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At least 505 records · Page 28Linked to original sources
PubMed2001

Olfactory perireceptor and receptor events in moths: a kinetic model.

A mathematical model of perireceptor and receptor events has been developed for olfactory sensilla on the antennae of the moth Antheraea polyphemus. The model includes the adsorptive uptake of pheromone molecules by the olfactory hair, their transport on and within the hair by diffusion, the formation of a complex of pheromone and the extracellular pheromone-binding protein (PBP), the interaction of the complex pheromone-PBP with the hypothetical receptor molecule on the plasma membrane of the olfactory cell, the deactivation of the pheromone and, finally, its enzymatic degradation. In the model the PBP with its reduced form (with one or two intramolecular disulfide bonds) first acts as a carrier of the odorant. Later, while the pheromone is bound, it changes to an oxidized form (three disulfide bonds) with a scavenger function (carrier-to-scavenger model). This process of pheromone deactivation rather than the enzymatic pheromone degradation is responsible for the fall of the receptor potential after stimulus offset. The model is based on morphometrical, radiometrical, electrophysiological and biochemical data reported by several authors. The study supports the idea that peripheral events rather than intracellular signalling processes govern the kinetics of the receptor potential in the unadapted receptor cell.

Animals↗
PubMedDate not supplied

[The effect of ouabain on the sugar receptor of the contact chemoreceptive sensilla of the fly Protophormia terraenovae].

Studies have been made on the inhibitory effect of ouabain solutions on bioelectrical activity of the labellar sensillae of flied. It was shown that 10(-2) M ouabain solution irreversibly inhibits the activity, where as 10(-3) and 10(-4) M concentrations decrease the frequency of impulses within 40-60 min. Ouabain solution is a specific stimulator of the sugar receptor of the sensillae with a threshold of 10(-7) M; in combination with 0.2 M glucose, it inhibits impulse activity with the first 200 msec of stimulation. The effect is observed in a narrow zone of ouabain concentrations, with a maximum approximately at 10(-4) M. Differences between the effects of the inhibitor at the vicinity of the onset of generator potential and those in the impulse activity zones on the membrane of the sensory cell are suggested.

Animals↗
PubMed1976

Response plasticity in hamster olfactory bulb: peripheral and central processes.

It is a well-established fact that prolonged odor stimulation leads to marked sensory adaptation. This study demonstrates comparable electrophysiological phenomena occurring at the level of the olfactory receptor and at more central olfactory structures. Recordings of overall receptor response and of olfactory bulb unit responses were made during repeated odor stimulation. During the course of a single, continuous odor presentation response decrements were seen in the EOG (at the olfactory receptors) and were mirrored at the mitral cell layer of the bulb. When brief periods without stimulation were introduced between such odor presentations, receptor responsiveness rebounded to its original level, but mitral cell responses did not. On the basis of this dissociation it is suggested that the pattern of response decrement within the bulb represents a case of stimulus-specific habituation in a simple cortical subsystem and is well worth future investigation as a model of neural plasticity. Surgical disconnection of the olfactory bulb from one or more of its centrifugal inputs results in hyperactive, hyperresponsive mitral cells, which habituate more rapidly and show longer recovery times than do those in the intact bulb. In addition, the synchronization of such units to the inhalation cycle is markedly reduced as compared with normal preparations. These facts together suggest that the habituation of mitral cell activity does not depend on centrifugal inputs, although one or more of such inputs act indirectly in an inhibitory fashion to modulate and tune mitral cell response characteristics.

Adaptation, Physiological↗
PubMed1990

[Fetal respiratory movements and their regulation].

In 1972, fetal breathing movements were clinically rediscovered. Details of their episodic occurrence, frequency, inspired volume, pleural pressure, and the nearly absolute independence of fetal blood gases were investigated in animal experiments. In the human being, there is also an association between fetal breathing and sleep state: fetal breathing movements were confined almost exclusively to periods of REM sleep. The pattern of respiratory frequency changes as gestation progresses; the rates decrease as term approaches. Hardly any breathing movement can be detected during labor. The fetal respiratory centre is capable of rhythmic movements, but there is a lack of response to basic chemical stimuli from the periphery of the body. The association between fetal breathing and REM sleep implies that the connection between breathing and behaviour is already established before birth; but in the fetus, the link between breathing and metabolism is not yet forged. Throughout postnatal life this linkage predominantly regulates breathing. The difference between fetus and newborn in the reaction to chemical stimuli implies a change at birth related to the glomera cells of the carotid bodies. Under the influence of the marked increase in the sympathetic tone there is a major increase in the sensitivity of the receptor cells to oxygen deficiency immediately after birth.

Asphyxia Neonatorum↗
PubMed1982

Cytospecific properties of arterial chemosensory neurons.

The carotid body of the cat was reinnervated either by the carotid branch or by the glossal branch of the IXth nerve and evaluated histologically and neurophysiologically. Regenerating foreign fibers re-established 90% fewer specialized terminals on glomus cells and displayed a greatly diminished chemosensory response, compared to axons of the regenerating carotid branch. Regenerating sensory neurons appear to develop chemosensitivity as a consequence of contact with glomus cells.

Animals↗
PubMed1989

Substance P and neurokinin A in the cat carotid body: localization, exogenous effects and changes in content in response to arterial pO2.

In the present work we studied the occurrence of substance P (SP) and neurokinin A (NKA) in the carotid bodies of cats by means of immunocytochemistry and radioimmunoassay (RIA). We also compared the exogenous effects of SP and NKA on carotid body sensory discharge. SP- and NKA-like immunoreactivities (SP-LI; NKA-LI) were seen in many glomus cells and in a sparse plexus of fine fibers. The SP-LI containing glomus cells and fibers also exhibited NKA-LI, suggesting that both these tachykinins coexist in the carotid body. Chemoreceptor discharge increased both by SP and NKA in a dose-dependent manner. The peak excitation produced by SP and NKA was the same when the effects were compared on an equimolar basis. The tachykinin content of the carotid bodies varied with changes in arterial pO2. During normoxia, SP and NKA levels were 57 +/- 8 and 85 +/- 14 fmol/mg, respectively. When the animals were exposed for 1 h to 100% O2, SP content was unchanged (51 +/- 4 fmol/mg), whereas NKA levels were significantly lower than during normoxia (29 +/- 3 fmol/mg, P less than 0.01). Following 1 h of hypoxia, SP content of the carotid body was 146 +/- 20 fmol/mg, a value higher than that obtained during normoxia and hyperoxia. NKA levels, on the other hand, were not significantly different from normoxic values. These results indicate that the cat carotid body (1) contains both SP and NKA, (2) both peptides augment neural discharge of the carotid body and (3) their levels in the carotid body are substantially altered by arterial oxygen, the natural stimulus to the chemoreceptors.

Action Potentials↗
PubMed1991

Carotid body chemoreception in the absence and presence of CO2-HCO3-.

Carotid body (CB) chemosensory responses to natural and pharmacological stimuli were studied in vitro in the presence and nominal absence of CO2-HCO3- in the perfusion-superfusion media. The CBs obtained from cats (n = 10), anesthetized with sodium pentobarbitone, were simultaneously perfused and superfused with a modified Tyrode solution at 36.5 +/- 0.5 degrees C, equilibrated respectively with PO2 of 120 and less than 20 Torr. The Tyrode, nominally free of CO2-HCO3- (HEPES-NaOH, pH 7.38, 310 mOsm), was used first. Subsequently the Tyrode containing HEPES-HCO3-, equilibrated with PCO2 of 36.8 Torr (pH 7.38) was used. Chemosensory discharges were recorded from the carotid sinus nerve. Both hypoxia (PO2 = 20-25 Torr) and ischemic hypoxia stimulated the discharge in the absence and presence of CO2-HCO3-. However, the presence of CO2-HCO3- significantly raised the baseline activity, augmented the speed, sensitivity and the maximal responses to both types of hypoxia. Hypercapnic perfusate (PCO2 = 65 Torr at pH 7.17) produced a peak response equally promptly in the absence and presence of CO2-HCO3- in the ongoing perfusate but generated a larger and more sustained response. Presence of CO2-HCO3- strongly potentiated the responses to cyanide (10(-10)-10(-7) mol) but less strikingly the responses to nicotine (10(-11)-10(-8) mol). Thus, the extracellular CO2-HCO3- significantly improved the response to hypoxia but was not essential for O2 chemoreception. The underlying mechanisms of the effect of CO2-HCO3- is likely to be mediated by the Cl(-)-HCO3- anion exchanger in the pH regulation of glomus cells.

Animals↗
PubMed1999

Activation of an anatomically distinct subpopulation of accessory olfactory bulb neurons by chemosensory stimulation.

Chemosensory cues known as pheromones play a key role in rodent reproductive physiology and social interactions. Pheromone molecules are detected by receptor cells located in the vomeronasal organ and conveyed exclusively to the accessory olfactory bulb, and then to limbic and hypothalamic sites for integration with other factors modulating reproductive physiology. We report here that chemosensory cues from the female mouse selectively activate a subpopulation of cells located in the anterior part of the accessory olfactory bulb of the male mouse. Exposure of male mice to female-soiled bedding resulted in a massive induction of c-fos expression, which was primarily confined to neurons located in the anterior part of the accessory olfactory bulb and was eliminated by removal of the vomeronasal organ. Exposure of the male to soiled bedding from a different stain of male mice also elevated c-fos expression, but immunoreactive cells were more evenly distributed along the anterior-posterior axis of the accessory olfactory bulb. No treatment effects were observed in the main olfactory bulb. Previous studies have indicated that vomeronasal receptor neurons are divided into two populations based on location within the organ, site of termination in the accessory olfactory bulb, second messenger content and putative pheromone receptor expression. The present study suggests that the two populations of vomeronasal receptor neurons detect different chemosensory stimuli. Since male mouse- and female mouse-specific urinary substances modulate different aspects of male mouse behavior, the present results suggest that anatomically segregated populations of vomeronasal organ receptor cells modulate distinct behavioral patterns.

Animals↗
PubMed1985

The brain of the planarian as the ancestor of the human brain.

The planarian is the simplest living animal having a body plan of bilateral symmetry and cephalization. The brain of these free-living flatworms is a bilobed structure with a cortex of nerve cells and a core of nerve fibres including some that decussate to form commissures. Special sensory input from chemoreceptors, photoreceptor cells of primitive eyes, and tactile receptors are integrated to provide motor responses of the entire body, and local reflexes. Many morphological, electrophysiological, and pharmacological features of planarian neurons, as well as synaptic organization, are reminiscent of the vertebrate brain. Multipolar neurons and dendritic spines are rare in higher invertebrates, but are found in the planarian. Several neurotransmitter substances identified in the human brain also occur in the planarian nervous system. The planarian evolved before the divergence of the phylogenetic line leading to vertebrates. This simple worm therefore is suggested as a living example of the early evolution of the vertebrate brain. An extraordinary plasticity and regenerative capacity, and sensitivity to neurotoxins, provide unique opportunities for studying the reorganization of the nervous system after injury. Study of this simple organism may also contribute to a better understanding of the evolution of the human nervous system.

Animals↗
PubMed1995

The perception of saltiness is eliminated by NaCl adaptation: implications for gustatory transduction and coding.

The tastes of salts to humans are complex. NaCl is the most purely salty of all salts, but even this stimulus tastes sweet at low concentrations and somewhat sour at mid-range intensities. Other salts taste significantly sour or bitter in addition to salty. Previous studies have shown that the saltiness of simple halide salts is reduced by adaptation to NaCl, suggesting that a single mechanism might be responsible for the salty taste of these stimuli. In electrophysiological studies in rodents, the response to NaCl is reduced by application to the tongue of the Na(+)-channel blocker amiloride. Organic Na+ salts are more heavily dependent on this amiloride-sensitive transduction component than NaCl, and are generally less salty and more sour. In order to investigate the relationship between NaCl saltiness and that evoked by other salts, we adapted the tongue to distilled H2O and to 0.1 M NaCl and obtained direct magnitude estimates of the taste intensity of 15 organic and inorganic Na+, Li+, K+ and Ca2+ salts, matched for total intensity. Subjects divided these magnitude estimates among the component taste qualities. Adaptation to NaCl abolished the taste of NaCl and LiCl, and eliminated the saltiness of all other salts. The magnitude estimates of the bitterness and sourness of many salts increased after NaCl adaptation. Since recent biophysical data suggest that adaptation in taste receptors may involve whole-cell mechanisms, we propose that saltiness is reduced by NaCl adaptation because it originates in the subset of taste receptors responsive to NaCl. This implies that saltiness is coded within the CNS in cells whose receptive fields include the NaCl-sensitive receptor cells and that the degree to which any salt tastes salty is determined by its ability to drive these receptors. This model proposes, for example, that KCl has a salty component because it stimulates some of the same receptor cells as NaCl, even though the transduction mechanisms for KCl are different than those engaged by NaCl. Adaptation to NaCl blocks the saltiness of KCl and other salts because they stimulate NaCl-sensitive receptor cells.

Adaptation, Psychological↗
PubMed1999

Diet-induced plasticity in the taste system of an insect: localization to a single transduction pathway in an identified taste cell.

We studied exposure-induced sensitivity changes in an identified taste cell from Manduca sexta, a herbivorous caterpillar. This taste cell occurs within the lateral styloconic sensillum and responds selectively to compounds that humans characterize as bitter (e.g. caffeine, salicin and aristolochic acid). We made extracellular recordings from several classes of identified taste cell within the lateral sensillum, both before and after dietary exposure (for 48 h) to a suprathreshold concentration of caffeine, salicin or aristolochic acid. Our results revealed (1) that dietary exposure to caffeine desensitized the bitter-sensitive taste cell to caffeine, whereas dietary exposure to salicin or aristolochic acid did not desensitize the same taste cell to salicin or to aristolochic acid; (2) that dietary exposure to caffeine failed to alter the responsiveness of the sugar-, salt- or inositol-sensitive taste cells within the same sensillum; (3) that the caffeine-induced desensitization phenomenon generalized to salicin, a compound that stimulates the same transduction pathway as caffeine, but not to aristolochic acid, a compound that stimulates a different pathway; and (4) that chronically stimulating the lateral sensillum with caffeine, in the absence of ingestion, was sufficient to induce desensitization. We conclude that caffeine causes desensitization through a direct effect on a single transduction pathway within the bitter-sensitive taste cell.

Animals↗