Activation of nicotinic receptors on GABAergic amacrine cells in the rabbit retina indirectly stimulates dopamine release
The retina possesses subpopulations of amacrine cells, which utilize different transmitters, including acetylcholine (ACh), GABA, and dopamine. We have examined interactions between these neurones by studying the effects of nicotinic agonists on GABA and dopamine release. Isolated rabbit retinas wer...
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Veröffentlicht in: | Visual neuroscience 2001-01, Vol.18 (1), p.55-64 |
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Zusammenfassung: | The retina possesses subpopulations of amacrine cells,
which utilize different transmitters, including acetylcholine
(ACh), GABA, and dopamine. We have examined interactions
between these neurones by studying the effects of nicotinic
agonists on GABA and dopamine release. Isolated rabbit
retinas were incubated with [3H]dopamine
and then superfused. Fractions of the superfusate (2 min)
were collected and the [3H]dopamine
in each sample was measured. Endogenous GABA release was
examined by incubating retinas in a small chamber. At 5-min
intervals, the medium was changed and the GABA measured
by high-pressure liquid chromatography (HPLC). Exposure
of the retina to nicotine, epibatidine, and other nicotinic
agonists increased the release of both GABA and dopamine.
The effects of nicotine and epibatidine were blocked by
mecamylamine, confirming an action on nicotinic receptors.
The action of epibatidine on dopamine release was unaffected
by glutamate antagonists but was blocked by picrotoxin
and gabazine. These results suggested that nicotine might
increase dopamine release indirectly by stimulating the
release of GABA, which in turn inhibited the release of
an inhibitory transmitter acting tonically on the dopaminergic
amacrines. Exposure of the retina to GABA caused a small
increase in dopamine release. This hypothetical inhibitory
transmitter was not GABA, an opioid, adenosine, glycine,
nociceptin, a cannabinoid, or nitric oxide because appropriate
antagonists did not affect the resting release of dopamine.
However, metergoline, a 5HT1/5HT2
receptor antagonist, and ketanserin, a 5HT2A
receptor antagonist, but not the 5HT1A antagonist
WAY100635, increased the resting release of dopamine and
blocked the effects of nicotine. The 5HT1A/5HT7
agonist 8-hydroxy DPAT inhibited both the nicotine and
GABA-evoked release of dopamine. We conclude that nicotinic
agonists directly stimulate the release of GABA, but the
evoked release of dopamine is indirect, and arises from
GABA inhibiting the input of an inhibitory transmitter,
which we tentatively identify as serotonin. |
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ISSN: | 0952-5238 1469-8714 |
DOI: | 10.1017/S0952523801181058 |