Biomedical subjects

J C Delaleu

Publications and source records attributed to J C Delaleu.

6 recordsLinked to original sources

PubMed1988

The activity of olfactory receptor cells is affected by acetylcholine and substance P.

The effects of acetylcholine (ACh) and substance P (SP) on the unit activity of receptor cells recorded from the superfused frog olfactory mucosa were studied. Single neurones were excited or, more rarely, depressed by the application of chemicals. Cholinergic antagonists were used to investigate the involvement of nicotinic and muscarinic receptors in the recorded responses. The ACh-evoked firing was antagonized by D-tubocurarine (D-TC), atropine (ATR) and SP. Responses to SP appeared to be D-TC resistant, but activation by the peptide was moderately antagonized by ATR. The results suggest that ACh and SP could affect the functioning of the olfactory receptor cells.

Acetylcholine↗

PubMed1987

Olfactory receptor cell function is affected by trigeminal nerve activity.

In the frog, antidromic electrical stimulation of the ophthalmic branch of the trigeminal nerve (NV-ob) evokes a slow potential in the olfactory mucosa, modifies the activity of receptor cells and modulates the responses to odour. Substance P (SP) application evokes similar electrical responses. These results imply that the functioning of the olfactory system might be controlled at the receptor cell level. It is suggested that the trigeminal system could modulate the activity of the olfactory receptor cells via a local axon reflex which may result in the release of SP.

Animals↗

PubMed1979

Olfactory receptor cell activity under electrical polarization of the nasal mucosa in the frog. I. Spontaneous activity.

The electrical activity of single olfactory receptor cells was studied under electrical polarization of the olfactory epithelium in the frog. 1. The spontaneous discharge frequency varied as a linear function of the polarizing current in the range 1--20 X 10(--6)A. 2. Surface positive polarizations caused the spike activity to increase; surface-negative polarizations suppressed the activity. 3. Partial accommodation to the current was observed. 4. After-effects of short duration occurred: Rebound suppression after positive polarization, rebound excitation after negative polarization. 5. A high percentage of receptor units found in the frog's mucosa displayed no spontaneous activity.

Animals↗

PubMed1976

Contribution of an electrogenic pump to the resting membrane polarization in a crustacean heart.

1. In the neurogenic heart of the isopod crustacean Porcellio dilatatus, external K+ removal depolarized the membrane (K0 effect) whereas subsequent restoration of K+ resulted in a rapid hyperpolarization (K1 effect). 2. The amplitude of the K1 effect depended on the duration of the prior K+ deprivation and on the subsequent K+ concentration. 3. The membrane resistance slightly increased during the K0 effect; during the K1 effect, it only returned to its control value. 4. Ouabain, cooling and replacement of external Na+ by Li+ also produced depolarization. 5. The K1 effect was suppressed by ouabain and markedly depressed by lowering the temperature to 4-6 degrees C. It was abolished if Li+ replaced Na+ during the prior privation of K+; moreover Li+ was unable to act as a substitute for external K+ in generating the K1 effect if used at equivalent concentration, but enhanced the effect at high concentration. 6. The findings are consistent with the presence of an electrogenic sodium pump in the myocardium of Porcellio contributing to the resting membrane potential. 7. Changes in the spontaneous rhythm observed during K0 and K1 are further suggestive of the presence of an electrogenic Na+ pump in the pacemaker neurons of the cardiac ganglion. Another explanation is also proposed. 8. The magnitude of the spontaneous contractions of the heart was increased during the K0 effect and markedly decreased during the K1 effect. An indirect effect of the changes in internal Na+ concentration on the contractile processes is suggested.

Animals↗

PubMed1976

Neural regulation of the heart muscle in an isopod crustacean: acceleration and peripheral inhibition.

1. In the neurogenic heart of the isopod crustacean Porcellio dilatatus, repetitive electrical stimulation of the cardiac nerves elicted either cardio-acceleratory or cardio-inhibitory effects depending on the stimulation parameters. 2. Acceleratory effects were accompanied by a decrease of membrane potential and by changes in the contour of the spontaneous electrical responses: increase in the speed of the rising phase and enhancement of the plateau phase. 3. Inhibitory stimulation acted on rhytjmicity and/or contour of spontaneous responses. At stimulation pulse frequencies beyond 25/s a hyperpolarization appeared after the cessation of the inhibitory train. 4. Inhibitory stimulation elicted IJPs in the myocardium. Their reversal potential was found to be close to the value of the resting membrane potential. During inhibitory stimulation, the membrane resistance of the heart muscle was frequently decreased. 5. The effects of changing the external chloride content, and of adding GABA and picrotoxin support the hypothesis that the inhibitory impulses increased the myocardium permeability to CL-. 6. On the basis of these findings it is assumed that cardio-inhibitory fibres act on both cardiac ganglion and myocardium. 7. Comparisons are established between the wood-louse's heart and the skeletal or heart muscle of some arthropods. The functional significance of peripheral inhibition is further discussed in relation to the nature of the spontaneous electrical responses and to contraction.

Animals↗

PubMed1976

Evidence for a synaptically mediated decrease in conductance in a crustacean myocardium.

1. In the neurogenic heart of the isopod Porcellio dilatatus, electrical stimulation of the cardio-regulatory nerves at rates greater than 20-25 pulses/s elicited inhibitory junctional potentials (IJPs) in the myocardium. Its cessation was followed by a long lasting hyperpolarization of myocardial membrane (post-stimulus hyperpolarization = PSH). 2. During the PSH the membrane resistance of the heart muscle increased. The PSH was enhanced by myocardium hyperpolarization, decreased by depolarization and reversed around -50 mV. 3. Picrotoxin inhibited the summated IJPs elicited by the stimulation and thus caused the membrane to maximally hyperpolarize during inhibitory train, thus suggesting a composite nature of the inhibitory processes. 4. The PSH was reversibly reduced in K+-free saline or in ouabain containing saline but partial restoration was obtained by injection of inward current to the myocardium. 5. The PSH was abolished in lithium saline and reduced in Na+-deficient (choline) solution. Cl-deficient solution that markedly affected the summated IJPs shortly after its introduction did not affect the PSH. 6. It is proposed that the PSH results from a decrease in conductance, presumably to both Na+ and K+. The implication of such a mechanism as a component of the inhibitory regulation of this crustacean heart is discussed.

Animals↗