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An aplysia dopamine 1 ‐like receptor: molecular and functional characterization
Author(s) -
Barbas Demian,
Zappulla Jacques P.,
Angers Stéphane,
Bouvier Michel,
Mohamed Habib A.,
Byrne John H.,
Castellucci Vincent F.,
DesGroseillers Luc
Publication year - 2006
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2005.03561.x
Subject(s) - dopamine , aplysia , agonist , neurotransmitter , biology , dopamine receptor , endogenous agonist , receptor , medicine , dopamine receptor d1 , endocrinology , stimulation , inhibitory postsynaptic potential , microbiology and biotechnology , neuroscience , chemistry , biochemistry
In Aplysia , the neurotransmitter dopamine is involved in the regulation of various physiological processes and motor functions, like feeding behaviour, and in the siphon‐gill withdrawal reflex. In this paper, we report the characterization of the first Aplysia D 1 ‐like dopamine receptor (Ap dop1 ) mainly expressed in the CNS, heart and buccal mass. Following expression of the Ap dop1 receptor in HEK293 cells, a higher level of cAMP was observed in the absence of the receptor ligand, showing that Ap dop1 is constitutively active. This activity was blocked by the inverse agonist flupentixol. Application of dopamine (EC 50 of 35 n m ) or serotonin (EC 50 of 36 μ m ) to Ap dop1 ‐transfected HEK293 cells further increased the level of cAMP, suggesting that the receptor is linked to the stimulatory G s protein pathway. When expressed in cultured sensory neurons, Ap dop1 immunoreactivity was observed in the cell body and neurites. Control sensory neurons responded to dopamine with a decrease in excitability mediated by a pertusis toxin‐sensitive G protein. Expression of Ap dop1 produced an increase in hyperpolarization in the absence of agonist and an increase in membrane excitability following stimulation by dopamine. In the presence of pertussis toxin to inhibit the G i protein inhibitory pathway responsible for decrease in excitability mechanism, Stimulation of membrane excitability was observed. Ap dop1 sensitivity to dopamine makes it a potential modulator of operant conditioning procedure.