Effect of serotonergic afferents on quantal release at central inhibitory synapses.
Although most examples of modulation of synaptic transmission have been obtained from excitatory rather than from inhibitory connections, serotonin (5HT) is now shown to cause a presynaptic facilitation of release of the inhibitory neurotransmitter glycine. Brief local injections of this amine, or application of a 5HT uptake blocker, produce a long-lasting enhancement of both spontaneous and evoked inhibitory currents in the teleost Mauthner cell. Quantal analysis showed that the probability of release is increased. Focal recording indicated that 5HT acts directly on the inhibitory terminals, possibly reducing potassium conductances. Double staining with specific antibodies demonstrated a morphological substrate for this effect. Nerve endings that contain 5HT contact inhibitory terminals directly apposed to postsynaptic glycine receptors.
Mintz
I
I
INSERM U261, Département des Biotechnologies, Institut Pasteur, Paris, France.
Gotow
T
T
Triller
A
A
Korn
H
H
D000344:Afferent Pathways; D000818:Animals; D005998:Glycine / Q000378:metabolism*; D006054:Goldfish; D008564:Membrane Potentials; D008839:Microelectrodes; D015221:Potassium Channels / Q000378:metabolism; D012701:Serotonin / Q000502:physiology*; D013569:Synapses / Q000502:physiology*
D015221:Potassium Channels; D012701:Serotonin; D005998:Glycine