Characterization of dopamine autoreceptors in the amygdala: A fast cyclic voltammetric study in vitro

Bull, David; Bakhtiar, Rahmat; Sheehan, Michael J.

doi:10.1016/0304-3940(91)90504-m

Cited by 27 publications

(15 citation statements)

References 9 publications

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“…Stable release was maintained for 25 min before superfusion with a drug. As has previously been reported (Bull et al ., 1991), superfusion with increasing concentrations of the dopamine D 2 receptor agonist quinpirole (0.1–100 n m ) reduced dopamine release in a concentration‐dependent manner. One hundred per cent inhibition ocurred at 100 n m quinpirole (IC 50 3.98 × 10 −8 m (Fig.…”

Section: Resultssupporting

confidence: 88%

“…The evidence to support this comes from the observation that the D 1 receptor antagonist SCH 23390 significantly attenuated the effect of CPA on dopamine release whilst 6‐chloro‐APB, a D 1 receptor agonist, increased the effect of CPA on dopamine release. Neither SCH 23390 nor 6‐chloro‐APB altered dopamine release on their own, which is in agreement with previous experiments measuring dopamine release in the amygdala (Bull et al ., 1991). These data therefore provide evidence for a novel functional interaction between striatal A 1 and D 1 receptors that is synergistic in nature.…”

Section: Discussionsupporting

confidence: 93%

“…Fast cyclic voltammetry has been used extensively for the detection of stimulated dopamine release in brain tissue both in vivo (Stamford et al ., 1991) and in vitro (Bull. et al ., 1991).…”

Section: Introductionmentioning

confidence: 99%

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Adenosine A₁ receptor‐mediated inhibition of dopamine release from rat striatal slices is modulated by D₁ dopamine receptors

O’Neill¹,

Nolan²,

Macari³

et al. 2007

Eur J of Neuroscience

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Dopamine release is regulated by presynaptic dopamine receptors and interactions between adenosine and dopamine receptors have been well documented. In the present study, dopamine release from isolated striatal slices from Wistar rats was measured using fast cyclic voltammetry. Single-pulse stimulation (0.1 ms, 10 V) was applied every 5 min over a 2-h period. Superfusion with the adenosine (A)(1) receptor agonist N(6)-cyclopentyladenosine (CPA), but not the A(2) receptor agonist 3-[4-[2-[[6-amino-9-[(2R,3R,4S,5S)-5-(ethylcarbamoyl)-3,4-dihydroxy-oxolan-2-yl]purin-2-yl]amino]ethyl] phenyl]propanoic acid (CGS 21680), inhibited dopamine release in a concentration-dependent manner (IC(50) 3.80 x 10(-7) m; n = 10). The dose-response curve to CPA was shifted to the right (IC(50) 6.57 x 10(-6) m; n = 6, P < 0.05 vs. control) by the A(1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). Neither the D(1) agonist 6-chloro-APB nor the D(1) antagonist R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3- benzazepine-7-ol (SCH 23390) altered dopamine release on their own. However, SCH 23390 (3 microm) significantly attenuated the response to CPA (IC(50) 1.44 x 10(-5) m; n = 6, P < 0.01 vs. control). Furthermore, the inhibitory effect of CPA was significantly increased in the presence of 6-chloro-APB (1 microm). In radioligand binding experiments, CPA interacted with high- and low-affinity states of [(3)H]DPCPX-lableled A(1) receptors. The high-affinity agonist binding to A(1) receptors was inhibited by the stable guanosine triphosphate analogue Gpp(NH)p. In contrast, neither the proportion nor the affinity of high-affinity A(1) receptors was altered by dopamine or SCH 23390. These results provide evidence that the inhibition of dopamine release by adenosine A(1) receptors is dependent, at least in part, on the simultaneous activation of D(1) dopamine receptors. While the mechanism underlying this interaction remains to be determined, it does not appear to involve an intramembrane interaction between A(1) and D(1) receptors.

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Section: Resultssupporting

confidence: 88%

Section: Discussionsupporting

confidence: 93%

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Adenosine A₁ receptor‐mediated inhibition of dopamine release from rat striatal slices is modulated by D₁ dopamine receptors

O’Neill¹,

Nolan²,

Macari³

et al. 2007

Eur J of Neuroscience

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“…D2-autoreceptors are particularly abundant in the striatum (Ford, 2014) but also present in the hippocampus (Rocchetti et al, 2015) and amygdala (Bull et al, 1991) and although dopaminestimulating effects in response to D2-antagonists seem to be less extreme in these structures compared to the striatum (Garris and Wightman, 1995), the relative sparseness of DAT in the hippocampus (Kwon et al, 2008) might lead to longer-lasting dopamine effects in the hippocampus (Prince et al, 2016). In particular, such increased stimulation of the postsynaptic D1-like receptors prevailing in hippocampus and amygdala (Köhler et al, 1991;Okubo et al, 1999;Rocchetti et al, 2015) by the dopaminergic midbrain might have led to the improved memory discrimination, possibly mediated by an increased signal-to-noise ratio (Frank, 2005;Warren et al, 2016;Yousif et al, 2016) of the representation of episodic information in these mnemonic structures.…”

Section: Discussionmentioning

confidence: 99%

Dopamine is a double-edged sword: Enhancing memory retrieval performance at the expense of metacognition

Clos

Bunzeck

Sommer

2018

Preprint

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While memory encoding and consolidation processes have been linked with dopaminergic signaling for a long time, the role of dopamine in episodic memory retrieval remained mostly unexplored. Based on previous observations of striatal activity during memory retrieval, we used pharmacological fMRI to investigate the effects of dopamine on retrieval performance and metacognitive memory confidence in healthy humans. Dopaminergic modulation by the D2 antagonist haloperidol administered acutely during the retrieval phase improved recognition accuracy of previously learned pictures significantly and was associated with increased activity in the SN/VTA, locus coeruleus, hippocampus and amygdala during retrieval. In contrast, confidence for new-decisions was impaired by unsystematically increased activity of the striatum across confidence levels and restricted range of responsiveness in frontostriatal networks under haloperidol. These findings offer new insights into the mechanisms underlying memory retrieval and metacognition and provide a broader perspective on the presence of memory problems in dopamine-related diseases and the treatment of memory disorders.

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“…The reason for this topographically specific covariance between these regions is currently unclear. It may be speculated that this link reflects autoreceptor expression as areas such as the amygdala are known to have potent terminal D2 autoreceptors (Bull et al, 1991), but data supporting or refuting such a hypothesis remain scarce.…”

Section: Discussionmentioning

confidence: 99%

The interrelationship of dopamine D2-like receptor availability in striatal and extrastriatal brain regions in healthy humans: A principal component analysis of [18F]fallypride binding

et al. 2010

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Individual differences in dopamine D2-like receptor availability arise across all brain regions expressing D2-like receptors. However, the inter-relationships in receptor availability across brain regions are poorly understood. To address this issue, we examined the relationship between D2-like binding potential (BP ND ) across striatal and extrastriatal regions in a sample of healthy participants. PET imaging was performed with the high affinity D2/D3 ligand [ 18 F]fallypride in 45 participants. BP ND images were submitted to voxel-wise principal components analysis to determine the pattern of associations across brain regions. Individual differences in D2-like BP ND were explained by three distinguishable components. A single component explained almost all of the variance within the striatum, indicating that individual differences in receptor availability vary in a homogenous manner across the caudate, putamen, and ventral striatum. Cortical BP ND was only modestly related to striatal BP ND , and mostly loaded on a distinct component. After controlling for the general level of cortical D2-like BP ND , an inverse relationship emerged between receptor availability in the striatum and the ventral temporal and ventromedial frontal cortices, suggesting possible cross-regulation of D2-like receptors in these regions. The analysis additionally revealed evidence of: 1) a distinct component involving the midbrain and limbic areas; 2) a dissociation between BP ND in the medial and lateral temporal regions; and 3) a dissociation between BP ND in the medial/midline and lateral thalamus. In summary, individual differences in D2-like receptor availability reflect several distinct patterns. This conclusion has significant implications for neuropsychiatric models that posit global or regionally specific relationships between dopaminergic tone and behavior.

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Characterization of dopamine autoreceptors in the amygdala: A fast cyclic voltammetric study in vitro

Cited by 27 publications

References 9 publications

Adenosine A₁ receptor‐mediated inhibition of dopamine release from rat striatal slices is modulated by D₁ dopamine receptors

Adenosine A₁ receptor‐mediated inhibition of dopamine release from rat striatal slices is modulated by D₁ dopamine receptors

Dopamine is a double-edged sword: Enhancing memory retrieval performance at the expense of metacognition

The interrelationship of dopamine D2-like receptor availability in striatal and extrastriatal brain regions in healthy humans: A principal component analysis of [18F]fallypride binding

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Characterization of dopamine autoreceptors in the amygdala: A fast cyclic voltammetric study in vitro

Cited by 27 publications

References 9 publications

Adenosine A1 receptor‐mediated inhibition of dopamine release from rat striatal slices is modulated by D1 dopamine receptors

Adenosine A1 receptor‐mediated inhibition of dopamine release from rat striatal slices is modulated by D1 dopamine receptors

Dopamine is a double-edged sword: Enhancing memory retrieval performance at the expense of metacognition

The interrelationship of dopamine D2-like receptor availability in striatal and extrastriatal brain regions in healthy humans: A principal component analysis of [18F]fallypride binding

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Adenosine A₁ receptor‐mediated inhibition of dopamine release from rat striatal slices is modulated by D₁ dopamine receptors

Adenosine A₁ receptor‐mediated inhibition of dopamine release from rat striatal slices is modulated by D₁ dopamine receptors