Phencyclidine-induced release of [3H]dopamine from chopped striatal tissue

Phencyclidine was examined for its ability to release [³H]dopamine ([³H]DA) from prelabelled chopped rat striatal tissue. A dynamic perfusion system was used in order to minimize the effects of drugs on uptake mechanisms. Cocaine and S-(+)-amphetamine were used to distinguish uptake inhibition from a neurotransmitter releasing action. Phencyclidine, starting at 3 μM, caused a dose-dependent increase in efflux of [³H]DA from chopped striatal tissue. In this same preparation, cocaine, a known neuronal uptake inhibitor of dopamine, was unable to release [³H]DA except in the largest dose of 100 μM. S-(+)Amphetamine, a known releaser of neuronal dopamine, was found to be about ten times more potent than phencyclidine in causing a dose-dependent release of [³H]DA. The results of the above experiments are discussed in relation to the ability of phencyclidine to decrease the synaptosomal accumulation of [³H]DA. It is concluded that some of the psychoactive effects of phencyclidine may be due to the ability of phencyclidine to elicit a release of dopamine from dopaminergic     

In vitro exposure to ambient fine and ultrafine particles alters dopamine uptake and release,and D2 receptor affinity and signaling

The exposure to environmental pollutants, such as fine and ultrafine particles (FP and UFP), has been associated with increased risk for Parkinson’s disease, depression and schizophrenia, disorders related to altered dopaminergic transmission. The striatum, a neuronal nucleus with extensive dopaminergic afferents, is a target site for particle toxicity, which results in oxidative stress, inflammation, astrocyte activation and modifications in dopamine content and D₂ receptor (D₂R) density. In this study we assessed the in vitro effect of the exposure to FP and UFP on dopaminergic transmission, by evaluating [³H]-dopamine uptake and release by rat striatal isolated nerve terminals (synaptosomes), as well as modifications in the affinity and signaling of native and cloned D₂Rs. FP and UFP collected from the air of Mexico City inhibited [³H]-dopamine uptake and increased depolarization-evoked [³H]-dopamine release in striatal synaptosomes. FP and UFP also enhanced D₂R affinity for dopamine in membranes from either rat striatum or CHO-K1 cells transfected with the long isoform of the human D₂R (hD_2LR)2LR). In CHO-K1-hD2L In CHO-K1-hD_2LR cells or striatal slices, FP and UFP increased the potency of dopamine or the D₂R agonist quinpirole, respectively, to inhibit forskolin-induced cAMP formation. The effects were concentration-dependent, with UFP being more potent than FP. These results indicate that FP and UFP directly affect dopaminergic transmission.     

Inhibitory effect of prostaglandins on dopamine release from the retina

1. Prostaglandins have been shown to modulate transmitter release from both central and peripheral neuroeffector junctions. In the present study, we examined the effect of prostaglandins on [³H]-dopamine release from isolated, superfused rabbit retina.2. Both naturally occurring and synthetic prostaglandins produced concentration-dependent reduction of electrically evoked [³H]-dopamine overflow without affecting basal tracer efflux. The rank order of potencies of the agonists was: sulprostone > 16, 16-dimethyl PGE₂>PGE₂> > 11-deoxy-PGE₁>PGF_2α.3. The PGE₂-mediated inhibition of field stimulated [³H]-dopamine release was not blocked by the selective EP₁-receptor antagonist, AH6809 (5–30 μM).4. The cyclooxygenase inhibitor, flurbiprofen (3 μM) had no effect on basal or evoked [³H]-dopamine overflow nor did it affect the inhibition caused by PGE₂ suggesting that endogenous prostaglandins are not involved in the regulation of dopamine release in the retina.5. The inhibition of [³H]-dopamine release produced by submaximal concentrations of PGE₂, apomorphine and melatonin were not additive indicating that presynaptic PGE₂, D₂- and melatonin receptors coexist at sites for neurotransmitter release and may share a common mechanism for regulation of dopamine release.6. We conclude that prostaglandin-induced inhibition of electrically evoked [³H]-dopamine release from the rabbit retina may be mediated by specific prostaglandin receptors of the EP₃ subtype.     

CAPTOPRIL INHIBITS BOTH DOPAMINERGIC AND CHOLINERGIC NEUROTRANSMISSION IN THE CENTRAL NERVOUS SYSTEM

1. The present study was performed to investigate the effects of captopril on both dopaminergic and cholinergic neurotransmission in the rat central nervous system . 2. Slices of rat striatum were prepared and prelabelled with [³H]-dopamine or [³H]-choline. Slices were continuously super-fused with Krebs'-Ringer solution and electrical stimulation (1 Hz) was performed . 3. Captopril significantly inhibited stimulation-evoked [³H]-dopamine release from rat striatal slices in a concentration-dependent manner (S2/S1 ratios: control 0.83S±0.018 (n= 6); 1×10^?5 mol/L captopril 0.597±0.035 (n= 6; P<0.05); 5 × 10^?5 mol/L captopril 0.561 ± 0.041 (n = 6; P<0.05)). However, the basal release of [³H]-dopamine was not affected by captopril . 4. Captopril also reduced stimulation-evoked [³H]-acetyl-choline release in the striatum (S2/S1 ratios: control 0.891 ±0.016 (n= 6); 1 × 10^?5 mol/L captopril 0.794±0.011 (n= 6; P<0.05)) . 5. These results show that captopril inhibits the release of both dopamine and acetylcholine in the rat striatum. Although the mechanisms underlying the neurosuppressive effects of captopril remain to be determined, the findings suggest that the inhibition of dopaminergic and cholinergic neurotransmission may be related to the central action of the angiotensin-converting enzyme inhibitor .     

EFFECTS OF VERAPAMIL AND DILTIAZEM ON DOPAMINE RELEASE IN THE CENTRAL NERVOUS SYSTEM OF SPONTANEOUSLY HYPERTENSIVE RATS

1. The purpose of the present study was to investigate the effects of Ca²⁺-antagonists (verapamil and diltiazem) on dopamine release in the central nervous system in hypertension. 2. Striatal slices obtained from spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats were prelabelled with [³H]-dopamine, and superfused with Krebs-Ringer solution in vitro. The slices were stimulated electrically at a frequency of 1 Hz. 3. Stimulation-evoked release of [³H]-dopamine from striatal slices was significantly decreased in SHR compared with WKY rats. 4. Exposure of slices to verapamil and diltiazem significantly increased the stimulation-evoked [³H]-dopamine release. The facilitatory effects of the Ca²⁺-antagonists on dopamine release were significantly greater in SHR than in WKY rats. 5. Because central nervous system dopaminergic mechanisms appear to be depressor, the results suggest that the pronounced effects of verapamil and diltiazem on dopamine release in SHR might be involved in the central hypotensive mechanisms of the Ca²⁺-antagonists.     

Effect of 3-PPP,a putative dopamine autoreceptor agonist,on [3H]ligand binding to dopamine receptors of calf and rat striatum

3-(3-Hydroxyphenyl)-N-n-propyliperidine (3-PPP) is most effective in inhibiting [³H]apomorphine binding in rat striatal membranes, with Ki values of 63 nM. 3-PPP was six to 27 times less effective when it competed with the binding of [³H]dopamine or [³H]spiperone in calf and rat striatal membranes. At concentrations up to 10 μM, 3-PPP failed to substitute for dopamine in the activation of adenylate cyclase in rat striatal membranes. 3-PPP at 4.8-5 μM caused 50% inhibition of catecholamine uptake in synaptosomes of corpus striatum and hypothalamus, therefore appearing to be a relatively weak uptake inhibitor. The higher affinity of 3-PPP for [³H]apomorphine binding sites is consistent with its binding to a subset of dopamine receptors which are characterized by a high affinity for both the agonist and antagonist of dopamine.     

Effect of morphine in vivo on uptake of [3H]choline and release of [3H]acetylcholine from rat striatal synaptosomes

The effect of morphine on the rat striatal cholinergic system was investigated in vitro by measuring the rates of [³H]choline uptake and [³H]acetylcholine release in striatal synaptosomes after in vivo injections of morphine sulfate. Morphine caused a 50 per cent increase in the V_max of [³H]choline uptake. Although a concomitant increase was also measured in the amount of [³H] acetylcholine released, it could be explained by the previous increase in uptake. It is suggested that morphine had an overall stimulatory effect on the striatal cholinergic system which may be a transynaptic phenomenon rather than a direct effect on the cholinergic cell.     

Effect of amperozide on rat cortical 5-HT2 and striatal and limbic dopamine D2 receptor occupancy: implications for antipsychotic action.

Amperozide (FG 5606, N-ethyl-4-[4',4'-bis(p-fluorophenyl)butyl]-1-piperazine-carboxamide) is an atypical antipsychotic drug which has relatively weak in vitro affinity for striatal dopamine2 (D2) receptors and strong affinity for cortical 5-HT2 receptors. The in vivo affinity for 5-HT2 binding sites in rat cortex was 1.1 mg/kg. In striatum or olfactory tubercle, doses of amperozide up to 40 mg/kg did not displace radioligand binding to D2 receptors. Amperozide, haloperidol and ritanserin had similar in vivo potency in blocking the 5-HT2 binding site, but only haloperidol displaced D2 receptor binding. Based on the clinically effective dose of amperozide (0.14-0.28 mg/kg per day), it is suggested that the antipsychotic effect of amperozide is related, in part, to its in vivo interaction with the 5-HT2 receptor and that amperozide cannot be expected to exert its antipsychotic action by blockade of D2 receptors in the striatum or limbic regions.     

Uptake of (3H)-catecholamines by homogenates of rat corpus striatum and cerebral cortex: effects of amphetamine analogues

The effects of isomers and metabolites of amphetamine on the uptake of [³H]-catecholamines in synaptosomal preparations of the striatum and cortex of the rat were investigated. Dextroamphetamine was found to be four times more potent than the (?)-enantiomer against the uptake of [³H]-dopamine with striatal tissue. This difference may help to clarify the effects of the isomers on the development of stereotyped behaviour in the rat. The p-hydroxylation of amphetamine did not alter its potency, while β-hydroxylation of amphetamine or p-OH-amphetamine reduced the inhibitory potency markedly. With cerebral cortex, less than a 2-fold difference was found for the potencies of (+)- and (?)-amphetamine against the uptake of [³H]-norepinephrine. Although pretreatment with reserpine resulted in a marked inhibition of the initial uptake of norepinephrine, reserpine did not alter the relative potencies of the stereoisomers of amphetamine against the uptake of norepinephrine by cortex.     

四氢巴马汀等异喹啉生物碱对突触体及囊泡摄取[3H]多巴胺的影响

本文报道四氢巴马汀(THP)等异喹啉生物碱对[³H]DA摄取的作用。突触体对[³H]DA的亲和力常数Km为0.23μmol。最大摄取速率Vmax为1.2 nmol/g(5 min)。d-THP,1-SPD和1-THP对突触体摄取[³H]DA均有抑制作用,其IC₅₀分别为0.44,2.24和18.5μmol。d-THP的作用比1-THP约强20倍。nomifensine,苯丙胺和氟哌啶醇亦能有效地抑制[³H]DA摄取(IC₍₅₀₎分别为0.05,0.27和3.18μmol)。动力学研究表明,d-THP和nomifensine为DA摄取的竞争性抑制剂。用低渗溶液处理溶胀的方法研究药物对递质贮存的作用发现,与利血平相似,d-THP显著降低贮存囊泡[³H]DA含量并使囊泡与突触体[³H]DA含量之比明显减小。实验结果表明,THP等能抑制突触体摄取,并直接作用于贮存囊泡抑制[³H]DA贮存,因此具有利血平样排空作用。     

Receptor binding properties of amperozide

The receptor pharmacology of amperozide was investigated with in vitro radioligand binding technique. Amperozide possessed a high affinity to the 5-HT₂ receptors (K_i= 16.5±2.1 nM) and a moderate affinity to α₁-adrenergic receptors of rat cerebral cortical membranes (K_i=172±14 nM). The affinity of amperozide for striatal and limbic dopamine D₂ receptors was low and not significantly different (K_i±S.E.M. = 540 ± 59 nM vs 403±42 nM; p<0.11, n = 4). The affinity for striatal and limbic 5-HT₂ receptors was measured as well and found to be very close to the affinity to the cerebral cortical 5-HT₂ receptor. The drug affinity for D₂ and 5-HT₂ receptors seems thus not to be influenced by the location of the receptor moiety. The affinity for several other rat brain receptors such as 5-HT_1A, α₂-adrenergic, dopamine D₁ muscarinic M1 and M2, opiate sigma and β₂-adrenergic was low. The pseudo-Hill coefficient of the amperozide competition binding curve was consistently higher than one indicating antagonistic and complex interactions with the 5-HT₂ receptor or with α₁-adrenergic and dopamine D₂ receptors. The antagonistic properties of amperozide were investigated by its ability to antagonize the serotonin-induced formation of inositol-1-phosphate in human blood platelets. Amperozide inhibited this 5-HT₂ receptor-mediated intracellular response with similar potency as ketanserin. These results suggest that amperozide is a selective 5-HT₂ receptor antagonist.     

Effects of omega-amino acids on tritiated dopamine release from rat striatum: evidence for a possible glycinergic mechanism.

The effects of GABA and glycine on the release of tritiated dopamine from prelabelled slices of rat striatum have been compared. Both GABA (>50 μM) and glycine (>200 μM) released tritiated dopamine, but had no effect on the release of radiolabelled 5-hydroxytryptamine and GABA. The GABA antagonist picrotoxin (50 μM) markedly reduced the ability of GABA to release [³H]dopamine, but had no effect on the glycine response. Conversely strychnine (0.5 μM), a specific glycine receptor antagonist at low concentrations, abolished both the GABA and the glycine response on [³H]dopamine release. Two other ω-amino acids, β-alanine and taurine, both at 500 μM, had no effect on [³H]dopamine release from rat striatal slices.In additional experiments, release of radioactivity was demonstrated from neonatal rat spinal cord and striatal slices after prelabelling with [³H]glycine. This release was calcium-dependent. The possibility that glycine may function as a neurotransmitter substance within the striatum is considered, and the hypothesis that GABA may partially exert some of its pharmacological effects through the glycine receptor is discussed.     

Effect of long term amineptine treatment on pre- and postsynaptic mechanisms in rat brain.

The effect of amineptine and its two metabolites on monoamine uptake, release and receptor binding was studied in vitro. Amineptine and its two metabolites did not displace labelled ligands for known neurotransmitters and drug receptor sites. Amineptine and its two metabolites did not influence [3H]-5-hydroxytryptamine ([3H]-5-HT) uptake or release by rat brain synaptosomes. Amineptine inhibited [3H]-dopamine and [3H]-noradrenaline ([3H]-NA) accumulation, with IC50 values of 1.4 and 10 microM, respectively. The effect was retained, though with lower efficacy, by the two metabolites. Amineptine released [3H]-dopamine from preloaded synaptosomes. Metabolite 1 had no effect on catecholamine release, and metabolite 2 was about half as active as the parent compound on [3H]-dopamine release. The releasing effect of amineptine on [3H]-dopamine was potentiated by reserpine pretreatment, suggesting that the drug acts on the cytoplasmic neurotransmitter pool. Chronic treatment with amineptine (20 mg kg-1, twice daily for 15 days followed by a 3 days drug withdrawal period) resulted in a decrease of [3H]-spiperone binding sites in striatum, and of [3H]-dihyroalprenolol and [3H]-clonidine in cortex. Chronic treatment with amineptine reduced basal [3H]-dopamine accumulation in striatal synaptosomes, without affecting [3H]-NA or [3H]-5-HT accumulation. The adaptive changes in the pre- and postsynaptic dopamine mechanisms observed after long term treatment with amineptine are consistent with the drug acting as an indirect dopamine agonist. The down regulation of beta- and alpha 2-noradrenoceptors observed after long term amineptine treatment may play a role in the antidepressant activity of the drug.     

Effects of phencyclidine on [3H]catecholamine and [3H]serotonin uptake in synaptosomal preparations from rat brain

Phencyclidine inhibited uptake in vitro of [³H]norepinephrine (ic₅₀ 0.52 μM), [³H]dopamine (ic₅₀ 0.73 μM) and [³H]serotonin (ic₅₀ 0.80 μM) in crude synaptosomal preparations from rat brain through a competitive mechanism. Phencyclidine was fairly similar in potency to d-amphetamine and methylphenidate in inhibiting catecholamine uptake but was 8 times more potent than d-amphetamine and 34 times more potent than methylphenidate in inhibiting [³H]serotonin uptake.     

Pharmacology: Ouabain-induced Increase in Dopamine Release from Mouse Striatal Slices is Antagonized by Riluzole

We have examined the effects of riluzole, a neuroprotective drug which stabilizes voltage-dependent sodium channels in their inactivated state and inhibits the release of glutamate in-vivo and in-vitro, on the release of newly taken up [³H]dopamine induced by ouabain, a potent and selective inhibitor of Na⁺/K⁺-ATPase in mouse striatal slices in-vitro. Riluzole potently (IC50 (concentration resulting in 50% inhibition) = 0.9±0.3 μM) and dose-dependently antagonized ouabain-stimulated [³H]dopamine release, the effect being observed at low concentrations. Tetrodotoxin (1 μM) and nomifensine (10 μM) also abolished ouabain-induced [³H]dopamine release. Blockade of glutamate receptors with dizocilpine (1 μM) and 6-(1H-imidazol-1-yl)-7-nitro-2,3(1H,4H)-quinoxalinedione (YM-90K; 10 μM), alone or in combination, was without effect. Incubation of striatal slices with 50 μM La³⁺, which blocks voltage-dependent calcium channels, did not inhibit [³H]dopamine release induced by ouabain. The potent effects of riluzole observed in this model are probably related to its ability to block voltage-dependent sodium channels. The consequences of this activity are critically discussed in relation to the protective action of riluzole previously reported in various models of Parkinson's disease and other neurodegenerative disorders.     

Effects of linopirdine,HP 749, and glycyl-prolyl-glutamate on transmitter release and uptake

Linopirdine, HP 749, and glycyl-prolyl-glutamate (GPE) are compounds that have been reported to alter the release of neurotransmitters. This study compares the potassium-stimulated neurotransmitter release enhancing properties maximal release enhancement. HP 749 increased the extracellular concentrations of the catecholamines, [³H]NE and [³H]DA, but not [³H]ACh or [³H]d-Asp. HP 749 was a potent inhibitor of both [³H]NE and [³H]DA uptake, and this may, in part, be responsible for the apparent release enhancing activity of the drug. GPE was devoid of release enhancing activity under the conditions of these compounds in parallel. While not affecting the apparent release of [³H]norepinephrine ([³H]NE), linopirdine at a concentration of 10 μM enhanced the potassium evoked release of cerebral cortical and hippocampal [³H]acetylcholine ([³H]ACh) release by 143% and 200% over control, respectively, and striatal [³H]dopamine ([³H]DA) and hippocampal [³H]d-aspartate ([³H]d-Asp) release by 236% and 65% over control, respectively. The release enhancing effects of linopirdine were not due to inhibition of high-affinity uptake processes, since the drug did not inhibit neurotransmitter uptake at the concentration (10 μM) which caused used in the present study. © 1993 Wiley-Liss, Inc.     

Stimulation of synaptosomal tyrosine hydroxylation by phencyclidine in vitro

Phencyclidine (PCP), a potent psychoactive drug, produces some animal behavior that are belived to be mediated by dopaminergic and/or cholinergic neurons in the basal ganglia. In this study, we have monitored the effects of PCP in vitro on the synthesis, uptake, and release of dopamine (DA) in rat striatal synaptosomes. Using tyrosine hydroxylation as an index of DA synthesis, we observed a concentration-dependent stimulation of DA synthesis by PCP. The stimulatory effect was antagonized by reserpine (1 μM) and was observed only when synaptosomes were preincubated under conditions which prevented the spontaneous release of [³H]DA. Two hydroxylated metabolites of PCP were also tested and found to have little effect on tyrosine hydroxylation. Like PCP these metabolites are potent inhibitors of synaptosomal [³H]DA uptake, but they apparently lack PCP's ability to release synaptosomal DA. Taken together, these results support our hypothesis that PCP stimulates synaptosomal DA synthesis by releasing DA from an inhibitory pool.     

Inhibition of neuronal uptake of 3H-biogenic amines into rat cerebral cortex by partially and fully saturated derivatives of imipramine and desipramine. The importance of the aromatic ring in adrenergic amines--part 3.

In order to assess the importance of the aromatic rings in inhibition of neuronal amine uptake produced by tricyclic antidepressant drugs, derivatives of imipramine (IMI) and dcsipramine (DMI) were prepared in which either one (IMIH, DMIH) or both (IMIH2, DMIH2) of the aromatic rings were fully reduced to cyclohexane rings. The relative abilities of these compounds to inhibit the uptake of $\text{l-[}{}^3\text{H}\text{]-}\text{norepinephrine}$ (NE), [³H]-dopamine (DA) and [³H]-5-hydroxytryptamine (5-HT) into chopped tissue of rat cerebral cortex were determined. Reduction of one or both aromatic rings did not alter significantly the inhibition of uptake of [³H]-DA or [³H]5-HT produced by either IMI or DMI (IC₅₀ values 25–80 μM). However, saturation of one or both rings abolished the selectivitv of DMI for inhibition of NE uptake (IC₅₀ 0.12 μM). decreasing potency 150-fold (IC₅₀ 18.3 μM) and 250-fold (IC₅₀ 29.4 μM) respectively. The effect of aromatic ring reduction on the IMI-induced inhibition of NE uptake was much less pronounced. The results suggest that hydrophobic rather than π-electron attractive forces are involved in the interaction of DMI or IMI with DA or 5-HT uptake sites. However, the loss in selectivity for inhibition of NE uptake upon reduction of DMI may reflect loss of π-electron interactions in the binding of DMI to the NE uptake site, or may reflect increased sensitivity to spatial disposition of the hydrophobic binding areas of the drug relative to that found at the DA or 5-HT amine uptake sites.     

Ca2+-DEPENDENT AND -INDEPENDENT MECHANISMS OF ISCHAEMIA-EVOKED RELEASE OF [3H]-DOPAMINE FROM RAT STRIATAL SLICES

1. Ischaemia was induced by 5 min of deprivation of glucose and an additional 5 min of deprivation of glucose and oxygen from Mg²⁺-free artificial cerebrospinal fluid in vitro. 2. During the ischaemic period, 11 ± 1.5% of the total [³H]-dopamine ([³H]-D A) was released into the incubation medium. 3. Ischaemia-evoked release of [³H]-DA from striatal slices was attenuated by tetrodotoxin (TTX), MgSO₄, dizocilpine, ketamine, 6,7-dinitroquinoxaline-2,3-dione (DNQX), or carbetapentane. 4. Release of [³H]-DA was attenuated by verapamil, ω-conotoxin GVIA and dantrolene. 5. Nomifensin inhibited the ischaemia-induced release of [³H]-DA. 6. Omission of Ca²⁺ from incubation media potentiated ischaemia-evoked [³H]-DA release. The inhibitory effect of nomifensin was potentiated in Ca²⁺-free incubation media. 7. These results suggest that ischaemia induces release of [³H]-DA by dual mechanisms; one is Ca²⁺-dependent exocytosis and the other is reversal of transporter.     

Interactions of dopamine and the release of [3H]-taurine and [3H]-glycine from the isolated retina of the rat

1 The dose-related, calcium-dependent, potassium-stimulated release of preloaded [³H]-dopamine from the superfused rat retina has been demonstrated.

2 A high-affinity uptake system for dopamine exists in rat retina in vitro; K_m value was calculated as 1.89 μM, V_max value as 1.4 nmol g^-1 tissue h^-1.

3 Dopamine (0.8 and 4 mM) inhibited the spontaneous release of [³H]-glycine from retina, and in the case of 0.8 mM dopamine this inhibitory effect was antagonized by 10 μM (+)-butaclamol but not by 10 μM (-)-butaclamol.

4 The potassium-evoked (25 mM) release of [³H]-glycine from rat retina was similarly inhibited by dopamine (0.4-4 mM) in a dose-related manner when added to the superfusate with the potassium. The effect of 0.8 mM dopamine was antagonized by 10 μM (+)-butaclamol but not by 10 μM (-)-butaclamol.

5 Dopamine (4 mM) significantly reduced the spontaneous release of [³H]-taurine from rat retina.

6 The potassium-stimulated (25 mM) release of [³H]-taurine occurred after the cessation of the depolarizing stimulus. This delayed release of [³H]-taurine was unaffected if dopamine was applied to the superfusate at the same time as the potassium, but it was significantly reduced if dopamine (0.8 and 4 mM) was applied after the depolarizing stimulus had been removed and during the actual amino acid release phase.

7 The inhibition of K⁺-stimulated (25 mM) delayed release of [³H]-taurine by applying dopamine (0.8 mM) after the depolarizing stimulus was blocked by 10 μM (+)-butaclamol but not by 10 μM (-)-butaclamol.

8 The results are discussed with respect to the possible neurotransmitter role for dopamine within the rat retina, and its possible interaction with glycine and taurine.