CNS Dopamine Receptors

Creese, Ian; Hamblin, Mark W.; Leff, Stuart E.; Sibley, David R.

doi:10.1007/978-1-4684-4361-5_3

Cited by 24 publications

(13 citation statements)

References 201 publications

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“…To determine a reason for these differential effects of systemically administered apomorphine has been a complicated matter because the drug acts on several DA pathways, as it acts differentially at different DA subtypes. For example, apomorphine has been reported to be a full agonist at D2 receptor sites (Creese et al, 1983). Moreover, although D2 receptors are found both pre-and postsynaptically, it has been reported that the presynaptic sites are between 6 and 10 times more sensitive to apomorphine than the postsynaptic sites (Skirboll et al, 1979).…”

Section: Discussionmentioning

confidence: 99%

Apomorphine Enhances Conditioned Responses Induced by Aversive Stimulation of the Inferior Colliculus

Troncoso¹,

Osaki²,

Mason³

et al. 2003

Neuropsychopharmacol

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Consistent evidence has shown that learning may be produced in paradigms using electrical stimulation of the inferior colliculus (IC) as unconditioned stimulus (UCS). Recent reports have also demonstrated that aversive stimulation of the IC, at the escape threshold, enhances dopamine (DA) release in the prefrontal cortex. The purpose of the present study was to determine whether dopaminergic mechanisms are involved in the Pavlovian conditioning and latent inhibition using IC stimulation as UCS and light as conditioned stimulus (CS). Rats were placed inside a shuttle box and subjected to a two-way avoidance paradigm. IC aversive electrical stimulation was used as UCS and shuttle box illumination as CS. The rats quickly learned to avoid or interrupt the IC stimulation. Apomorphine injections produced a dose-dependent increase in the number of avoidance responses. On the other hand, chlorpromazine administration promoted a dose-dependent reduction of the avoidance responses. Previous injections of chlorpromazine inhibited the effects of apomorphine. Also, previous exposure to unreinforced light weakened the strength of the conditioning. Apomorphine blocked this latent inhibition effect, which was antagonized by previous injections of chlorpromazine. These findings bring evidence for the involvement of DA in the setting up of adaptive responses to aversive states generated at the IC level, which may underlie stressful situations present in anxiety.

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Section: Discussionmentioning

confidence: 99%

Apomorphine Enhances Conditioned Responses Induced by Aversive Stimulation of the Inferior Colliculus

Troncoso¹,

Osaki²,

Mason³

et al. 2003

Neuropsychopharmacol

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“…Since it has been well documented that other neurotransmitter receptors (e.g. 13-adrenoceptors, dopaminergic receptors) are up-regulated after a long-term treatment with their respective antagonists (see Creese et al, 1983;Weiss et al, 1984), one could speculate that the increase in the density of the cortical al-adrenoceptors results from their prolonged blockade with the investigated antidepressant drugs. In fact, a moderate affinity of amitriptyline, mianserin and imipramine to brain al-adrenoceptors was reported (Hall and Ogren, 1981) and confirmed by our unpublished results (the drugs displaced [3H] prazosin in the rat cerebral cortex, the K i value being 17, 46 and 85 nM, respectively).…”

Section: Discussionmentioning

confidence: 99%

Effect of repeated treatment with antidepressant drugs and electroconvulsive shock (ECS) on [3H] prazosin binding to different rat brain structures

Nowak

Przegaliński

1988

J. Neural Transmission

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The influence of acute and repeated treatment with imipramine, amitriptyline, mianserin, citalopram and ECS on alpha 1-adrenoceptors in different structures of the rat brain (cerebral cortex, hippocampus and thalamus) was measured using [3H] prazosin as a ligand. Repeated, but not acute, treatment with all the above antidepressant drugs and ECS induced an increase in the density of alpha 1-adrenoceptors in the cerebral cortex. On the other hand, no changes were found in the hippocampus and thalamus, with an exception of the increased number of [3H] prazosin binding sites in the thalamus after imipramine. The results suggest that the up-regulation of alpha 1-adrenoceptors following repeated antidepressant treatment is not a general phenomenon within the central nervous system.

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“…Of the many classifications available, the simplest system, based essentially on adenylate cyclase, holds the greatest sway at the present time for the mammalian central nervous system (Kebabian & Calne, 1979;Creese et al, 1983). In this system, DI-receptors mediate adenylate cyclase stimulation, and there is abundant evidence that SKF 38393 and SCH 23390, are, respectively, selective agonists and antagonists at DI-receptors (Setler et al, 1978;Stoof & Kebabian, 1981;Cross et al, 1983;lorio et al, 1983;O'Boyle & Waddington, 1984); in contrast, D2-receptor activation has either no effect or inhibits adenylate cyclase, and there is evidence that the compound LY 141865 is a selective agonist at this receptor site (Tsuruta et al, 1981;Stoof & Kebabian, 1981;Scatton, 1982).…”

Section: Administration Of Drugsmentioning

confidence: 99%

Vasomotor responses of cerebral arterioles in situ to putative dopamine receptor agonists

Edvinsson

McCulloch

Sharkey

1985

British J Pharmacology

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1 The vasomotor responses of individual cerebral pial arterioles on the convexity of the cerebral cortex to subarachnoid perivascular micro-injections ofdopamine and the putative dopamine receptor agonists, apomorphine, SKF 38393 and LY 141865, have been examined in 38 anaesthetized cats. 2 The perivascular microapplication of dopamine (10-9-10-M) effected dose-dependent reductions in pial arteriolar calibre, with the maximum reductions in calibre (22 ± 2% from preinjection levels: mean ± s.e.) being observed at 10-3M. The cerebrovascular constriction produced by dopamine (10-sM) could be significantly attenuated by the concomitant perivascular administration of phentolamine (10-6M) or methysergide (10-6M). 3 The perivascular microapplication of apomorphine (10-8 10-4M) effected dose-dependent increases in arteriolar calibre, with the maximum increase (31 ± 6%) being observed with apomorphine (10-5M). 4 The perivascular administration of the putative dopamine Di-receptor agonist, SKF 38393 (10-9 1O-4 M) increased arteriolar calibre, with the maximum response (24 ± 3%) being observed with injection of 10-0M. The putative dopamine D2-receptor agonist, LY 141865, also increased cerebral arteriolar calibre, but only at high concentrations (maximum calibre increase 25 ± 6.1 with 10-4 M). 6 These results point to the presence on cat cerebral arterioles ofdopamine receptors (probably of DI subtype) mediating dilatation.

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CNS Dopamine Receptors

Cited by 24 publications

References 201 publications

Apomorphine Enhances Conditioned Responses Induced by Aversive Stimulation of the Inferior Colliculus

Apomorphine Enhances Conditioned Responses Induced by Aversive Stimulation of the Inferior Colliculus

Effect of repeated treatment with antidepressant drugs and electroconvulsive shock (ECS) on [3H] prazosin binding to different rat brain structures

Vasomotor responses of cerebral arterioles in situ to putative dopamine receptor agonists

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