Emetic, central nervous system and pulmonary activities of rolipram in the dog

Heaslip, Richard J.; Evans, Deborah Y.

doi:10.1016/0014-2999(95)00457-2

Cited by 82 publications

(51 citation statements)

References 30 publications

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“…The behavioral pattern of the anxiogenic-like effect and reduced immobility in the FST observed in PDE4BÀ/À mice appears not uncommon; it also occurs in BDNF transgenic mice (Govindarajan et al, 2006) and in rats treated acutely with pentylenetetrazol (Cannizzaro et al, 1993) or fluoxetine (Zienowicz et al, 2006). Thus, the present data suggest that PDE4B plays a role in the anxiogenic-like effects of acute rolipram (Heaslip and Evans, 1995;Imaizumi et al, 1994), which also exerts antidepressant activity.…”

Section: Pde4b-deficiency and Behavior H-t Zhang Et Alsupporting

confidence: 51%

“…other studies have shown that PDE4 inhibitors, including rolipram, result in anxiogenic-like behavior in dogs and mice (Heaslip and Evans, 1995;Imaizumi et al, 1994). The reasons for the inconsistent results may be due, at least partially, to the sedative effect of PDE4 inhibitors (Griebel et al, 1991;Silvestre et al, 1999b) and/or the different contributions of PDE4 subtypes to anxiety regulation.…”

Section: Discussionmentioning

confidence: 97%

“…They also may induce anxiogenic-like effects and sedation (Heaslip and Evans, 1995;Imaizumi et al, 1994;Silvestre et al, 1999b), although an anxiolytic-like effect also has been reported (Silvestre et al, 1999a). While studies have shown that PDE4D plays an important role in the mediation of antidepressant-like effect (Zhang et al, 2002) and may be involved in memory , the role of PDE4B has not been investigated due to the lack of highly selective inhibitors of individual PDE4 subtypes and the complexity of the PDE4 family in terms of its numerous variants and compartmentation (Conti et al, 2003;Houslay et al, 2005;Terrin et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

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Anxiogenic-Like Behavioral Phenotype of Mice Deficient in Phosphodiesterase 4B (PDE4B)

Zhang

Huang

Masood

et al. 2007

Neuropsychopharmacol

157

143

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Phosphodiesterase-4 (PDE4), an enzyme that catalyzes the hydrolysis of cyclic AMP and plays a critical role in controlling its intracellular concentration, has been implicated in depression-and anxiety-like behaviors. However, the functions of the four PDE4 subfamilies (PDE4A, PDE4B, PDE4C, and PDE4D) remain largely unknown. In animal tests sensitive to anxiolytics, antidepressants, memory enhancers, or analgesics, we examined the behavioral phenotype of mice deficient in PDE4B (PDE4BÀ/À). Immunoblot analysis revealed loss of PDE4B expression in the cerebral cortex and amygdala of PDE4BÀ/À mice. The reduction of PDE4B expression was accompanied by decreases in PDE4 activity in the brain regions of PDE4BÀ/À mice. Compared to PDE4B + / + littermates, PDE4BÀ/À mice displayed anxiogenic-like behavior, as evidenced by decreased head-dips and time spent in head-dipping in the holeboard test, reduced transitions and time on the light side in the light-dark transition test, and decreased initial exploration and rears in the open-field test. Consistent with anxiogenic-like behavior, PDE4BÀ/À mice displayed increased levels of plasma corticosterone. In addition, these mice also showed a modest increase in the proliferation of neuronal cells in the hippocampal dentate gyrus. In the forced-swim test, PDE4BÀ/À mice exhibited decreased immobility; however, this was not supported by the results from the tail-suspension test. PDE4BÀ/À mice did not display changes in memory, locomotor activity, or nociceptive responses. Taken together, these results suggest that the PDE4B subfamily is involved in signaling pathways that contribute to anxiogenic-like effects on behavior.

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Section: Pde4b-deficiency and Behavior H-t Zhang Et Alsupporting

confidence: 51%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Anxiogenic-Like Behavioral Phenotype of Mice Deficient in Phosphodiesterase 4B (PDE4B)

Zhang

Huang

Masood

et al. 2007

Neuropsychopharmacol

157

143

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“…This result demonstrates that clinical dosage levels of cisplatin elicit increases in salivary amylase in rats. It is well known that cisplatin (12,17,18) and rolipram (19 -24) are strong emetic agents in humans, dogs, and ferrets; and the latency to the first vomiting is 1 -1.5 h after cisplatin administration to humans, dogs, monkeys and ferrets (12, 13, 25 -27) and within 0.5 h after rolipram administration to humans, ferrets, and dogs (21,22,28). In this study, significant increases in amylase activity were observed at 1.5 h after the administration of cisplatin and at 0.5 h after the administration of rolipram.…”

Section: Discussionmentioning

confidence: 99%

Various Emetogens Increase the Secretion of Salivary Amylase in Rats: a Potential Model in Emesis Research

et al. 2010

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Abstract. We investigated the effects of various emetic agents: cisplatin, apomorphine, lithium chloride (LiCl), rolipram, sibutramine, and the β 3 -adrenoceptor (AR) agonist CL316243 on salivary amylase secretion in rats. We also determined the inhibitory effect of granisetron, a 5-HT 3 -receptor antagonist, on cisplatin-induced increased salivary amylase activity and the inhibitory effect of bilateral abdominal vagotomy on increases in salivary amylase activity induced by cisplatin and LiCl. Granisetron was administered 15 min before and 1 h after cisplatin administration. Cisplatin (10 -15 mg/kg, i.v.) increased salivary amylase activity dose-dependently and induced an acute increase from 1.5 h post-treatment with 15 mg/kg. Apomorphine (1 -3 mg/kg, s.c.), LiCl (120 mg/kg, i.p.), rolipram (3 -10 mg/kg, p.o.), and sibutramine (10 mg/kg, p.o.) induced significant increases in salivary amylase secretion. On the other hand, CL316243 did not stimulate salivary amylase secretion. The increased amylase activity induced by cisplatin (15 mg/kg, i.v.) was inhibited significantly by granisetron (1 or 3 mg/kg × 2, i.v.) or tended to be inhibited by bilateral abdominal vagotomy, whereas an increase in amylase activity produced by LiCl was not inhibited by abdominal visceral nerve section. These results suggest that salivary amylase activity is useful as a marker for emesis in rats, a species that does not exhibit vomiting.

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“…They are effective in animal models of asthma (3) and chronic obstructive pulmonary disease (COPD) (4). However, PDE4 inhibitors (rolipram, a prototypic PDE4 inhibitor, and its related derivatives) have side effects, including nausea and emesis (5), that limit their therapeutic potential. Potentiation of apomorphineinduced emesis in dogs by Ro20-1724 (another prototypic PDE4 inhibitor) implies that the emesis via PDE4 inhibitors is produced, at least in part, in the area postrema neurons in the emesis centers (6).…”

Section: Introductionmentioning

confidence: 99%