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Synaptic Vesicle Depletion in Reticulospinal Axons is Reduced by 5‐hydroxytryptamine: Direct Evidence for Presynaptic Modulation of Glutamatergic Transmission
Author(s) -
Shupliakov O.,
Pieribone V. A.,
Gad H.,
Brodin L.
Publication year - 1995
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1995.tb01099.x
Subject(s) - synaptic vesicle , glutamatergic , lamprey , neuroscience , neurotransmission , axon , axon terminal , synaptic pharmacology , chemistry , glutamate receptor , vesicle , synapse , active zone , neurotransmitter , inhibitory postsynaptic potential , biology , synaptic augmentation , biophysics , excitatory postsynaptic potential , central nervous system , biochemistry , receptor , membrane , fishery
Abstract 5‐hydroxytryptamine (5‐HT; serotonin) is known to depress glutamatergic synaptic transmission in the spinal cord of vertebrates. To test directly whether 5‐HT inhibits synaptic glutamate release, we examined its effect on the ultrastructure of synaptic vesicle clusters in giant reticulospinal axons in a lower vertebrate (lamprey; Lampetra fluviatilis ). The size of these axons makes it possible to selectively expose only a part of the presynaptic element to 5‐HT, while another part of the same axon is maintained in control solution. Action potential stimulation at 20 Hz for 20 min caused a marked reduction in the number of synaptic vesicles in active zones maintained in control solution, while in the part exposed to 5‐HT (20 μM) the number of synaptic vesicles per active zone was ‐3‐fold higher. In contrast, 5‐HT had no effect on the number of vesicles in resting axons. To examine whether 5‐HT acts by reducing presynaptic Ca 2+ influx, intra‐axonal recordings of Ba 2+ potentials were performed. No reduction of the axonal Ba 2+ potential could be detected after application of 20 or 200 pM 5‐HT. The present results show that 5‐HT reduces the rate of synaptic exocytosis in reticulospinal axons. The effect appears to be mediated by a mechanism distinct from the presynaptic Ca 2+ channels.