Neuroanatomical and pharmacological assessment of Fos expression induced in the rat brain by the phosphodiesterase-4 inhibitor 6-(4-pyridylmethyl)-8-(3-nitrophenyl) quinoline

Bureau, Y; Handa, Minoru; Zhu, Yanqiu; Laliberté, France; Moore, Craig S.; Liu, S.; Huang, Zheng; Macdonald, D.D.; Xu, Daigen; Robertson, G.S.

doi:10.1016/j.neuropharm.2006.06.018

Cited by 20 publications

(12 citation statements)

References 42 publications

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“…Results showed that acute 3 rd ICV administration of exendin-4 produced a pica response of comparable magnitude to that observed after day 1 of IP exendin-4 treatment. This CNS-mediated pica response may be based, in part, on GLP-1R activation in the mNTS as parenchymal exendin-4 delivered to the mNTS produced a pica response and a suppression of food intake, an outcome that is consistent with findings showing that neurons in the NTS are activated by various emetic agents, including cisplatin (De Jonghe and Horn, 2009; Horn, 2009), phosphodiesterase-4 inhibitors (Bureau et al, 2006), and X-ray irradiation (Yamada et al, 2000). However, our findings are inconsistent with some features of previous work.…”

Section: Discussionsupporting

confidence: 81%

The role of nausea in food intake and body weight suppression by peripheral GLP-1 receptor agonists, exendin-4 and liraglutide

et al. 2012

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The FDA-approved glucagon-like-peptide-1 receptor (GLP-1R) agonists exendin-4 and liraglutide reduce food intake and body weight. Nausea is the most common adverse side effect reported with these GLP-1R agonists. Whether food intake suppression by exendin-4 and liraglutide occurs independently of nausea is unknown. Further, the neurophysiological mechanisms mediating the nausea associated with peripheral GLP-1R agonist use are poorly understood. Using two established rodent models of nausea [conditioned taste avoidance (CTA) and pica (ingestion of non-nutritive substances)], results show that all peripheral doses of exendin-4 that suppress food intake also produce CTA, whereas one dose of liraglutide suppresses intake without producing CTA. Chronic (12 days) daily peripheral administration of exendin-4 produces a progressive increase in pica coupled with stable, sustained food intake and body weight suppression, whereas the pica response and food intake reduction by daily liraglutide are more transient. Results demonstrate that the nausea response accompanying peripheral exendin-4 occurs via a vagal-independent pathway involving GLP-1R activation in the brain as the exendin-4-induced pica response is attenuated with CNS co-administration of the GLP-1R antagonist exendin-(9-39), but not by vagotomy. Direct administration of exendin-4 to the medial subnucleus of the nucleus tractus solitarius (mNTS), but not to the central nucleus of the amygdala, reduced food intake and produced a pica response, establishing the mNTS as a potential GLP-1R-expressing site mediating nausea responses associated with GLP-1R agonists.

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Section: Discussionsupporting

confidence: 81%

The role of nausea in food intake and body weight suppression by peripheral GLP-1 receptor agonists, exendin-4 and liraglutide

et al. 2012

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“…Thus, clearly defining the CPG region in the least shrew will require the development of markers which can differentiate the region from its surrounding fiber tracts and other cell groups. In addition, other studies have reported the central nucleus of the amygdala as being activated following administration of known emetogens (Bureau et al, 2006; Horn et al, 2006). In the shrew, Fos-IR in the amygdala was extensive in both experimental and control conditions, but the cytoarchitectonic subdivisions of the amygdala were not as clear as those of the DVC (see figure 1A).…”

Section: Discussionmentioning

confidence: 98%

“…Studies examining emesis-related Fos-IR across different species or various nonspecific emetogens such as radiation and cisplatin, found certain consistently activated areas, including the DVC nuclei (Bureau et al, 2006; Horn et al, 2006; Ito et al, 2003; Miller et al, 1994; Yip and Chahl, 1999). Previous studies have utilized Fos with nonspecific emetogens (Miller et al, 1994; Watson et al, 1995), or with receptor-specific compounds in non-emetic animals (Yip and Chahl, 1999).…”

Section: Discussionmentioning

confidence: 99%

“…Thus, Fos-IR in the PVT is likely related to thalamocortical gating of the negative sensations associated with vomiting. Indeed, previous studies have linked emesis-related Fos-IR in several diencephalic nuclei including the PVT and central nucleus of the amygdala to emotional state and memory (Bureau et al, 2006; Horn et al, 2006). Fos-IR in serotonergic DRN neurons might, at first glance, imply the stimulation of central 5-HT nuclei concomitantly with the emesis-related peripheral surge of 5-HT (Andrews, 1992; Darmani et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…These activate specific nuclei in the medulla (Endo et al, 2000; Hesketh et al, 2003; Higa et al, 2006), and the resulting output is an intestinal retroperistaltic wave, relaxation of the lower esophageal sphincter, and powerful contractions of the stomach and abdominal/intracostal musculature (Travagli et al, 2006; Veyrat-Follet et al, 1997), finally expelling the toxic GI contents from the stomach. Although cisplatin and other emetogenic conditions, such as exposure to non-chemical stimuli (e.g., motion) or enteric bacterial toxins, demonstrate overlapping activation patterns (Bureau et al, 2006; Ito et al, 2002; Miller and Ruggiero, 1994), cisplatin and its related chemotherapeutic agents are some of the most potent emetogens known (du Bois et al, 1997). …”

Section: Introductionmentioning

confidence: 99%

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Receptor-selective agonists induce emesis and Fos expression in the brain and enteric nervous system of the least shrew (Cryptotis parva)

Ray

Chebolu

Darmani

2009

Pharmacology Biochemistry and Behavior

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Research on the mechanisms of emesis has implicated multiple neurotransmitters via both central (dorsal vagal complex) and peripheral (enteric neurons and enterochromaffin cells) anatomical substrates. Taking advantage of advances in receptor-specific agonists, and utilizing Fos expression as a functional activity marker, this study demonstrates a strong, but incomplete, overlap in anatomical substrates for a variety of emetogens. We used cisplatin and specific agonists to 5-HT 3 serotonergic, D 2 /D 3 dopaminergic, and NK 1 tachykininergic receptors to induce vomiting in the least shrew (Cryptotis parva), and quantified the resulting Fos expression. The least shrew is a small mammal whose responses to emetic challenges are very similar to its human counterparts. In all cases, the enteric nervous system, nucleus of the solitary tract, and dorsal motor nucleus of the vagus demonstrated significantly increased Fos immunoreactivity (Fos-IR). However, Fos-IR induction was notably absent from the area postrema following the dopaminergic and NK 1 receptor-specific agents. Two brain nuclei not usually discussed regarding emesis, the dorsal raphe nucleus and paraventricular thalamic nucleus, also demonstrated increased emesis-related Fos-IR. Taken together, these data suggest the dorsal vagal complex is part of a common pathway for a variety of distinct emetogens, but there are central emetic substrates, both medullary and diencephalic, that can be accessed without directly stimulating the area postrema.

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Therapeutic Strategies for Huntington’s Disease

Mrzljak

Muñoz-Sanjuán

2013

Behavioral Neurobiology of Huntington's Disease and Parkinson's Disease

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Huntington's disease (HD) is a devastating autosomal dominant neurodegenerative disease, caused by expansion of the CAG repeat in the huntingtin (HTT) gene and characterized pathologically by the loss of pyramidal neurons in several cortical areas, of striatal medium spiny neurons, and of hypothalamic neurons. Clinically, a distinguishing feature of the disease is uncontrolled involuntary movements (chorea, dyskensias) accompanied by progressive cognitive, motor, and psychiatric impairment. This review focuses on the current state of therapeutic development for the treatment of HD, including the preclinical and clinical development of small molecules and molecular therapies.

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Neuroanatomical and pharmacological assessment of Fos expression induced in the rat brain by the phosphodiesterase-4 inhibitor 6-(4-pyridylmethyl)-8-(3-nitrophenyl) quinoline

Cited by 20 publications

References 42 publications

The role of nausea in food intake and body weight suppression by peripheral GLP-1 receptor agonists, exendin-4 and liraglutide

The role of nausea in food intake and body weight suppression by peripheral GLP-1 receptor agonists, exendin-4 and liraglutide

Receptor-selective agonists induce emesis and Fos expression in the brain and enteric nervous system of the least shrew (Cryptotis parva)

Therapeutic Strategies for Huntington’s Disease

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