Fox odour affects corticosterone release but not hippocampal serotonin reuptake and open field behaviour in rats.
ABSTRACT Group-housed Sprague-Dawley (SD) rats exposed for 1 h to 2,5-dihydro-2,4,5-trimethylthiazoline (TMT, a component of fox feces) did not display changes in hippocampal serotonin (5-HT) metabolism and [3H]5-HT reuptake, compared to water or butyric acid. Such an observation extended to isolated SD and Fischer 344 rats. When group-housed SD rats were tested 1 week after a 1-h exposure to TMT, hippocampal 5-HT metabolism, [3H]5-HT reuptake, and [3H]paroxetine binding at the 5-HT transporter remained unchanged. This study questions TMT as a specific predatory stimulus as both butyric acid and TMT increased plasma corticosterone levels whilst leaving intact open field behaviour (at least in group-housed SD rats).
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ABSTRACT: An intricate interplay between different brain neurotransmitter and neuropeptide systems coordinates the neuroendocrine, autonomic and behavioural responses to stress. Under normal conditions, the body has appropriate mechanisms to respond to acute stressful challenges, but chronic stress may evolve in maladaptive coping processes, resulting in an enhanced risk for illness. Disturbances at the level of both corticotropin-releasing factor (CRF) and serotonin (5-HT) have been implicated in the etiology of stress-related psychiatric disorders, such as major depression and anxiety. Therefore, this chapter is dedicated to the effects of stress on serotonergic neurotransmission and the role of CRF herein. The first part of this chapter covers the neuroanatomical evidence for interactions between CRF and 5-HT at the level of the raphe nuclei. Further, the effects of stress and CRF on different aspects of serotonergic neurotransmission will be addressed, including expression of c-fos in the raphe nuclei, serotonin synthesis and firing rate of serotonergic neurons. Moreover, the effects of five selected stressors (immune stress, forced swimming, tail pinch, electric shock/fear conditioned stress and predator stress), differing in their physical and psychological impact, on the levels of 5-HT and its metabolite 5-hydroxyindoleacetic acid in forebrain regions will be discussed. The data presented here underscore the concept that stress, possibly via activation of the CRF system, affects serotonergic neurotransmission. Stress seems to exert predominantly stimulatory effects on the 5-HT system, at least in higher brain structures such as the hippocampus. Long-term changes in the CRF system, e.g. chronic elevation of brain levels of CRF or dysfunctioning of CRF receptor type 1, have profound consequences for the stress responsiveness of the hippocampal 5-HT system. Notwithstanding the vast amount of data on the effects of stress on serotonergic neurotransmission, the wide variety of experimental protocols used until now has uncovered the clear need for more systematic and neuroanatomically detailed approaches to further elucidate the interactions between stress, CRF and 5-HT. Such strategies will increase our knowledge on ‘healthy’ stress processing and may consequently lead to a better understanding of the putative maladaptive processes involved in the etiology of stress-related psychiatric and other disorders.Techniques in the Behavioral and Neural Sciences 01/2005; 15:503-524. DOI:10.1016/S0921-0709(05)80028-8
European Neuropsychopharmacology 09/2011; 21. DOI:10.1016/S0924-977X(11)70904-X · 5.40 Impact Factor
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ABSTRACT: We aimed to quantify stress-induced hyperglycemia and differentiate the glucose response between normal animals and those with diabetes. We also examined the pattern in glucose fluctuation induced by stress according to type of diabetes. To load psychological stress on animal models, we used a predator stress model by exposing rats to a cat for 60 minutes and measured glucose level from the beginning to the end of the test to monitor glucose fluctuation. We induced type 1 diabetes model (T1D) for ten Sprague-Dawley rats using streptozotocin and used five Otsuka Long-Evans Tokushima Fatty rats as obese type 2 diabetes model (OT2D) and 10 Goto-Kakizaki rats as nonobese type 2 diabetes model (NOT2D). We performed the stress loading test in both the normal and diabetic states and compared patterns of glucose fluctuation among the three models. We classified the pattern of glucose fluctuation into A, B, and C types according to speed of change in glucose level. Increase in glucose, total amount of hyperglycemic exposure, time of stress-induced hyperglycemia, and speed of glucose increase were significantly increased in all models compared to the normal state. While the early increase in glucose after exposure to stress was higher in T1D and NOT2D, it was slower in OT2D. The rate of speed of the decrease in glucose level was highest in NOT2D and lowest in OT2D. The diabetic state was more vulnerable to stress compared to the normal state in all models, and the pattern of glucose fluctuation differed among the three types of diabetes. The study provides basic evidence for stress-induced hyperglycemia patterns and characteristics used for the management of diabetes patients.Diabetes & metabolism journal 12/2013; 37(6):475-483. DOI:10.4093/dmj.2013.37.6.475This article is viewable in ResearchGate's enriched formatRG Format enables you to read in context with side-by-side figures, citations, and feedback from experts in your field.