Dopamine receptor and transporter levels are altered in the brain of Purkinje Cell Degeneration mutant mice

Delis, Foteini; Mitsacos, Ada; Giompres, Panagiotis

doi:10.1016/j.neuroscience.2004.01.020

Cited by 28 publications

(26 citation statements)

References 88 publications

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“…Given that ␤-adrenoceptors exert an excitatory action on hippocampus pyramidal neurons (Curet and de Montigny, 1988b), it is possible that the net biological response to DA results from opposite effects exerted on various adrenoceptors. In keeping with a weak expression of DA receptors and raclopride binding sites in the dorsal hippocampus (Dubois et al, 1986;Delis et al, 2004), it was reported that neither the iontophoretic application of raclopride nor the systemic injection of haloperidol blocked DA-or NE-induced inhibition in the dorsal hippocampus. Although haloperidol is known to bind and antagonize both D 2 and ␣ 1 -receptors (Cohen and Lipinski, 1986), the possibility that it blocked the adrenoceptors in the present study can be excluded, because the administration of the selective ␣ 1 -adrenoceptor antagonist prazosin reduced the effect of NE in a dose-dependent manner (Curet and de Montigny, 1988a) and was here devoid of antagonistic activity.…”

Section: Downloaded Frommentioning

confidence: 89%

“…The involvement of DAT was somewhat unexpected because in brain regions in which DAT is weakly expressed, as in the hippocampus (Delis et al, 2004;Dahlin et al, 2007), a limited role of DAT in removing DA from the extracellular space has been reported (Morón et al, 2002). An alternative mechanism could be that residual DA uptake was mediated by the recently cloned and characterized polyspecific cation-monoamine transporters organic cation transporters (2 and 3) or plasma membrane monoamine transporter.…”

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confidence: 99%

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Cross-Talk between Dopaminergic and Noradrenergic Systems in the Rat Ventral Tegmental Area, Locus Ceruleus, and Dorsal Hippocampus

Guiard

Mansari²,

Blier³

2008

Mol Pharmacol

132

114

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A decreased central dopaminergic and/or noradrenergic transmission is believed to be involved in the pathophysiology of depression. It is known that dopamine (DA) neurons in the ventral tegmental area (VTA) and norepinephrine (NE) neurons in the locus ceruleus (LC) are autoregulated by somatodendritic D 2 -like and ␣ 2 -adrenoceptors, respectively. Complementing these autoreceptor-mediated inhibitory feedbacks, anatomical and functional studies have established a role for noradrenergic inputs in regulating dopaminergic activity, and reciprocally. In the present study, a microiontophoretic approach was used to characterize the postsynaptic catecholamine heteroreceptors involved in such regulations. In the VTA, the application of DA and NE significantly reduced the firing activity of DA neurons. In addition to a role for D 2 -like receptors in the inhibitory effects of both catecholamines, it was demonstrated that the ␣ 2 -adrenoceptor antagonist idazoxan dampened the DA-and NE-induced attenuations of DA neuronal activity, indicating that both of these receptors are involved in the responsiveness of VTA DA neurons to catecholamines. In the LC, the effectiveness of iontophoretically applied NE and DA to suppress NE neuronal firing was blocked by idazoxan but not by the D 2 -like receptor antagonist raclopride, which suggested that only ␣ 2 -adrenoceptors were involved. In the dorsal hippocampus, a forebrain region having a sparse dopaminergic innervation but receiving a dense noradrenergic input, the suppressant effects of DA and NE on pyramidal neurons were attenuated by idazoxan but not by raclopride. The suppressant effect of DA was prolonged by administration of the selective NE reuptake inhibitor desipramine and, to lesser extent, of the selective DA reuptake inhibitor 1-(2-[bis(4-fluorophenyl)methoxy]ethyl)-4-(3-phenylpropyl)-piperazine (GBR12909), suggesting that both the NE and DA transporters were involved in DA uptake in the hippocampus. These findings might help in designing new antidepressant strategies aimed at enhancing DA and NE neurotransmission.The catecholamines neurotransmitters dopamine (DA) and norepinephrine (NE) are believed to be involved in psychiatric disorders, and a better knowledge of the reciprocal interactions between these two systems should improve our understanding of the pathophysiology and treatment of mood disorders. Anatomical evidence indicates that noradrenergic neurons of the locus ceruleus (LC) send projections to the ventral tegmental area (VTA) in the vicinity of DA neuron cell bodies (Simon et al., 1979). Several subtypes of ␣-adrenergic receptors have been identified in the VTA (Lee et al., 1998), raising the possibility that NE inputs play a role in modulating DA neuronal activity. Consistent with this assumption, it was recently demonstrated that a selective lesion of LC NE neurons increases the mean firing activity of DA neurons by 70% and their burst activity by almost 50%, thus revealing a net inhibitory effect of NE in the VTA (Guiard et al., 2008). In con...

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Section: Downloaded Frommentioning

confidence: 89%

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confidence: 99%

Cross-Talk between Dopaminergic and Noradrenergic Systems in the Rat Ventral Tegmental Area, Locus Ceruleus, and Dorsal Hippocampus

Guiard

Mansari²,

Blier³

2008

Mol Pharmacol

132

114

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“…Even if not traditionally considered as a prominent cerebellar neuromodulator, there is evidence for dopaminergic transmission in the cerebellum (Takada et al, 1993; Hurley et al, 2003; Delis et al, 2004; Schweighofer et al, 2004; Giompres and Delis, 2005) There is also some evidence that dopamine levels in the cerebellum follow a circadian cycle (Owasoyo et al, 1979). However, the role of dopamine in the cerebellum remains poorly understood (Schweighofer et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Diurnal influences on electrophysiological oscillations and coupling in the dorsal striatum and cerebellar cortex of the anesthetized rat

Frederick

Bourget-Murray

Chapman

et al. 2014

Front. Syst. Neurosci.

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Circadian rhythms modulate behavioral processes over a 24 h period through clock gene expression. What is largely unknown is how these molecular influences shape neural activity in different brain areas. The clock gene Per2 is rhythmically expressed in the striatum and the cerebellum and its expression is linked with daily fluctuations in extracellular dopamine levels and D2 receptor activity. Electrophysiologically, dopamine depletion enhances striatal local field potential (LFP) oscillations. We investigated if LFP oscillations and synchrony were influenced by time of day, potentially via dopamine mechanisms. To assess the presence of a diurnal effect, oscillatory power and coherence were examined in the striatum and cerebellum of rats under urethane anesthesia at four different times of day zeitgeber time (ZT1, 7, 13 and 19—indicating number of hours after lights turned on in a 12:12 h light-dark cycle). We also investigated the diurnal response to systemic raclopride, a D2 receptor antagonist. Time of day affected the proportion of LFP oscillations within the 0–3 Hz band and the 3–8 Hz band. In both the striatum and the cerebellum, slow oscillations were strongest at ZT1 and weakest at ZT13. A 3–8 Hz oscillation was present when the slow oscillation was lowest, with peak 3–8 Hz activity occurring at ZT13. Raclopride enhanced the slow oscillations, and had the greatest effect at ZT13. Within the striatum and with the cerebellum, 0–3 Hz coherence was greatest at ZT1, when the slow oscillations were strongest. Coherence was also affected the most by raclopride at ZT13. Our results suggest that neural oscillations in the cerebellum and striatum, and the synchrony between these areas, are modulated by time of day, and that these changes are influenced by dopamine manipulation. This may provide insight into how circadian gene transcription patterns influence network electrophysiology. Future experiments will address how these network alterations are linked with behavior.

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“…Although pharmacodynamic effects of SCH23390 acting at the D1 receptor were initially reported in rat studies (e.g., 19,31,57,64), the strain-specific effects of SCH23390 could alternatively be due to pharmacokinetics with SCH23390 acting as a poor D1 antagonist in some murine strains and a strong D1 antagonist in others. For instance, SCH23390 binding is significantly reduced in homozygous mice for the recessive gene weaver (55, but see 50), dopamine D(1A) receptor knockout mice (43,44), and diabetic mice (60), but is increased in Purkinje Cell Degeneration mutant mice (23). In contrast, SCH23390 binding is unchanged in hypoxic mice (5), MPTP-treated mice (4), methamphetamine-treated mice (77), 6-hydroxydopamine and iron-deficient mice (81), mu-opioid receptor knock-out mice (71), and cannabinoid CB1 receptor knockout mice (32).…”

Section: Discussionmentioning

confidence: 99%

Genetic variance contributes to dopamine receptor antagonist-induced inhibition of sucrose intake in inbred and outbred mouse strains

Dym¹,

Pinhas²,

Robak³

et al. 2009

Brain Research

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Preference and intake of sucrose varies across inbred and outbred strains of mice. Pharmacological analyses revealed that the greatest sensitivity to naltrexone-induced inhibition of sucrose (10%) intake was observed in C57BL10/J and C57BL/6J strains, whereas 129P3/J, SWR/J and SJL/J strains displayed far less sensitivity to naltrexone-induced inhibition of sucrose intake. Given that dopamine D1 (SCH23390) and D2 (raclopride) receptor antagonism potently reduce sucrose intake in outbred rat and mouse strains, the present study examined the possibility of genetic variance in the dose-dependent (50–1600 nmol/kg) and time-dependent (5–120 min) effects of these antagonists upon sucrose (10%) intake in the eight inbred (BALB/cJ, C3H/HeJ, C57BL/6J, C57BL/10J, DBA/2J, SJL/J, SWR/J, 129P3/J) and one outbred (CD-1) mouse strains previously tested with naltrexone. SCH23390 significantly reduced sucrose intake across all five doses in 129P3/J and SJL/J mice, across four doses in C57BL/6J and BALB/cJ mice, across three doses in DBA/2J, SWR/J, C3H/HeJ and C57BL/10J mice, but only at the two highest doses in CD-1 mice. SCH23390 was 2–3-fold more potent in inhibiting sucrose intake in 129P3/J and SJL/J mice relative to CD-1 mice. In contrast, only the highest equimolar 1600 nmol/kg dose of raclopride significantly reduced sucrose intake in the BALB/cJ, C3H/HeJ, C57BL/6J, C57BL/10J, DBA/2J, SJL/J and 129P3/J, but not the SWR/J and CD-1 strains. The present and previous data demonstrate specific and differential patterns of genetic variability in inhibition of sucrose intake by dopamine and opioid antagonists, suggesting that distinct neurochemical mechanisms control sucrose intake across different mouse strains.

show abstract

Dopamine receptor and transporter levels are altered in the brain of Purkinje Cell Degeneration mutant mice

Cited by 28 publications

References 88 publications

Cross-Talk between Dopaminergic and Noradrenergic Systems in the Rat Ventral Tegmental Area, Locus Ceruleus, and Dorsal Hippocampus

Cross-Talk between Dopaminergic and Noradrenergic Systems in the Rat Ventral Tegmental Area, Locus Ceruleus, and Dorsal Hippocampus

Diurnal influences on electrophysiological oscillations and coupling in the dorsal striatum and cerebellar cortex of the anesthetized rat

Genetic variance contributes to dopamine receptor antagonist-induced inhibition of sucrose intake in inbred and outbred mouse strains

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