathecally-administered clonidine inhibited the spontaneous firing of single neurons in the pontine nucleus locus coeruleus of rats. Such inhibition of neuron firing was not observed when the non-lipophilic alpha 2 adrenoceptor agonist (oxymetazoline) was administered intrathecally. It is concluded that lipophilic drugs like clonidine, when administered intrathecally, can have profound supraspinal actions and thus caution should be exercised in interpreting the sites of action of such drugs.
Animals↗
NEURAL INHIBITION IN A BIRD: EFFECT OF STRYCHNINE AND PICROTOXIN.
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Animals↗
[Effect of autonomic neural inhibition on the tumor process].
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Animals↗
The failure of morphine to depress selectively non-adrenergic neural inhibition of the guinea-pig taenia caeci.
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Animals↗
Xenopus msx1 mediates epidermal induction and neural inhibition by BMP4.
Epidermal fate in Xenopus ectoderm has been shown to be induced by a secreted growth factor, Bone Morphogenetic Protein 4 (BMP4). However, the molecular mechanism mediating this response is poorly understood. Here, we show that the expression of the homeobox gene, msx1, is an immediate early response to BMP4 in Xenopus embryos. The timing of expression and embryonic distribution of msx1 parallel those described for BMP4. Moreover, overexpression of msx1 in early Xenopus embryos leads to their ventralization as described for BMP4. Consistent with mediating a BMP type of signaling, overexpression of msx1 is sufficient to induce epidermis in dissociated ectoderm cells, which would otherwise form neural tissue. Finally, msx1 can also rescue neuralization imposed by a dominant negative BMP receptor (tBR) in ectodermal explants. We propose that Xenopus msx1 acts as a mediator of BMP signaling in epidermal induction and inhibition of neural differentiation.
Animals↗
Neural inhibition during maximal eccentric and concentric quadriceps contraction: effects of resistance training.
Despite full voluntary effort, neuromuscular activation of the quadriceps femoris muscle appears inhibited during slow concentric and eccentric contractions. Our aim was to compare neuromuscular activation during maximal voluntary concentric and eccentric quadriceps contractions, hypothesizing that inhibition of neuromuscular activation diminishes with resistance training. In 15 men, pretraining electromyographic activity of the quadriceps muscles [vastus medialis (VM), vastus lateralis (VL), and rectus femoris (RF)] was 17-36% lower during slow and fast (30 and 240 degrees/s) eccentric and slow concentric contractions compared with fast concentric contractions. After 14 wk of heavy resistance training, neuromuscular inhibition was reduced for VL and VM and was completely removed for RF. Concurrently, electromyographic activity increased 21-52, 22-29, and 16-32% for VL, VM, and RF, respectively. In addition, median power frequency decreased for VL and RF. Eccentric quadriceps strength increased 15-17%, whereas slow and fast concentric strength increased 15 and 8%, respectively. Pre- and posttraining median power frequency did not differ between eccentric and concentric contractions. In conclusion, quadriceps motoneuron activation was lower during maximal voluntary eccentric and slow concentric contractions compared with during fast concentric contraction in untrained subjects, and, after heavy resistance training, this inhibition in neuromuscular activation was reduced.
Adult↗
Wnt signalling inhibits neural differentiation of embryonic stem cells by controlling bone morphogenetic protein expression.
Wnt signalling plays an important role in both embryonic development and in tumourigenesis. Activation of the signalling cascade by wnt, but also mutations of the adenomatous polyposis coli (APC) protein and of the phosphorylation domain of beta-catenin, result in accumulation of active beta-catenin in the nucleus, where it binds to TCF/LEF transcription factors. We studied the effect of wnt signalling in embryonic stem cells by either inactivating APC or by introducing a dominant active form of beta-catenin. Both resulted in inhibition of neural differentiation in vitro and after brain grafting and in activation of downstream targets of wnt signalling, such as cyclins, c-myc, and bone morphogenetic proteins (BMP). Neural differentiation could be partially restored by the addition of the BMP antagonist noggin. This suggests a mechanism regulating the fate of differentiating embryonic stem cells.
Adenomatous Polyposis Coli Protein↗
Neural inhibition in the rat lower esophageal sphincter: role of beta 3-adrenoceptor activation.
1. Electrical field stimulation (EFS) of the rat lower esophageal sphincter produced tetrodotoxin-sensitive relaxant responses. 2. The relaxant responses were not significantly affected by propranolol but were attenuated by 6-hydroxydopamine and cyanopindolol, indicating beta 3-adrenoceptor activation. 3. The relaxant responses were significantly reduced in tissues previously exposed to BRL 37344, a beta 3-adrenoceptor agonist. 4. It was concluded that EFS-induced relaxation was adrenergic in origin and was mediated by beta 3-adrenoceptors.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
GABAergic and glycinergic neural inhibition in excitatory frequency tuning of bat inferior collicular neurons.
This study examined the effect of GABAergic and glycinergic inhibition on excitatory frequency tuning curves (FTCs) of inferior collicular (IC) neurons of the big brown bat, Eptesicus fuscus. The excitatory FTCs of 70 IC neurons were either V-shaped (57, 81%), closed (11, 16%), or double-peaked (2, 3%). By means of a two-tone stimulation paradigm, inhibitory FTCs were obtained at one frequency flank only (low-frequency flank: 11, 16%; high-frequency flank: 7, 10%), at both frequency flanks (36, 51%) of excitatory FTCs, or between two excitatory FTCs (2, 3%). IC neurons that had inhibitory FTCs typically had larger Q(10) and Q(30) values (i.e., sharper excitatory FTCs) than neurons that did not have inhibitory FTCs. Neurons with inhibitory FTCs at both frequency flanks had larger Q(10) and Q(30) values than neurons with inhibitory FTCs at one frequency flank only. IC neurons with a small difference between excitatory and inhibitory best frequencies typically had sharper excitatory frequency tuning. Bicuculline (an antagonist for GABAA) application produced a greater degree of abolishing inhibitory FTCs than strychnine (an antagonist for glycine) application. Application of both drugs was most effective in abolishing the inhibitory FTCs of IC neurons. The implications of these findings for bat echolocation are discussed.
Acoustic Stimulation↗
Vasoactive intestinal polypeptide (VIP) inhibits neurally evoked smooth muscle activity of rat uterine cervix in vitro.
VIP inhibits the spontaneous motor activity (including tone) in isolated preparations of uterine cervix from oophorectomized rats, but has no direct effect on preparations from estrogen-treated animals. Electrical field stimulation of nerves in the tissue evokes a contractile response that is inhibited by VIP in a concentration-dependent manner. The neuronal link probably involves a cholinergic mechanism, since the contraction is blocked by atropine. The results suggest the presence of VIP receptors both in cholinergic nerves and in smooth muscle cells of the rat uterine cervix.
Animals↗
Direct neural inhibition of insulin secretion in response to systemic hypoglycemia.
The innervated pancreas of an anesthetized small "pancreas" dog was cross-perfused with blood from a large "support" dog in order to separate neural from blood-borne influences on the immunoreactive insulin secretion rate (ISR). The arterial plasma reducing sugar (sugar) concentration could be varied independently in the pancreas dog systemic circulation and in its pancreas. After tying of the hepatic arteries and portal vein in the pancreas dog, its systemic arterial plasma sugar concentration was allowed to fall in 10 experiments. This was prevented in five control experiments by intravenous glucose infusion (7 mg/kg-min). In all experiments, pancreatic arterial plasma sugar concentration was sustained, and at 40 min it was elevated 50 mg/100 ml by glucose infusion into the pancreatic blood supply. Bilateral splanchnic nerve section at 120 min caused an increase of the ISR in all experiments, but a greater rise occurred from the pancreases of the 10 dogs allowed to become hypoglycemic (P less than .02). In two further experiments, the splanchnic nerves were not cut, and no rise in ISR occurred. In conclusion, systemic hypoglycemia can inhibit insulin secretion by means of the splanchnic nerves.
Animals↗
Neural inhibition of inflammation: the cholinergic anti-inflammatory pathway.
The innate immune system is activated by infection and injury to release pro-inflammatory cytokines, which activate macrophages and neutrophils and modulate specific cellular responses. The magnitude of the cytokine response is critical, because a deficient response may result in secondary infections, while an excessive response may be more injurious than the original insult. We recently described a neural pathway, termed the "cholinergic anti-inflammatory pathway", that reflexively monitors and adjusts the inflammatory response by inhibiting pro-inflammatory cytokine synthesis. Efferent signals in the vagus nerve provide a direct mechanism for neural regulation of the immune response that is rapid, localized, and integrated. Vagus nerve stimulation inhibits the release of TNF, HMGB1, and other cytokines, and protects against endotoxemia and ischemia-reperfusion injury. This newly identified physiological mechanism of maintaining immunological homeostasis suggests that novel therapeutics may effectively modulate inflammatory responses by activating the cholinergic anti-inflammatory pathway.
Acetylcholine↗
The FLT3 tyrosine kinase receptor inhibits neural stem/progenitor cell proliferation and collaborates with NGF to promote neuronal survival.
The FLT3 receptor tyrosine kinase (FLT3) was originally identified on hematopoietic stem cells (HSCs) and its ligand (FL) induces HSC proliferation. As stem cells originating from various tissues are more similar than once thought, the goal of this study was to determine whether neural stem cells express FLT3 and proliferate in response to FL. In fact, a subset of neural stem/progenitor cells does express FLT3, but contrary to our expectations, FL inhibited EGF and FGF-2 stimulated proliferation. Since FLT3 is expressed weakly by proliferative neuroepithelia but strongly by subsets of neurons in the CNS and PNS, we tested its ability to support neuronal survival. FL synergized with NGF to promote the survival of cultured DRG neurons, although it lacked any neurotrophic activity alone. We conclude that FL serves as an adjunct trophic factor in the nervous system, which differs from its role in the hematopoietic system.
Animals↗
Evidence that endogenous thyrotropin-releasing hormone (TRH) may control vagal efferents to thyroid gland: neural inhibition by central administration of TRH antiserum.
The intracerebroventricular (i.c.v.) injection of rabbit antiserum to thyrotropin-releasing hormone (TRH) to the urethane anesthetized rat inhibited the spontaneous electrical discharge of the superior laryngeal nerve (n.sl). On the other hand, the i.c.v. injection of rabbit antiserum to somatostatin (SRIF) failed to influence the nerve activity whereas SRIF itself is capable of inhibiting the n.sl activity. These findings suggest that TRH in the brain takes a role continuously in regulating the neural activity while SRIF is involved in the neuronal circuits as an agent for the down regulation of the autonomic nervous system.
Animals↗
The membrane effects, and sensitivity to strychnine, of neural inhibition of the Mauthner cell, and its inhibition by glycine and GABA.
1. Anionic conductance changes in Mauthner neurones of goldfish were measured during synaptically evoked inhibition and inhibition caused by iontophoretic application of the putative inhibitory transmitters glycine and gamma-aminobutyric acid (GABA).2. The effects of either amino acid were indistinguishable from those of the neural inhibitory transmitter(s). The membrane permeability during the neural or drug response was increased to Br(-), Cl(-), I(-), SCN(-), NO(3) (-), ClO(3) (-), and formate (HCOO(-)), but not to HCO(3) (-), BrO(3) (-), IO(3) (-), SO(4) (-), HPO(4) (-), H(2)PO(4) (-), acetate and citrate.3. Strychnine was injected intramuscularly, iontophoretically, or applied topically to the exposed brain in order to compare quantitatively its ability to prevent inhibition evoked by synaptic activation and by pharmacological means. Inhibitions were measured by the increase in membrane conductance.4. Strychnine, at concentrations just adequate to block completely the late collateral inhibition (LCI) and crossed VIII nerve inhibition, had little effect on the pharmacological inhibition caused by glycine, and sometimes there was no detectable effect at all. In one experiment even a local iontophoretic application of strychnine in a sufficient dose to diffuse over the cell and block the LCI almost completely, merely halved the effect of a small dose of glycine applied to the same localized region of the membrane.5. Higher concentrations of strychnine than those necessary to block synaptically evoked inhibition would reduce the effect of glycine but not that of GABA. The evidence indicated that any apparent effect of strychnine upon GABA could be explained by displacement of the GABA-containing iontophoretic pipette.6. The glycine-blocking action of iontophoretic pulses of strychnine was of relatively very slow onset and long duration compared to the effects of pulses of glycine and GABA.7. These findings can be interpreted as either (1) strychnine has a presynaptic action, preventing the release of inhibitory neurotransmitter, in addition to its less potent post-synaptic one in blocking pharmacological inhibition, or (2) strychnine acts entirely post-synaptically, but the physiological transmitter action differs from that of glycine and GABA in being considerably more sensitive to strychnine antagonism. In either case, the use of strychnine as evidence for the claim that glycine is an inhibitory neurotransmitter at the Mauthner cell is questionable.
Aminobutyrates↗
Ammonia inhibits neural cell adhesion molecule polysialylation in Chinese hamster ovary and small cell lung cancer cells.
Ammonia is a major concern in biotechnology because it often limits recombinant protein production by animal cells. Conditions, such as ammonia accumulation, in large-scale production systems can parallel those that develop within fast-growing solid tumors such as small cell lung cancer (SCLC). Ammonia's specific inhibition of the sialylation of secreted glycoproteins is well documented, but it is not known how ammonia affects membrane-bound proteins, nor what role it may have on important glycosylation determinants in cancer. We therefore examined the effects of NH4Cl on polysialic acid (PolySia) in the neural cell adhesion molecule (NCAM). By using flow cytometry combined with two NCAM antibodies, one specific for the peptide backbone and another that recognizes PolySia chains, we show that ammonia causes rapid, dose-dependent, and reversible inhibition of NCAM polysialylation in Chinese hamster ovary (CHO) and SCLC NCI-N417 cells. The decrease in PolySia was accompanied by a small increase in NCAM, suggesting that the changes were specific to the oligosaccharide. Inhibition by ammonia was greater for CHO cells, with PolySia cell surface content decreasing to 10% of control after a 4-day culture with 10 mM NH4Cl, while N417 cell PolySia was reduced by only 35%. Ammonia caused a 60% decrease in the CHO cell yield from glucose, while N417 cells were barely affected, suggesting that increased resistance to ammonia by N41 7 cells is a global rather than glycosylation-specific phenomenon. The data presented show that the tumor microenvironment may be an important factor in the regulation of PolySia expression.
Ammonia↗