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Role of histamine in the sensory motor integration of gill lateral cell cilia in the bivalve mollusc, Crassostrea virginica (1131.1)
Author(s) -
Akande Patrick,
Duncan Jened,
Catapane Edward,
Carroll Margaret
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.1131.1
Subject(s) - mantle (geology) , sensory system , anatomy , cilium , biology , neuroscience , sensory receptor , escape response , microbiology and biotechnology , paleontology
Lateral gill cells of Crassostrea virginica are innervated by serotonin and dopamine nerves from their ganglia. Most bivalves have lateral cell cilia that respond to serotonin and dopamine. The motor aspects have been well studied, but not the sensory side. There is limited information about sensory inputs. We found C. virginica can sense and adjust gill cilia beating to the presence of food and a variety of chemical cues including histamine (HIS). HIS does not alter beating when applied to gill, but when applied to mantle rim decreases beating. Detaching the mantle rim or transecting the branchial nerve prevents this. We hypothesize HIS is a sensory neurotransmitter in mantle rim involved in sensory‐motor integration of gill lateral cilia. We studied actions of HIS and 3 different classes of HIS receptor antagonists. Cilia beating was measured by stroboscopic microscopy. Adding HIS (10 ‐6 ‐ 10 ‐3 M) to mantle rim decreased cilia beating. H1 antagonist diphenhydramine and H2 antagonist famotidine blocked HIS over the range of 10 ‐3 ‐ 10 ‐9 . Conessine a H3 antagonist did not block HIS. The study further demonstrates a sensory‐motor integration of beating of lateral cilia involving the sensory mantle rim and visceral ganglia and suggests HIS is a sensory neurotransmitter in mantle receptor cells that synapses with afferents going to the VG where signals are integrated resulting in a motor response to the gill lateral cells. Grant Funding Source : NIH‐2R25GM06003, NSF‐0622197, NYSED‐ 0516041071