The phenylephrine blood pressure clamp in pharmacologic magnetic resonance imaging: reduction of systemic confounds and improved detectability of drug-induced BOLD signal changes

Kalisch, Raffaël; Delfino, Marina; Murer, Mario Gustavo; Auer, Dorothee P.

doi:10.1007/s00213-005-2252-0

Cited by 13 publications

(20 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…for the phMRI sessions. Usage of higher drug doses than in behavioral experiments is in line with earlier studies from our group (Kalisch et al, 2005) and other groups (eg, Chen et al, 1997).…”

Section: Experimental Designsupporting

confidence: 90%

“…BP was also monitored continuously via the tail artery. Druginduced BP changes can generate correlated BOLD signal changes, which may mask neurally mediated drug effects on BOLD (Kalisch et al, 2001;Nagaoka et al, 2002;Tuor et al, 2002;Kalisch et al, 2005;Wang et al, 2006). In order to minimize such BP changes, all animals received domperidone (0.4 mg i.v.…”

Section: Phmri Methodologymentioning

confidence: 99%

“…; Motilin, BYK, Germany), an antagonist of peripheral D2 family receptors, 10 min before scanning. Furthermore, we used a recently established BP clamping technique (Kalisch et al, 2005) by which BP is kept constant with the help of a continuous i.v. infusion of the adrenergic agonist phenylephrine (PEP; 10 mg/ml in phosphate-buffered saline (PBS); Sigma, Germany).…”

Section: Phmri Methodologymentioning

confidence: 99%

“…In this method, PEP infusion volumes are continuously adjusted by the experimenter whenever BP begins to deviate from the baseline level. The method has been shown by us to reduce BP confounds and to improve the detectability of non-BPmediated drug-induced BOLD signal changes (Kalisch et al, 2005).…”

Section: Phmri Methodologymentioning

confidence: 99%

“…The so-called blood oxygenation level-dependent (BOLD) signal can be used not only to study activity changes induced by sensory or cognitive stimuli but also changes induced by drugs, a variant that is termed pharmacological fMRI (phMRI). Several studies have been able to demonstrate BOLD signal increases following administration of non-selective dopamine agonists in animal models of PD (Chen et al, 1997(Chen et al, , 1999Nguyen et al, 2000;Kalisch et al, 2005). The value of this technique is demonstrated by the contrasting effects that apomorphine and the dopamine releasing compound amphetamine have on behavior and basal ganglia signal in rats with unilateral nigrostriatal lesions induced by 6-OHDA.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Mapping the Effects of Three Dopamine Agonists with Different Dyskinetogenic Potential and Receptor Selectivity Using Pharmacological Functional Magnetic Resonance Imaging

Delfino

Kalisch

Czisch

et al. 2007

Neuropsychopharmacol

Self Cite

View full text Add to dashboard Cite

The mechanisms underlying dopamine agonist-induced dyskinesia in Parkinson's disease remain poorly understood. Similar to patients, rats with severe nigrostriatal degeneration induced by 6-hydroxydopamine are more likely to show dyskinesia during chronic treatment with unselective dopamine receptor agonists than with D2 agonists, suggesting that D1 receptor stimulation alone or in conjunction with D2 receptor stimulation increases the chances of experiencing dyskinesia. As a first step towards disclosing drug-induced brain activation in dyskinesia, we examined the effects of dopamine agonists on behavior and blood oxygenation level-dependent (BOLD) signal in the striatum and motor cortex of rats with unilateral nigrostriatal lesions. Rats were rendered dyskinetic before pharmacologic functional magnetic resonance imaging by means of a repeated treatment regime with dopamine agonists. The unselective agonist apomorphine and the selective D1/D5 agonist SKF-81297 induced strong forelimb dyskinesia (FD) and axial dystonia and increased BOLD signal in the denervated striatum. Besides, SKF-81297 produced a significant but smaller BOLD increase in the intact striatum and a symmetric bilateral increase in the motor cortex. The D2 family agonist quinpirole, which induced mild dyskinesia on chronic treatment, did not produce BOLD changes in the striatum or motor cortex. Further evidence to support an association between BOLD changes and dyskinesia comes from a direct correlation between scores of FD and magnitude of drug-induced BOLD increases in the denervated striatum and motor cortex. Our results suggest that striatal and cortical activation induced by stimulation of D1/D5 receptors has a primary role in the induction of peak dose dyskinesia in parkinsonism.

show abstract

Section: Experimental Designsupporting

confidence: 90%