Factors affecting release of 3H-dopamine from perfused carp retina

Abstract

The effects of putative retinal neurotransmitters and several neuropeptides on 3H-dopamine release from isolated perfused carp (Cypriuus curpio) retinas were studied. Of the transmitter candidates tested, only serotonin (S-HT) and the 5-HT agonist tryptamine released "H-dopamine. However, the release evoked by these agents was calcium (Ca*+) independent and not blockable by the 5-HT antagonist methysergide. We also investigated the antagonism of inhibitory inputs as a potential regulatory mechanism for dopamine release and found that the GABA antagonists, bicuculline and picrotoxin, stimulated a dose-dependent release of 3Hdopamine. The effects of the GABA antagonists were dependent on extracellular Ca*+ and could be inhibited by perfusion of the retina with GABA. Bicuculline and picrotoxin also stimulated an increase in CAMP accumulation, which was inhibited by the dopamine antagonist haloperidol. Our results support the hypothesis that the dopaminergic interplexiform cells of the teleost retina are under GABAergic inhibitory control.

Dopamine in the rabbit retina and striatum: Diurnal rhythm and effect of light stimulation

“…1980). Althought DA release from the vertebrate retina stimulated by both potassium ions (Thomas et al, 1978;Bauer et al, 1980;Frederick et al, 1982), electric current (Dubocovich and Weiner, 1981;Nowak, 1987), and some compounds (O'Connor et al, 1986) has been described in detail by many authors, that evoked by light was studied only in few laboratories. Thus, Kramer (1971) showed that [3H]-DA, perfused pre-retinally, is taken up by the cat's retina, and stimulation by flickering (and not by steady) light increased the rate of release of the [3H]-neurotransmitter (chemical analysis revealed that the major part of the released radioactivity was in the form of DA).…”

Glutamate antagonists that block hyperpolarizing bipolar cells increase the release of dopamine from turtle retina

“…The effects of glutamate antagonists were first examined to determine whether depolarizing or hyperpolarizing bipolar cells control the release of dopamine. In addition, the involvement of GABAergic circuitry was also tested by examining the influence of GABA-related compounds on dopamine release (Marshburn & Iuvone, 1981;O'Connor et al, 1986O'Connor et al, , 1987Piccolino et al, 1982Piccolino et al, , 1987Proll & Morgan, 1983;Teranishi et al, 1984;Ishita et al, 1988). Finally, the agents that increased dopamine efflux were also examined for their effects on retinal levels of cAMP.…”

Evidence for D2 Receptor Regulation of Dopamine Release in the Goldfish Retina

“…Fish were killed by decapitation, enucleated, and each retina was removed by inverting the hemisected eyecup on filter paper and severing the optic nerve. Two retinas from each fish were incubated in the dark in 1 ml of Ringer's solution (80 mM NaCI, 3.5 m M KC1, 22.7 m M NaHCO,, 2.4 mM MgSO,, 2.3 mMCaCI,, 10 mMD-glucose, 10 mMHEPES, 0.1 m M sodium ascorbate, and 15 pM pargyline, pH 7.4) (OConnor et al, 1986) (Marc, 1982). The preparation was continuously bubbled with a mixture of 95% 0, and 5% COz.…”