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5-HT receptors on identified Lymnaea neurones in culture. Pharmacological characterization of 5-HT1A receptors
Affiliation:1. Department of Biology, University of Virginia, Charlottesville, VA 22904, USA;2. Division of Embryology and Genetics, Institute for Amphibian Biology, Hiroshima University, Higashihiroshima 739-8526, Japan;3. Department of Cellular Biology, University of Georgia, Athens, GA, 30602, USA;4. Department of Ophthalmology, University of Virginia School of Medicine, Charlottesville, VA 22908, USA;1. Department of Neurobiology and Anatomy, W.M. Keck Center for the Neurobiology of Learning and Memory, McGovern Medical School at the University of Texas Health Science Center, Houston, TX 77030, USA;2. Department of Biology, Case Western Reserve University, Cleveland, OH 44106-7080, USA;3. Department of Neurosciences, Case Western Reserve University, Cleveland, OH 44106-7080, USA;4. Department of Biomedical Engineering, Case Western Reserve University, Cleveland, OH 44106-7080, USA;5. Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109, USA
Abstract:The ability of the selective 5-HT1A receptor agonist R(+)-8-hydroxydipropylaminotetralin hydrobromide (8-OH-DPAT) to bind with 5-HT receptor(s) on cultured, identified neurones in Lymnaea stagnalis was examined. The identified neurones studied were from the buccal ganglia and the serotonin-containing cerebral giant cells (CGCs). 5-HT and its agonists were applied from puffer pipettes, whilst 5-HT antagonists were applied in the bathing medium. At 10−3 M, the 5-HT1A agonist, always produced paroxysmal depolarizing shifts (PDS) while at a lower concentration (10−4 M), it always mimicked the effects of 10−3 M 5-HT. 8-OH-DPAT (10−4 M) and 5-HT 10−3 M produced dose-dependent increases in the responses they evoked. At 10−4 M, the 5-HT3 receptor agonist 1-(m-chlorophenyl)-biguanide hydrochloride (m-CPBG), failed to hyperpolarize most of the neurones hyperpolarized by 5-HT. At 10−4 M, the antagonists ketanserin (5-HT2), MDL 72222 (5-HT3), and pindobind-5-HT1A (5-HT1A) consistently abolished spike generation ii spontaneously active neurones. Both ketanserin and MDL 72222 failed to block the actions of 8-OH-DPAT and only partially blocked those of 5-HT, but pindobind-5-HT1A completely, but reversibly,blocked the 8-OH-DPAT effects while greatly reducing those of 5-HT. These results suggest that 5-HT1A receptor subtypes might be involved in the hyperpolarizing responses of the CGCs and their follower motor neurones in the buccal ganglia of Lymnaea stagnalis to 5-HT. The presence of 5-HT1A receptors on these neurones can be considered to correspond with those found in mammals because their pharmacological responses resemble those of mammalian 5-HT1A receptors.
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