The University of Southampton
University of Southampton Institutional Repository

Adenosine, dopamine and octopamine pharmacology of identified Helix asperacentral neurones

Adenosine, dopamine and octopamine pharmacology of identified Helix asperacentral neurones
Adenosine, dopamine and octopamine pharmacology of identified Helix asperacentral neurones

Electrophysiological recordings were made from identified neurones in the isolated suboesophageal ganglionic mass of Helix aspersa. The modulatory effects of adenosine (AD) and its derivatives were studied in detail. The dopamine (DA) and Octopamine (OA) inhibitory responses were investigated and compared. Bath applied AD (60-600nM) depressed the depolarisation induced in cell F1 by bath or iontophoretically applied Acetylcholine (Ach). If the proportion of the Ach response that was carried by calcium ions was increased, the percentage depression of this response by AD was significantly greater. A residual Ach induced inward current was observed in sodium free/high calcium Ringer. This Ach induced current was antagonised by cobalt or verapamil suggesting that it was calcium mediated. This residual current was also completely abolished by 0.6μM AD. The depressive effect of AD on the Ach response was blocked by 8 - Phenyltheophylline and is believed to be mediated by an A_1 receptor. Lower bath concentrations of AD (0.6-6nM) and also Adenosine Triphosphate (ATP) and its analogue α, β Methylene ATP enhanced the Ach excitatory response of F1. The potency ranking of AD and its 2 analogues L-phenylisopropyladenosine (L-PIA) and N-5'Ethylcarboxamideadenosine (NECA) was the same as that described for an A_2 receptor. The possible physiological role of these two modulatory effects of AD is discussed. The DA and OA inhibitory responses were both shown to be potassium mediated events. They were preferentially antagonised by low micromolar concentrations of the potassium channel antagonist by low micromolar concentrations of the potassium channel antagonist 4-Aminopyridine. Bath addition of dibutyrylcyclic Adenosine 5' Monophosphate caused a time dependent enhancement of an evoked dopaminergic-IPSP and the DA and OA induced outward currents. Two compounds which alter Adenylate cyclase activity, Forskolin and MDL 12,330A, also modulated these responses. Cell sensitivity to DA or OA was greatly enhanced in calcium free/2mM cobalt Ringer. The reversal potential of the DA response was shifted to a more negative value in calcium free Ringer. Sodium free Ringer was also found to alter the responses to DA or OA, but these results were more variable. The DA and OA inhibitory responses are contrasted and compared. The possible classification of the receptor mediating the Helix Da inhibitory response is also discussed. (D72314/87)

University of Southampton
Cox, Rosalind Tania Lucia
Cox, Rosalind Tania Lucia

Cox, Rosalind Tania Lucia (1986) Adenosine, dopamine and octopamine pharmacology of identified Helix asperacentral neurones. University of Southampton, Doctoral Thesis.

Record type: Thesis (Doctoral)

Abstract

Electrophysiological recordings were made from identified neurones in the isolated suboesophageal ganglionic mass of Helix aspersa. The modulatory effects of adenosine (AD) and its derivatives were studied in detail. The dopamine (DA) and Octopamine (OA) inhibitory responses were investigated and compared. Bath applied AD (60-600nM) depressed the depolarisation induced in cell F1 by bath or iontophoretically applied Acetylcholine (Ach). If the proportion of the Ach response that was carried by calcium ions was increased, the percentage depression of this response by AD was significantly greater. A residual Ach induced inward current was observed in sodium free/high calcium Ringer. This Ach induced current was antagonised by cobalt or verapamil suggesting that it was calcium mediated. This residual current was also completely abolished by 0.6μM AD. The depressive effect of AD on the Ach response was blocked by 8 - Phenyltheophylline and is believed to be mediated by an A_1 receptor. Lower bath concentrations of AD (0.6-6nM) and also Adenosine Triphosphate (ATP) and its analogue α, β Methylene ATP enhanced the Ach excitatory response of F1. The potency ranking of AD and its 2 analogues L-phenylisopropyladenosine (L-PIA) and N-5'Ethylcarboxamideadenosine (NECA) was the same as that described for an A_2 receptor. The possible physiological role of these two modulatory effects of AD is discussed. The DA and OA inhibitory responses were both shown to be potassium mediated events. They were preferentially antagonised by low micromolar concentrations of the potassium channel antagonist by low micromolar concentrations of the potassium channel antagonist 4-Aminopyridine. Bath addition of dibutyrylcyclic Adenosine 5' Monophosphate caused a time dependent enhancement of an evoked dopaminergic-IPSP and the DA and OA induced outward currents. Two compounds which alter Adenylate cyclase activity, Forskolin and MDL 12,330A, also modulated these responses. Cell sensitivity to DA or OA was greatly enhanced in calcium free/2mM cobalt Ringer. The reversal potential of the DA response was shifted to a more negative value in calcium free Ringer. Sodium free Ringer was also found to alter the responses to DA or OA, but these results were more variable. The DA and OA inhibitory responses are contrasted and compared. The possible classification of the receptor mediating the Helix Da inhibitory response is also discussed. (D72314/87)

This record has no associated files available for download.

More information

Published date: 1986

Identifiers

Local EPrints ID: 460801
URI: http://eprints.soton.ac.uk/id/eprint/460801
PURE UUID: e0edb363-1cd9-4664-831d-eadcd45b8841

Catalogue record

Date deposited: 04 Jul 2022 18:29
Last modified: 04 Jul 2022 18:29

Export record

Contributors

Author: Rosalind Tania Lucia Cox

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×