A comparative study of the dopamine-acetylcholine interaction in telencephalic structures of the rat and of a reptile, the lizardGekko gecko (original) (raw)
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Brain Research, 1991
Activation of the N.methyl.D.aspartate (NMDA) receptor increases and that of the D2 dopamine (DA) receptor inhibits the release of acetylcholine (ACh) from mammalian neostriatal tissue. Similar effects have been described in the ventral striatum of the rat, however, in the caudomedial part of the nucleus accumbens. D 2 receptor activation does not inhibit the release of ACh. Likewise, the NMDA-induced stimulation of the release of ACh in this part of the striatum is much smaller. In the present study we demonstrated that in the striatal complex or striatum of reptiles Dz receptor activation did not result in an inhibition of the release of ACh, whereas the release of DA could be inhibited to a significant extent. These findings indicate that, although D2 receptors are present in the striatum of reptiles, these receptors do not regulate the release of ACh in this brain structure. We observed in the striatum of reptiles a potassium induced and calcium-dependent release of [3H]D-aspartate indicating a neurotransmitter role for aspartate or glutamate (GLU). However GLU and NMDA have only a marginal effect on the release of ACh in the striatum of the reptiles as compared to the effects in the neostriatum of the rat. It is concluded that with respect to the effects of Da and NMDA receptor activation on the release of ACh, the striatum of reptiles bears most similarity to the caudomedial part of the nucleus accumbens.
Naunyn-Schmiedeberg's Archives of Pharmacology, 1992
The possible involvement of dopamine D~ receptors in the regulation of acetylcholine release in the rabbit caudate nucleus was investigated. Caudate slices, preincubated with [3H]choline, were superfused continuously and subjected to electrical field stimulation with only a single pulse. In agreement with the view that the release of acetylcholine evoked by a single electrical pulse is not influenced by endogenous transmitters, atropine and domperidone failed to icnrease the evoked release of [3H]acetylcholine, whereas oxotremorine and quinpirole caused a concentration-dependent inhibition of transmitter release. Neither the dopamine D1 receptor antagonist SCH 23390 nor the D~ agonist SKF 38393 in a concentration range of 0.01-1 gmol/1 changed the evoked [3H]acetylcholine release. The inhibitory effect of the dopamine D 2 receptor agonist quinpirole was virtually abolished in the presence of 0.1 gmol/l domperidone and diminished in the presence of 1 ~mol/1 SCH 23390. It remained unchanged in the presence of 1 gmol/1 SKF 38393. It is concluded that the inhibition of acetylcholine release by dopamine is mediated exclusively via presynaptic dopamine D a receptors and that the antagonistic effect of SCH 23390 on the inhibition of acetylcholine release by quinpirole is due to its interaction with dopamine D 2 rather than D 1 receptors located on cholinergic nerve terminals.
Neuroscience, 1983
Electrophysioiogical recordings from the cells of the neostriatum in rats anaesthetised with halothane revealed only inhibitory actions of dopamine applied iontophoretically close to the cells. Inhibition of cortical driving seemed to have a slightly higher threshold in most cells but dopamine inhibited spontaneous action potentials, glutamate-induced responses, and cortical driving in the cells studied. Fluphenazine applied iontophoretically blocked the actions of dopamine but was itself without effect on the neuronal responses. Sulpiride, in contrast, was without effect on the spontaneous activity of the cells and was ineffective in blocking the action of applied dopamine. Sulpiride, nevertheless, increased the response to cortical stimulation though it had no action on the response to applied glutamate. These results suggest that the sub-class of dopamine receptors on the terminals of the corticostriatal pathway may be inhibitory on glutamate release and preferentially sensitive to blockade by sulpiride. While several different binding sites for dopamine have been described in the central nervous system6," the number of receptors at which dopamine can be shown to exert a physiological effect is considerably smaller in mammals.'3.27,40 In their simpler scheme, Kebabian and Calne17 suggested that sites at which there is a known biochemical effect of dopamine on adenylate cyclase be called D, receptors while the binding sites for dopamine-at that time not associated with known biochemical changes in the post synaptic elements-be called D, receptors. With this simplified scheme it is possible to suggest from lesion studies that the two "receptors" in the neostriatum may in fact be preferentially located on different neuronal elements. The D, receptors are associated with neurones of the neostriatum and with those which project to the substantia nigra (SN). They appear to be associated with the outer membrane of these neurones and are present on their terminals in the SN as well as on their cell bodies in the striatum.32 Kainic acid lesions which destroy the neurones of the striatum, also reduce the activity of adenylate cyclase in the nucleus and result in a 94% reduction in the stimulation of the enzyme by dopamine? Such lesions of the striatum lead to a reduction of the dopamine ligand binding sites in the striatum, presumably as a result of the destruction of striatal neurones.20- .
European Journal of Pharmacology, 1992
In vivo microdialysis was used to determine the effects of 6-hydroxydopamine (6-OHDA) lesions of the mesotelencephalic dopamine system on dopamine receptor agonist induced changes in extracellular acetylcholine (ACh) concentrations in the striatum. Such lesions increased the inhibitory effect of a low dose of the D2 receptor agonist quinpirole (0.05 mg/kg s.c.) on striatal ACh release. In addition, 6-OHDA lesions enhanced the facilitatory effect of the selective D1 receptor agonist CY 208-243 on striatal ACh release, enabling a subthreshold (0.2 mg/kg s.c.) dose to increase striatal dialysate concentrations of ACh by over 60%. These results indicate that denervation supersensitivity potentiates both the facilitatory effects of D1 receptor agonists and the inhibitory effects of D2 receptor agonists on striatal cholinergic activity. It was also found that the 6-OHDA lesions reduced basal interstitial ACh concentrations by 75% in the ipsilateral striatum. The later results are consistent with the hypothesis that the prepotent action of dopamine in the forebrain is to enhance striatal ACh release via a D1 receptor mechanism.
Brain Research, 1996
The dopamine (DA)-acetylcholine (ACh) interactions were investigated in dorsal (nucleus caudate, NC) and ventral (olfactory tubercle, OT) striatal regions, of rats and rabbits. Both regions receive a dense dopaminergic innervation and have high ACh concentrations. Brain slices of NC and OT from both animal species were prelabeled with [3H]choline and superfused. In rat and rabbit OT and NC, higher ACh release per pulse was elicited by lower than higher stimulation frequencies; in addition, rabbit tissues released a greater fraction of tissue [3H]transmitter than rat tissues. Blockade of D 2 DA-receptors with sulpiride (1 ~M), did not modify ACh release in OT and NC of rats and rabbits; suggesting that the lower ACh release observed in rat tissues is not due to an inhibitory dopaminergic tone on cholinergic neurons. Apomorphine (APO), a D 2 DA-receptor agonist, inhibited in a concentration-dependent manner the evoked release of ACh from rat and rabbit NC (maximal inhibition = 90%). In rabbit OT, maximal inhibition induced by APO was 49 _+ 2% and in the rat OT, it was 23 ± 1%. Sulpiride antagonized APO-induced inhibition of ACh release from rat and rabbit NC; however, it failed to prevent APO-induced inhibition in rat OT, and in the rabbit OT reduced it from 47% to 20 _+ 5%. These results indicate differences in the wiring of DA and cholinergic neurons and terminals in dorsal and ventral striatal structures, as well as between rat and rabbit tissues. Cholinergic ventral striatal structures may not receive a direct DA input, and afferent cholinergic nerve terminals (rather than interneurons) predominate in the ventral striatum.
British Journal of Pharmacology, 1997
1 The eect of two D 3/2 dopamine receptor agonists, LY-171555 (quinpirole) and 7-hydroxy-N,N-di-npropyl-2-aminotetralin (7-OH-DPAT) on spontaneous [ 3 H]-acetylcholine ([ 3 H]-ACh) release were investigated in rat striatal synaptosomes. 2 Quinpirole and 7-OH-DPAT inhibited in a concentration-dependent manner the basal eux of [ 3 H]-ACh with similar E max (maximal inhibitory eect) values (29.95+2.91% and 33.19+1.21%, respectively). Signi®cant dierences were obtained between the pEC 50 (7log of molar concentration) of quinpirole (7.87+0.12) and 7-OH-DPAT (7.21+0.17; P50.01).
British Journal of Pharmacology, 1997
The eect of two D 3/2 dopamine receptor agonists, LY-171555 (quinpirole) and 7-hydroxy-N,N-di-npropyl-2-aminotetralin (7-OH-DPAT) on spontaneous [ 3 H]-acetylcholine ([ 3 H]-ACh) release were investigated in rat striatal synaptosomes. 2 Quinpirole and 7-OH-DPAT inhibited in a concentration-dependent manner the basal eux of [ 3 H]-ACh with similar E max (maximal inhibitory eect) values (29.95+2.91% and 33.19+1.21%, respectively). Signi®cant dierences were obtained between the pEC 50 (7log of molar concentration) of quinpirole (7.87+0.12) and 7-OH-DPAT (7.21+0.17; P50.01). 3 Dierent concentrations (0.3 ± 10 nM) of haloperidol (D 2/3 dopamine receptor antagonist) shifted to the right the concentration-response curves elicited by quinpirole and 7-OH-DPAT, without modi®cations in the E max. 4 Slopes of a Schild plot obtained with haloperidol in the presence of quinpirole and 7-OH-DPAT were not sign®cantly dierent from unity (0.85+0.05 and 1.17+0.11, respectively) and consequently haloperidol interacted with a homogeneous receptor population. The pK B values of haloperidol obtained from Schild regression were 9.96+0.15 (in presence of quinpirole) and 9.90+0.09 (in presence of 7-OH-DPAT). 5 Speci®c binding of [ 3 H]-YM-09151-2 to membranes of striatal synaptosomes and cells expressing D 2 and D 3 dopamine receptors was inhibited by haloperidol. Analysis of competition curves revealed the existence of a single population of receptors. There were no dierences between the estimated pK i (7log of molar concentration) values for synaptosomes (8.96+0.02) and cells expressing D 2 receptors (8.81+0.05), but the pK i value from cells expressing D 3 dopamine receptors diered signi®cantly (8.48+0.06; P50.01). 6 In conclusion, the data obtained in the present study indicate that quinpirole and 7-OH-DPAT, two D 3/2 dopamine receptor agonists, inhibit the spontaneous [ 3 H]-ACh eux and this eect is competitively antagonized by haloperidol and probably mediated through dopamine D 2 receptors.