Anxiolytic effect of serotonin depletion in the novelty-induced hypophagia test

Bechtholt, Anita J.; Hill, Tiffany E.; Lucki, Irwin

doi:10.1007/s00213-006-0615-9

Cited by 40 publications

(25 citation statements)

References 37 publications

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“…NIH outcomes for latency were generally similar to those of intake but more variable as previously reported (Bechtholt et al, 2007;Dulawa and Hen, 2005). Vehicletreated animals showed increased latencies to feed in the novel environment that were reduced, but not significantly, by acute chlordiazepoxide treatment (Figure 2, right panels).…”

Section: Effects Of Acute Chlordiazepoxide On Nihsupporting

confidence: 79%

“…Acute chlordiazepoxide or chronic fluoxetine mitigated this anxiety by decreasing the difference in intake between the home and novel cage. Latency score analyses yielded similar results, however, these scores were typically highly variable in this test (Bechtholt et al, 2007;Dulawa and Hen, 2005). Thus, although significant for chronic fluoxetine treatment, only a tendency toward a decrease in novel cage latencies was observed following chlordiazepoxide, which may be due to the sedative effects of this drug.…”

Section: Discussionmentioning

confidence: 51%

“…This time was required to reach stable intakes and latencies to begin eating (Bechtholt et al, 2007). Ninety minutes prior to daily feeding sessions an opaque Plexiglas divider was inserted into the home cage, separating the two animals.…”

Section: Novelty-induced Hypophagiamentioning

confidence: 99%

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Overlapping and Distinct Brain Regions Associated with the Anxiolytic Effects of Chlordiazepoxide and Chronic Fluoxetine

Bechtholt

Valentino

Lucki

2007

Neuropsychopharmacol

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Little is known about the sites of action for the behavioral effects of chronic antidepressants. The novelty-induced hypophagia (NIH) test is one of few animal behavioral tests sensitive to acute benzodiazepines and chronic antidepressants. The goals of these experiments were to examine patterns of brain activation associated with the behavioral response to novelty and identify regions that could regulate the anxiolytic effects of acute benzodiazepine and chronic antidepressant treatments, measured using the NIH test. In the first experiment, rats were treated acutely with the anxiolytic, chlordiazepoxide (2.5 or 5 mg/kg, i.p.). In separate experiments, animals were implanted with osmotic minipumps delivering vehicle or fluoxetine (5 or 20 mg/kg per day s.c.) for 3 or 28 days. NIH was assessed by giving animals access to a familiar palatable food in a novel environment. Associated brain areas were identified using c-fos immunohistochemistry. NIH was mitigated by acute chlordiazepoxide and chronic fluoxetine. Both drugs reversed novelty-induced changes in c-fos expression in the lateral division of the posterolateral part of the bed nucleus of the stria terminalis (STLP), cingulate cortex (Cg), and dorsal field CA2 of the hippocampus (dCA2). Chronic fluoxetine additionally increased c-fos expression in the anterior nucleus accumbens (aAcb) and the piriform cortex (Pir). The effects of the drugs on c-fos expression in many regions correlated with anxiolytic efficacy. These findings identified brain regions where the effects of chronic antidepressants and benzodiazepines may converge to produce anxiolytic activity, as well as distinct sites of action for the two classes of drugs.

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Section: Effects Of Acute Chlordiazepoxide On Nihsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 51%

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Overlapping and Distinct Brain Regions Associated with the Anxiolytic Effects of Chlordiazepoxide and Chronic Fluoxetine

Bechtholt

Valentino

Lucki

2007

Neuropsychopharmacol

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“…Rats were monitored for anxiety-like behavior using hypophagia procedures as previously described (40, 41). Briefly, rats were habituated to a quiet testing room illuminated by red light (see Supplemental Information).…”

Section: Methodsmentioning

confidence: 99%

Constitutive Increases in Amygdalar Corticotropin-Releasing Factor and Fatty Acid Amide Hydrolase Drive an Anxious Phenotype

Natividad

Buczynski

Herman

et al. 2017

Biological Psychiatry

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Background Corticotropin-releasing factor (CRF) mediates anxiogenic responses by activating CRF1 receptors in limbic brain regions. Anxiety is further modulated by the endogenous cannabinoid (eCB) system that attenuates the synaptic effects of stress. In the amygdala, acute stress activates the enzymatic clearance of the eCB N-arachidonoylethanolamine (anandamide; AEA) via fatty acid amide hydrolase (FAAH), although it is unclear whether chronic stress induces maladaptive changes in amygdalar eCB signaling to promote anxiety. Here, we used genetically-selected Marchigian Sardinian P (msP) rats carrying an innate overexpression of CRF1 receptors to study the role of constitutive upregulation in CRF systems on amygdalar eCB function and persistent anxiety-like effects. Methods We applied behavioral, pharmacological, and biochemical methods to broadly characterize anxiety-like behaviors and amygdalar eCB clearance enzymes in msP versus non-selected Wistar rats. Subsequent studies examined the influence of dysregulated CRF and FAAH systems in altering excitatory transmission in the central amygdala (CeA). Results MsPs display an anxious phenotype accompanied by elevations in amygdalar FAAH activity and reduced dialysate AEA levels in the CeA. Elevations in CRF-CRF1 signaling dysregulate FAAH activity, and this genotypic difference is normalized with pharmacological blockade of CRF1 receptors. MsPs also exhibit elevated baseline glutamatergic transmission in the CeA, and dysregulated CRF-FAAH facilitates stress-induced increases in glutamatergic activity. Treatment with a FAAH inhibitor relieves sensitized glutamatergic responses in msPs and attenuates the anxiety-like phenotype. Conclusions Pathological anxiety and stress hyper-sensitivity are driven by constitutive increases in CRF1 signaling that dysregulate AEA signaling mechanisms and disable neuronal constraint of CeA glutamatergic synapses.

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“…Recent studies suggest that various nutrients affect the mind of mammals; administration of caffeine [1], succinic acids [2] and dietary soy phytoestrogens [3] improved anxiety in rats. Dietary amino acid imbalance is also involved in emotion [4].…”

Section: Introductionmentioning

confidence: 99%

Anxiolytic effects of short- and long-term administration of cacao mass on rat elevated T-maze test

Yamada

Yumura

Okano

et al. 2009

The Journal of Nutritional Biochemistry

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Anxiolytic effect of serotonin depletion in the novelty-induced hypophagia test

Cited by 40 publications

References 37 publications

Overlapping and Distinct Brain Regions Associated with the Anxiolytic Effects of Chlordiazepoxide and Chronic Fluoxetine

Overlapping and Distinct Brain Regions Associated with the Anxiolytic Effects of Chlordiazepoxide and Chronic Fluoxetine

Constitutive Increases in Amygdalar Corticotropin-Releasing Factor and Fatty Acid Amide Hydrolase Drive an Anxious Phenotype

Anxiolytic effects of short- and long-term administration of cacao mass on rat elevated T-maze test

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