PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 38131

Action of putative neurotransmitters in the guinea pig cochlea.

S D Comis·G Leng
View original source ↗Export metadata ↓

Abstract

Scala tympani of the guinea pig was perfused with artificial perilymph containing putative transmitter substances. Single auditory nerve fibre activity was recorded during these perfusions and the responses of these fibres were studied using computer-controlled routine. Acetylcholine significantly inhibited tone-induced responses of a large proportion of the fibres tested. Glutamate appeared to be a potent depolarising agent when applied in concentrations between 2 and 10 mM. Noradrenaline did not affect tone-induced activity, but inhibited the spontaneous activity of some fibres. The results support the view that acetylcholine is the transmitter at synapses of the olivocochlear bundle, and that glutamate may be involved in the afferent synapse. The data do not support the hypothesis that noradrenaline is the afferent transmitter.

Explore related subjects

AcetylcholineAcoustic StimulationAnimalsAspartic AcidAuditory PathwaysCochleaEvoked PotentialsGlutamatesGuinea PigsNerve FibersNeurotransmitter AgentsNorepinephrineOlivary NucleusVestibulocochlear NerveJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S D Comis, G Leng. 1979-06-01. Action of putative neurotransmitters in the guinea pig cochlea.. https://doi.org/10.1007/bf00238472

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1979

Interaction of local anesthetics with Torpedo californica membrane-bound acetylcholine receptor.

The effects of local anesthetics on the rate of the agonist-induced increase in ligand affinity of membrane-bound acetylcholine receptor from Torpedo californica were examined. The rate of the transition in receptor affinity was determined by following the time-dependent increase in inhibition of iodinated alpha-bungarotoxin binding caused by 1 microM carbamylcholine. At concentrations below those that directly inhibited the binding of iodinated alpha-bungarotoxin, dibucaine increased the rate of the transition to a high-affinity state and tetracaine decreased this rate. The measured rate constants were 0.026 +/- 0.008 s-1 in the presence and 0.010 +/- 0.002 s-1 in the absence of dibucaine while tetracaine decreased the rate to 0.006 +/- 0.002 s-1 as compared to a control value of 0.012 +/- 0.003 s-1. A parallel was observed between the effectiveness of a compound in increasing or decreasing the rate of the agonist-induced transition in affinity and the change in its apparent inhibition constant in the presence of carbamylcholine (increase or decrease) measured by the displacement of tritiated perhydrohistrionicotoxin. This parallel could be explained by assuming (a) that local anesthetics bound directly to the specific histrionicotoxin binding site or (b) that they bound to a different site and the observed effects were caused by conformational changes.

Acetylcholine↗
PubMed1979

Ca2+-dependent protein phosphorylation of purely cholinergic Torpedo synaptosomes.

Preincubation of intact, purely cholinergic Torpedo synaptosomes with [32P]Pi results in the incorporation of 32P into about 10 specific proteins. Depolarizing the Torpedo synaptosomes by a high K+ buffer or treatment with the Ca2+ ionophore A23187 result in Ca2+ uptake, in acetylcholine (ACh) release, and in a marked increase of 32P incorporation into a specific protein band with an apparent subunit molecular weight of 100,000 (band alpha). The kinetics of synaptosomal 45Ca2+ uptake, of 32P incorporation into band alpha, and of ACh release is similar and reach maximal values about 45 s after the synaptosomes have been treated. Sr2+ and Ba2+ can replace Ca2+ in evoking both K+ depolarization-dependent ACh release and 32P incorporation into band alpha. The effectiveness of these ions (Ca2+ greater than Sr2+ greater than Ba2+) is similar in both cases. The data presented suggest that Ca2+ accumulation by Torpedo synaptosomes leads to an increase in the phosphorylation of a specific protein and to ACh release. This phosphoprotein may be involved in the regulation of presynaptic processes which underly ACh release.

Acetylcholine↗