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At least 19 recordsLinked to original sources
PubMed1979

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↗
PubMed1975

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↗
PubMed1976

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↗
PubMed1977

The effects of hyperphenylalaninaemia on the concentrations of aminoacyl-transfer ribonucleic acid in vivo. A mechanism for the inhibition of neural protein synthesis by phenylalanine.

An acute administration of phenylalanine to neonatal animals has been reported to result in large decreases in the intracellular concentrations of several essential amino acids in neural tissue, as well as an inhibition of neural protein synthesis. The present report evaluates the effects of the loss of amino acids on the concentrations of aminoacyl-tRNA in vivo, with the view that an alteration in the concentrations of specific aminoacyl-tRNA molecules could be the rate-limiting step in brain protein metabolism during hyperphenylalaninaemia. tRNA was isolated from saline- and phenylalanine-injected mice 30-45 min after injection, by using a procedure designed to maintain the concentrations of aminoacyl-tRNA present in vivo. Periodate oxidation of the non-acylated tRNA and aminoacylation with radioactively labelled amino acids was used to determine the proportion of tRNA that was present in vivo as aminoacyl-tRNA. Although decreases in the intracellular concentrations of alanine, lysine and leucine were observed after phenylalanine administration, the concentrations of alanyl-tRNA, lysyl-tRNA and leucyl-tRNA actually increased by 15%. Although tryptophan has been suggested to be rate-limiting during hyperphenylalaninaemia, the proportion of tryptophan tRNA that was acylated was maximal in both normal and hyperphenylalaninaemic animals. This unexpected increase in aminoacyl-tRNA concentration is discussed as perhaps a secondary effect resulting from the phenylalanine-induced inhibition of protein synthesis. In contrast, the proportion of methionine tRNA that was acylated in vivo after phenylalanine administration was demonstrated to be decreased by approx. 17%. When the isoaccepting species of methionine tRNA were separated by reverse-phase column chromatography, three species were separated, one of which was demonstrated to be the initiator species, tRNAfMet, by the selective aminoacylation and formylation with Escherichia coli enzymes. After the administration of phenylalanine, the acylation of each of the three methionine tRNA species was decreased, with the initiator species being lowered by 10%. This effect on aminoacylation of tRNAfMet may be the primary step by which phenylalanine affects neural protein synthesis, and this is consistent with previous reports that re-initiation may be inhibited during hyperphenylalaninaemia.

Acylation↗
PubMed1976

A pharmacological analysis of neurally induced inhibition of carotid body chemoreceptor activity in cats.

Experiments were performed to determine the mechanism by which centrifugal impulses in the carotid sinus nerve (CSN) reduce the frequency of impulse traffic in afferent chemoreceptor fibers from the carotid body in cats. Recordings of chemoreceptor activity were made from single- or few-fiber preparations dissected off the CSN, while the remainder of the CSN was stimulated electrically to produce neurally induced inhibition of chemoreceptor activity. Various drugs were injected either intravenously or directly into the arterial blood supply to the carotid body. We found that catecholamines (dopamine, norepinephrine and epinephrine) inhibited spontaneous chemoreceptor activity, and that alpha adrenergic antagonists abolished both this inhibition and that produced by electrical stimulation of the CSN in the same preparation. Atropine, but not nicotinic antagonists of acetylcholine, consistently blocked neurally induced inhibition but not that produced by catecholamines. Muscarinic agonists had no effect on spontaneous chemoreceptor activity. We conclude that centrifugal activity in the CSN causes release of endogenous catecholamines in the carotid body, and that these catecholamines mediate neurally induced inhibition of chemoreceptor activity is due to the vasomotor effects of acetylcholine.

Acetylcholine↗
PubMed1990

Inhibition of neural crest cell migration by aggregating chondroitin sulfate proteoglycans is mediated by their hyaluronan-binding region.

We have recently shown that the large hyaluronan-aggregating chondroitin sulfate proteoglycan from cartilage (PG-LA) is unfavorable as a substrate for neural crest cell migration in vitro and that this macromolecule inhibits cell dispersion on fibronectin substrates when included in the medium (R. Perris and S. Johansson, 1987, J. Cell Biol. 105, 2511-2521). In this study we present data on the specificity of the migration-repressing activity of PG-LA and data on the molecular mechanisms by which the proteoglycan might impair neural crest cell motility. Soluble PG-LA potently impaired cell migration on substrates of laminin/laminin-nidogen, vitronectin, and collagen types I, III, IV, and VI. When tested in solid-phase binding assays, PG-LA bound avidly to substrates of collagen types I-III and V. Conversely, minimal amounts of the proteoglycan bound to substrates of laminin-nidogen, vitronectin, collagen types IV and VI, and fibronectin or to a proteolytic fragment encompassing its cell-binding domain (105 kDa). Preincubation of these substrates with soluble PG-LA prior to plating of the cells had no effect on their locomotory behavior. These results indicate that PG-LA affects neural crest cell movement primarily through an interaction with the cell surface, rather than by association with the cell motility-promoting substrate molecules. The molecular interaction of soluble PG-LA with neural crest cells was further examined by analyzing the effects of isolated domains of the proteoglycan on cell migration on fibronectin. Addition of chondroitin sulfate chains, the core protein free of glycosaminoglycans, the isolated hyaluronan-binding region (HABr), or a proteolytic fragment corresponding to the keratan sulfate-enriched domain of the PG-LA to neural crest cells migrating on fibronectin or the 105-kDa fibronectin fragment had no significant effect on their motility. After reduction and alkylation, PG-LA was considerably less efficient in perturbing cell movement on fibronectin substrates and virtually ineffective in altering migration on the 105-kDa fragment. In the presence of hyaluronan fragments of 16-30 monosaccharides in length, or an antiserum against the HABr, the migration repressing activity of PG-LA was reduced in a dose-dependent fashion. Furthermore, the inhibitory action of PG-LA was significantly reduced by treatment of the cells with Streptomyces hyaluronidase.(ABSTRACT TRUNCATED AT 400 WORDS)

Ambystoma↗
PubMed1979

The development of inducibility for glutamine synthetase in embryonic neural retina: inhibition by BrdU.

The hydrocortisone-mediated induction of glutamine synthetase (GS) in the neural retina of the chick embryo is a characteristic and unique feature of differentiation of this tissue. The induction involves genomic activity elicited by the inducer resulting in synthesis and accumulation of the enzyme. We describe correlations between the growth of embryonic retina tissue in vivo and in vitro and the development of its inducibility for GS, and demonstrate that this development proceeds through two phases: competence-acquisition phase (before the 7th day of development), and maturation phase. BrdU applied for 24 h to retinas of 5-day embryos irreversibly suppresses the development of induction-competence. However, BrdU does not affect the progressive maturation of inducibility when applied to retinas that already are fully induction-competent (8 days and older). The short treatment with BrdU of 5-day retinas also causes defective histogenesis resulting in drastic malformation of the tissue. The nature of the processes involved in competence-acquisition and in the maturation of inducibility for GS are examined. Possible mechanisms by which BrdU prevents the development of induction-competence for GS in the early embryonic retina and elicits defective histogenesis are discussed.

Animals↗
PubMed1991

Hypovolaemia inhibits acid-induced alkaline transport in the rat duodenum via an alpha-2 adrenergic mechanism.

Acid exposure of the duodenal mucosa is a well-known stimulant of the mucosal alkaline secretion. We have previously reported that a minor blood loss inhibits this secretory increment via activation of the splanchnic nerves. In the present study the pharmacological characteristics of the splanchnic neural inhibition of the alkaline secretion were investigated. Duodenal HCO3- secretion was measured by in-situ titration in chloralose-anaesthetized rats. Exposure of the duodenal mucosa to hydrochloric acid (0.01 M, 5 min) increased the secretion by approximately 60%. A 10% decrease in blood volume simultaneously to the luminal acidification abolished the secretory increase, as previously reported. Treatment with either guanethidine or yohimbine blocked the bleeding-induced inhibition of the secretion after acid-exposure. Neither prazosin nor propranolol did prevent such hypovolaemia-induced inhibition of duodenal alkaline secretion. The present results suggest that the splanchnic neural inhibition of acid-induced duodenal HCO3- secretion is mediated via adrenergic nerve fibres and alpha-2 adrenoceptors.

Animals↗
PubMed1991

Inhibition in the nervous system: models of its roles in choice and context determination.

Neural inhibition has often been regarded as playing an important role in stabilizing and tuning the responses of networks of excitatory neurons. Some partial quantitative bases for this qualitative notion are discussed in the context of current neural network models. Such neural network principles as associative learning, competition, opponent processing, and interlevel resonant feedback are explained and related to behavioral and neurochemical data. Tentative analogies of parts of these model networks with specific neurotransmitter systems are explored; these analogies are likely to become more precise as the networks are further refined.

Animals↗
PubMed1992

Steroid inhibition of neural microvessel morphogenesis in vitro: receptor mediation and astroglial dependence.

Steroid hormones alter several aspects of microvascular function within the CNS. Both microvessel formation and blood-brain barrier expression appear to be influenced by interactions between astrocytes and endothelial cells. To determine if steroids alter astrocyte-endothelial interactions, we studied their effects on astroglial-induced microvessel morphogenesis in vitro. C6 astroglial cells induce bovine retinal microvascular endothelial cells to differentiate into capillary-like structures. Dexamethasone, hydrocortisone, and progesterone at 10 nM inhibited C6-induced microvessel morphogenesis by 75, 35, and 30%, respectively. Inhibition by dexamethasone was both time and concentration dependent, reaching 80-100% at 1 microM. Tetrahydrocortisone and 17 alpha-hydroxyprogesterone had only marginal inhibitory effects. Cortexolone, a glucocorticoid receptor antagonist, blocked inhibition by dexamethasone. Progesterone receptors were expressed in C6 but not bovine retinal microvascular endothelial cells, identifying the astroglial cell as the likely effector of progesterone-mediated inhibition. Astroglial cells were further implicated as the effectors of steroid-mediated inhibition because none of the steroids inhibited astroglial-independent capillary-like structure formation in response to a reconstituted extracellular matrix, Matrigel. These findings are evidence that steroids modulate neural microvascular endothelial cell functions indirectly through perivascular astrocytes via a receptor-mediated mechanism.

Animals↗
PubMed1992

Activation of histamine H3 receptors produces presynaptic inhibition of neurally evoked cat nictitating membrane responses in vivo.

This study was undertaken in order to determine the potential role of prejunctional histamine H3 receptors in an in vivo adrenergic model system. Frequency-dependent nictitating membrane responses were elicited by sympathetic nerve stimulation in anesthetized cats. Systemic administration of the selective histamine H3 receptor agonist, (R)-alpha-methylhistamine (R alpha MeHA) produced a dose-related depression of amplitude of the evoked nictitating membrane responses with a threshold of about 10 micrograms/kg and maximal effect (50% depression at the lowest frequency; 0.5 Hz) seen at 100-300 micrograms/kg. Responses obtained with low frequency stimulation were more sensitive to depression by R alpha MeHA than were responses evoked with higher frequencies of stimulation. Larger doses of R alpha MeHA given to the same animals, failed to produce additional inhibition. R alpha MeHA depressed the amplitude of nictitating membrane responses evoked by either pre- or postganglionic nerve stimulation to an equivalent degree. This depressant action of R alpha MeHA was antagonized by pretreatment with the specific histamine H3 antagonist, thioperamide (3 mg/kg), but not by combined pretreatment with histamine H1 and H2 blockers chlorpheniramine (300 micrograms/kg) and cimetidine (5 mg/kg). Intravenous administration of adrenaline (1-30 micrograms/kg) also produced graded nictitating membrane responses that were not altered by subsequent administration of R alpha MeHA. These results suggest that histamine H3 receptors are involved in the modulation of neurally evoked noradrenaline release in the cat nictitating membrane by an inhibitory presynaptic action.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Inhibition of neural crest cell differentiation by embryo ectodermal extract.

The white mutation in Mexican axolotls has long been thought to be a defect associated with the embryonic extracellular environment, but not with embryonic neural crest cells. Thus it was believed that pigment cells in white axolotls disappear from the skin during early development, not because they are intrinsically defective but because they have no choice but to move into an unfavorable environment. We present evidence to suggest that: (1) white neural crest cells are in fact intrinsically different from dark (wild-type) cells, and (2) an inhibitor is produced in white embryonic ectoderm that actively suppresses the migration, differentiation, and survival of pigment cells in this animal. How these observations fit into the existing body of literature on the white mutant and a model for how the white phenotype might develop are discussed.

Ambystoma mexicanum↗
PubMed1976

Dynamic properties of excitation and two-tone inhibition in the cochlear nucleus studied using amplitude-modulated tones.

The dynamic properties of excitation and two-tone inhibition in the cochlear nucleus were studied from extracellularly recorded unit responses to two simultaneously presented tones. One tone was presented at the unit's characteristic frequency, CF, the other at the unit's best inhibitory frequency, BIF. One or both of the tones were amplitude-modulated with pseudorandom noise. The system under study is in general nonlinear, but can be considered to function as a linear system for small changes in sound intensity around a certain operating point. The dynamic properties are likely to be different at different operating points. A suitable method for the study of dynamic properties of such a system employs tones that are amplitude-modulated with pseudorandom noise. In the present study, the dynamic properties were assessed by cross-correlating the unit discharge rate with the modulation. This was accomplished by computing the cross-covariance function between a period of noise and a period histogram of the discharges, the histogram being locked to the periodicity of the pseudorandom noise. In this way, it has been shown in previous works (Moller, 1973, 1974b), that the cross-covariance function is a valid approximation of the system's impulse response function at a certain sound intensity, provided the modulation is kept at a low value. In the present study the computed cross-covariance function is thus an approximation of the change in discharge rate of the cochlear nucleus units in response to a brief increase in stimulus intensity. As the response of the system under the given circumstances is approximately that of a linear system, the integrated cross-covariance is an approximation of the system's step response function, i.e the change in discharge rate that resulte from a hypothetical step increase in stimulus intensity. The results of the present study can be summarized as follows: 1. The impulse and step response functions computed from the responses to the modulated inhibitory tone of the great majority of units from which recording was made were found to be virtual mirror images of those obtained when the excitatory tone was modulated, the inhibitory response being somewhat smaller in amplitude than the excitatory. 2. When both tones were modulated simultaneously, the step response function was approximately the algebraic sum of the two responses obtained when the tones were modulated singly, further indicating that the system functions as a linear system when the stimulus amplitude is varied slightly around a certain operating point. 3. The shape of the cross-covariance functions is similar for all three stimulus situations, but varies with stimulus intensity and is different in different units. 4. The implication of the results is that the inhibition studied may either originate from the inhibition (suppression) seen in primary fibers or it may be the result of a true neural inhibition in the cochlear nucleus that occurs without any interneurons.

Animals↗
PubMed1991

Partial kindling of the ventral hippocampus: identification of changes in limbic physiology which accompany changes in feline aggression and defense.

This study examined the interictal consequences of partial kindling of the ventral perforant path on attack and defensive behavior in the domestic cat. Partial kindling produced a lasting increase in defense response of cats to both rats and conspecific threat howls. In addition, there was a lasting suppression of approach-attack behaviors directed toward rats. The suppression of some components of approach-attack were shown to be independent of the increases in defensive response. The effects of partial kindling of the ventral perforant path on spread of seizure activity into the amygdala, and on the output of the amygdala to both the ventromedial hypothalamus (VMH) and bed nucleus of the stria terminalis (BNST) were also examined. In addition, the effects of repeated hippocampal seizures on recurrent inhibition in the trisynaptic circuit (areas CA1 and CA3) were investigated. Growth of seizure activity in the amygdala and VMH as partial kindling progressed was essential for behavioral change. In addition, interictal long-term potentiation of potentials evoked in the VMH and in the BNST by pulsed stimulation of the amygdala followed partial kindling or afterdischarge threshold determination in the ventral perforant path. A lasting interictal increase in inhibition in area CA3 and a lasting interictal failure of inhibition in area CA1 of the ventral hippocampus also followed partial kindling. These changes in limbic physiology were related to the behavioral changes produced by partial kindling. The analysis revealed the importance of the amygdalo-VMH pathway in increased defensive response to rats. The amygdalo-BNST pathway is not important in mediating defensive response to prey, but it is implicated in suppression of some types of predatory aggression. Finally, changes in neural inhibition in the ventral hippocampus in areas CA1 and CA3 are associated with changes in both defensiveness and predatory aggression.

Aggression↗
PubMed1992

Nitric oxide as a putative nonadrenergic noncholinergic inhibitory transmitter in the canine pylorus in vivo.

Antropyloroduodenal motility was recorded in seven anesthetized dogs to assess the role of nitric oxide and L-arginine metabolites in nonadrenergic noncholinergic (NANC) mediation of pyloric relaxation. Pyloric activity induced by duodenal field stimulation was inhibited by antral field stimulation and electrical vagal stimulation. Intra-arterial NG-L-arginine-methyl-ester (L-NAME) reduced the inhibition from antral or vagal stimulation (P less than 0.05). Intravenous infusion of L-NAME also blocked the inhibitory effect of vagal and antral stimulation but left the tetrodotoxin-insensitive action of intra-arterial vasoactive intestinal peptide (VIP) and sodium nitroprusside unchanged. L-Arginine reversed the effect of L-NAME whereas D-arginine did not. L-NAME enhanced pyloric contractions to intra-arterial acetylcholine. The NANC inhibition of the substance P-stimulated pyloric response in vitro was blocked by L-NAME and reversed by addition of L-arginine. Sodium nitroprusside was effective as a relaxant in vitro but VIP was not. These data suggest that metabolites of L-arginine mediate neural inhibition of canine pyloric motor activity.

Animals↗