The action of serotonin on excitatory nerve terminals in lobster nerve‐muscle preparations.

Abstract

1. The action of serotonin on excitatory transmission in the opener muscle of the dactyl of the lobster walking leg was examined by intracellular recording techniques. 2. Serotonin, at concentrations as low as 5 x 10(‐9) M, caused a sustained increase in the size of the excitatory junctional (synaptic) potential (e.j.p.). When serotonin was washed out of the bath the e.j.p. declined in two steps (T 1/2 approximately equal to 1‐2 min; T 1/2 approximately equal to 30 min) to the control size. The increased e.j.p. size was predominantly due to a serotonin‐induced increase in the release of quanta of excitatory transmitter with nerve stimulation. 3. The increase in transmitter release did not require nerve stimulation or the presence of Na+ or Ca2+ ions in the bathing medium during the period of serotonin treatment. 4. Three types of experiments suggested that a part of the action of serotonin on excitatory nerve terminals might involve a long‐term metabolic change within terminals, possibly involving the buffering or storage of Ca2+ ions. First, serotonin increased the frequency of spontaneous release of transmitter in both normal saline (26 mM‐Ca2+) and saline with very low levels of Ca2+ (less than 10(‐8) M). Secondly, serotonin greatly potentiated increases in miniature excitatory junctional potential frequency induced by the loading of the nerve terminal with Na+ either by veratridine or by inhibition of the Na+ pump or by the addition of the Na‐ionophore monensin in low‐Ca2+ salines. Thirdly, in some experiments, serotonin treatment produced a partial restoration of the nerve‐evoked release of transmitter in the low‐Ca2+ medium (less than 10(‐8) M).

The actions of serotonin on frog primary afferent terminals and cell bodies

“…However, depolarization per se cannot be equated with presynaptic inhibition since the Mn 2+ sensitivity of serotonin's direct action suggests an effect of 5-HT on a calcium sensitive process. An influence of 5-HT on calcium entry or mobilization could lead to presynaptic inhibition, as has been proposed for cultured chick DRG cell 5-HT responses (Dunlap and Fischbach, 1978;Fischback et al, 1981), or presynaptic facilitation as has been proposed for molluscan ganglion cell (Klein and Kandel, 1978), and lobster neuromuscular junction (Glusman and Kravitz, 1982) 5-HT responses. Additionally, the repetitive firing of primary afferents during 5-HT depolarizations suggests that transmission in afferent terminal arborizations may be altered by serotonin's influence on spike generation.…”

Serotonin and the Small Cardioactive Peptides Differentially Modulate Two Motor Neurons That Innervate the Same Muscle Fibers inAplysia

“…At both crayfish and lobster skeletal muscles, 5HT has been shown to facilitate EJPs (Dudel, 1965;Kravitz et al, 1980;Glusman and Kravitz, 1982;Dixon and Atwood, 1985). This effect has been shown to be mediated by an increase in transmitter release, perhaps involving a change in presynaptic calcium metabolism.…”

Heart rate within male crayfish: social interactions and effects of 5-HT

“…Two particular monoamines, 5-HT and octopamine, are released into the animal's hemolymph from neuro-secretory organs (Evans et al, 1976;Livingston et al, 1980). 5-HT affects motor nerve terminals, in general, by increasing transmitter release (Florey and Rathmayer, 1978;Fischer and Florey, 1982;Glusman and Kravitz, 1982), but the behavioral extension or flexion of extremities is thought to result from selective modification of CNS output (Livingston et al, 1980;Harris-Warrick and Kravitz, 1984). Due to experimental difficulties by inadvertently stressing the animals when taking samples of hemolymph to test 5-HT levels while the animals are behaving, direct measures have not yet been forthcoming that relate intrinsic levels of biogenic amines to behaviors.…”