Premium
Presence of inhibitory GABA receptors on serotonin neurons in the bivalve mollusc Crassostrea virginica (1059.5)
Author(s) -
Welsh Christopher,
Saunders A.C.,
Carroll Margaret,
Catapane Edward
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1059.5
Subject(s) - inhibitory postsynaptic potential , biology , serotonin , serotonergic , neurotransmitter , excitatory postsynaptic potential , glutamate receptor , 5 ht receptor , dopaminergic , neuroscience , receptor , dopamine , medicine , central nervous system , biochemistry
GABA is a major inhibitory neurotransmitter in molluscs and other animals, but has not been well studied in bivalves. In several bivalves, including Crassostrea virginica , beating of gill lateral cilia is controlled by a reciprocal serotonergic‐dopaminergic innervation from their ganglia. Serotonin (HT) increases beating rates, dopamine slows it down. GABA has no direct effects on cilia beating in C. virginica, however, GABA blocked the cilio‐excitation of HT when both are applied to the cerebral ganglia. We hypothesize cerebral and visceral ganglia contain GABA neurons and the cilio‐excitatory HT neurons in the ganglia contain inhibitory GABA receptors. We used immunofluorescence histochemistry to visualize GABA receptors and HT neurons in cerebral and visceral ganglia. Tissues were dissected, snap frozen, sectioned on a cryostat, fixed with paraformaldehyde, treated with blockers, incubated with 1̊ and 2̊ antibodies and viewed with a fluorescence microscope with FITC and Texas Red filters. We found cerebral and visceral ganglia contained GABA neurons and some HT neurons had GABA receptors on their soma. This study confirms our earlier pharmacological studies indicating a role for GABA in this bivalve, working centrally as an inhibitory ganglionic neurotransmitter to inhibit cilio‐excitatory HT neurons that innervate the gill and helps to explain the ganglionic circuitry by which this could be done. Grant Funding Source : NIH‐2R25GM0600309, NYSED‐0516041071, NSF‐0622197