Neuroanatomical characterization of Fos induction in rat behavioral models of anxiety

Duncan, Gary E.; Knapp, Darin J.; Breese, George R.

doi:10.1016/0006-8993(95)01486-1

Cited by 302 publications

(188 citation statements)

References 37 publications

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“…Brains were then placed in paraformaldehyde and kept in cold storage until cut with a vibratome. Sections (50 m thick) were taken for selected brain regions, and a standard avidin-biotin/horseradish peroxidase method was used for the Fos-LI assay, as previously described (Duncan et al 1996). Briefly, Fos-LI was detected using an affinity-purified sheep polyclonal antibody (1:10,000) raised to a synthetic peptide of fos (Cambridge Research Biochemicals, Inc., Wilmington, DE; current source is Biogenesis, Brentwood, NH), and visualized with Vectastain ABC kits (Vector Laboratories, Inc., Burlingame, CA) containing rabbit antigoat IgG, and 3,3 Ј -diamino-benzidene tetrahydrochloride (DAB; Polysciences, Inc., Warrington, PA).…”

Section: Measurement Of Fos-like Immunoreactivity (Fos-li)mentioning

confidence: 99%

Effect of Olanzapine on Functional Responses from Sensitized D1-Dopamine Receptors in Rats with Neonatal Dopamine Loss

Moy

Knapp

Breese

2001

Neuropsychopharmacology

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(Breese et al. 1985a,b). For example, neonate-lesioned animals have increased locomotion following treatment with SKF-38393, a D 1 -DA receptor agonist, at doses that have minimal impact on control rats (Breese et al. 1985a,b). Repeated treatment with D 1 -DA agonists can lead to extremely high rates of activity in lesioned rats, and this "priming" effect can still be observed 6 months after the chronic drug treatment (Breese et al. 1985b;Criswell et al. 1989b). Supersensitivity of D 1 -DA receptors in neonatal-6-OHDA rats has also been linked to stereotyped responses and self-injurious behavior (SIB) following treatment with L-Dopa or apomorphine, suggesting that these animals can provide a valuable model for the self-injury and DA loss associated with Lesch-Nyhan disease (Breese et al. 1984a,b), a metabolic disorder primarily observed in male children (Lesch and Nyhan 1964).Paradoxically, although the aberrant responses in the neonate-lesioned rats can be completely blocked with selective D 1 -DA receptor antagonists (Breese et al. 1985a), these animals are remarkably subsensitive to haloperidol, even at doses which induce catalepsy in normal controls and in rats given 6-OHDA as young adults (Bruno et al. 1985;Duncan et al. 1987). Similarly, treatment with typical antipsychotic agents does not prevent the painful self-injury that occurs in LeschFrom the Departments of Psychiatry (SSM, DJK, GRB), Anesthesiology (GRB) and Pharmacology (GRB), Skipper Bowles Center For

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Section: Measurement Of Fos-like Immunoreactivity (Fos-li)mentioning

confidence: 99%

Effect of Olanzapine on Functional Responses from Sensitized D1-Dopamine Receptors in Rats with Neonatal Dopamine Loss

Moy

Knapp

Breese

2001

Neuropsychopharmacology

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“…The induction of c-Fos mRNA or protein has been widely used as a marker to map neuronal populations activated in vivo after pharmacological treatments or environmental stimuli. Exposure to EPM anxiety has been reported to moderately induce c-Fos expression in several limbic brain regions (Graeff et al, 1993;Duncan et al, 1996;Hinks et al, 1996). Stronger and more widespread c-Fos induction is observed after more severe stressors (Stone and Zhang, 1995;Duncan et al, 1996;Chowdhury et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…Exposure to EPM anxiety has been reported to moderately induce c-Fos expression in several limbic brain regions (Graeff et al, 1993;Duncan et al, 1996;Hinks et al, 1996). Stronger and more widespread c-Fos induction is observed after more severe stressors (Stone and Zhang, 1995;Duncan et al, 1996;Chowdhury et al, 2000). Moreover, the suppression of stress-induced c-Fos expression in the rat brain has been associated with the anxiolytic effects of benzodiazepines in the fear-conditioning model of anxiety (Beck and Fibiger, 1995).…”

Section: Introductionmentioning

confidence: 99%

Anxiolytic Activity of the MGLU2/3 Receptor Agonist LY354740 on the Elevated Plus Maze is Associated with the Suppression of Stress-Induced c-Fos in the Hippocampus and Increases in c-Fos Induction in Several Other Stress-Sensitive Brain Regions

Lindén

Greene

Bergeron

et al. 2003

Neuropsychopharmacol

100

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LY354740 is a potent and selective agonist for group II metabotropic glutamate (mGlu) receptors, mGlu2 and mGlu3 receptors, with anxiolytic activity in several animal models of anxiety, including the elevated plus maze (EPM) test. Here, we studied neuronal activation in mouse brain after EPM exposure in saline-and LY354740-treated mice using c-Fos immunoreactivity as a marker. The effect of LY354740 on c-Fos expression was also studied in cage control (no EPM) mice. Pretreatment with LY354740 (20 mg/kg, s.c.) produced robust anxiolytic behavior on the EPM. LY354740 administration decreased EPM-induced increases in c-Fos expression in the CA3 of the hippocampus, while having no significant effects on basal c-Fos expression in the hippocampus. LY354740 administration significantly increased c-Fos expression in specific limbic regions, including the lateral division of the central nucleus of the amygdala (CeL), lateral parabrachial nucleus, locus coeruleus, and Edinger-Westphal nucleus, whether or not animals were exposed to the EPM. Moreover, LY354740 administration per se significantly increased c-Fos expression in regions processing sensory information, including the paraventricular and lateral geniculate nucleus of the thalamus as well as the nucleus of the optic tract and superior colliculus. In particular, the suppression of fear-evoked neuronal activity in the hippocampus and drug-induced increases in neuronal activation in the CeL have been previously linked to the anxiolytic effects of clinically effective drugs such as benzodiazepines, and thus may contribute to anxiolytic actions of LY354740 in animal models and human anxiety patients.

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“…The expression of c-fos is induced by a variety of stimuli (Smith et al 1992;Melia et al 1994;Duncan et al 1996) and after some forms of learning (McCabe and Horn 1994;Radulovic et al 1998;Wan et al 1999;Vann et al 2000). Accordingly, Fos expression is considered a mechanism by which brief stimuli can trigger long-term changes in gene expression and alter the structural and functional properties of nerve cells (Goelet et al 1986;Morgan and Curran 1991).…”

mentioning

confidence: 99%

A Role of Fos Expression in the CA3 Region of the Hippocampus in Spatial Memory Formation in Rats

Yamada

Nabeshima

2002

Neuropsychopharmacology

115

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Neuroanatomical characterization of Fos induction in rat behavioral models of anxiety

Cited by 302 publications

References 37 publications

Effect of Olanzapine on Functional Responses from Sensitized D1-Dopamine Receptors in Rats with Neonatal Dopamine Loss

Effect of Olanzapine on Functional Responses from Sensitized D1-Dopamine Receptors in Rats with Neonatal Dopamine Loss

Anxiolytic Activity of the MGLU2/3 Receptor Agonist LY354740 on the Elevated Plus Maze is Associated with the Suppression of Stress-Induced c-Fos in the Hippocampus and Increases in c-Fos Induction in Several Other Stress-Sensitive Brain Regions

A Role of Fos Expression in the CA3 Region of the Hippocampus in Spatial Memory Formation in Rats

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