Stress-related Behavioral Changes Research Articles

Pituitary adenylate cyclase-activating polypeptide deficient (PACAP-/-) mice display reduced c-Fos response to forced swim stress

Event Abstract Back to Event Pituitary adenylate cyclase-activating polypeptide deficient (PACAP-/-) mice display reduced c-Fos response to forced swim stress B. Gaszner1*, V. Kormos2, D. Reglődi3, T. Kozicz4 and Z. Helyes2 1 Univ. of Pecs, Hungary 2 Pécs University, Department of Pharmacol., Hungary 3 Pécs University, Dept. of Anat., Hungary 4 Radboud University, Dept. of Cell. Animal Physiol., Netherlands PACAP-/- mice show depression-like behavior in forced swim test (FST) and hyperlocomotion in open field (OF). Examination of c-Fos expression could explore which nuclei are involved in the behavioral changes. Here we hypothesized that PACAP-/- mice vs. wildtype counterparts upon OF and FST show altered neuronal activity in stress-related areas. Our results revealed that both locomotor activity in OF and immobility in FST were greater in PACAP-/- mice in accordance with the literature. Counting of c-Fos immunoreactive neurons revealed that stress increased the activity of all examined brain areas. Stressed PACAP-/- mice showed reduced c-Fos response in the oval, anterolateral and anteromedial bed nucleus of the stria terminalis (BNST), dorsal raphe (DR) and Edinger-Westphal nuclei (EW) moreover we found stress x genotype interaction. The c-Fos expression of the periaqueductal gray matter (PAG), paraventricular nucleus (PVN) and basolateral amygdaloid nucleus (BLA) did not drop significantly in stressed PACAP-/- mice but a clear interaction between stress and genotype was observed. The ventral lateral septum (LSv) showed markedly reduced c-Fos expression in transgenic mice without interaction. c-Fos expression in the central and medial amygdala and dorsal lateral septal nucleus were not influenced by PACAP. Based on these we conclude that specific PACAP influence on the BNST, DR, EW, PAG, PVN, BLA and LSv nuclei could play a role in stress-related behavioral changes. Keywords: Behaviour and cognition, Neuroscience Conference: 13th Conference of the Hungarian Neuroscience Society (MITT), Budapest, Hungary, 20 Jan - 22 Jan, 2011. Presentation Type: Abstract Topic: Behaviour and cognition Citation: Gaszner B, Kormos V, Reglődi D, Kozicz T and Helyes Z (2011). Pituitary adenylate cyclase-activating polypeptide deficient (PACAP-/-) mice display reduced c-Fos response to forced swim stress. Front. Neurosci. Conference Abstract: 13th Conference of the Hungarian Neuroscience Society (MITT). doi: 10.3389/conf.fnins.2011.84.00128 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 03 Mar 2011; Published Online: 23 Mar 2011. * Correspondence: Dr. B. Gaszner, Univ. of Pecs, Pécs, Hungary, balazs.b.gaszner@aok.pte.hu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers B. Gaszner V. Kormos D. Reglődi T. Kozicz Z. Helyes Google B. Gaszner V. Kormos D. Reglődi T. Kozicz Z. Helyes Google Scholar B. Gaszner V. Kormos D. Reglődi T. Kozicz Z. Helyes PubMed B. Gaszner V. Kormos D. Reglődi T. Kozicz Z. Helyes Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

From Classic Aspects of the Stress Response to Neuroinflammation and Sickness: Implications for Individuals and Offspring

Accumulating evidence suggests that exposure to psychological stressors leads to increased expression of pro-inflammatory cytokines and activation of inflammatory-related pathways in the central nervous system. Several logical predictions arise from these findings: (1) stressor exposure should produce changes in behavior that are reminiscent of acute illness; (2) administration of antiinflammatory agents should ameliorate some behavioral consequences of stressor exposure; and (3) there should be convergence between anatomical and neurochemical pathways activated by stressor exposure and those involved in mitigating sickness behaviors. Importantly, these predictions have been tested in our laboratory across multiple stressor paradigms (footshock, maternal separation, and during acute alcohol withdrawal) using two species (rats and guinea pigs), suggesting that sickness may represent a more general motivational state that can be elicited by a diverse range of psychological challenges. Implications of these findings for understanding stress-related changes in behavior, mood and neuroinflammatory processes will be discussed with special reference to implications for the individual and reproductive fitness.

Antidepressant-like effects of the vasopressin V1b receptor antagonist SSR149415 in the Flinders Sensitive Line rat

There is an increased interest in the potential of vasopressin receptor antagonists as antidepressants because of the involvement of vasopressin in stress-related behavioral changes. The present study sought to provide confirmatory evidence for the antidepressant-like effects of the selective vasopressin V1b receptor antagonist SSR149415, which had been previously demonstrated in a variety of animal models. The Flinders Sensitive Line (FSL) rat, a selectively bred animal model of depression, was chronically treated for 14 days with SSR149415 (1, 10, and 30 mg/kg), vehicle, or desipramine (5 mg/kg) as a positive control. Approximately 22–24 h after the last treatment, the rats were exposed to a single 5-min session in a cylinder containing 25 °C water and immobility was recorded. A control group of Flinders Resistant Line (FRL) rats was included as a reference group as well as one treated with 10 mg/kg SSR149415. Vehicle-treated FSL rats exhibited much more immobility than the FRL rats, and desipramine-treated FSL rats had much lower scores, as expected. Treatment with SSR149415 reduced immobility in the FSL rats at all doses, but only the higher doses reduced it such that they were no longer different from the FRL rats. In contrast, SSR149415 did not alter the lower immobility of the FRL rats. The social interaction test of anxiety was also examined in the FSL rats, at 20–22 h after the last of the 14 injections. Results showed that the 10 and 30 mg/kg doses of SSR149415 increased the time spent in social interaction in the FSL rats, suggesting anxiolytic effects. These findings confirm the antidepressant-like potential of SSR149415 and suggest that it may also have anxiolytic effects. It is likely that the strategy of testing selective vasopressin V1b receptor antagonists will be fruitful.

Involvement of brain endogenous cholecystokinin in stress-induced impairment of spatial recognition memory

The central fragment of cholecystokinin, CCK8, plays a critical role in stress-related changes in behavior and memory. Therefore, we investigated whether the endogenous cholecystokininergic system is involved in the impairment of attention and/or memory induced by stressful conditions. Plasma corticosterone concentrations increased three-fold and plasma adrenocorticotropin (ACTH); concentrations increased five-fold when rats were maintained in the open arm of an elevated plus maze for 5 min. The same stress conditions impaired spatial recognition in the two-trial memory task. In addition, this stress led to a significant decrease in the extracellular levels of cholecystokinin-like immunoreactivity in the dorsal subiculum/CA1 of the hippocampus and partially suppressed the increase obtained during the acquisition phase of memory. This suggests that the cholecystokininergic system in the hippocampus is involved in stress-induced impairment of spatial recognition memory.

β-adrenergic receptors are involved in stress-related behavioral changes

Cerebral noradrenergic systems have been implicated in stress-related changes in behavior. Previous studies with receptor antagonists suggested that α 1-adrenergic receptors were involved in defensive withdrawal in rats and in investigatory behavior in mice tested in the multicompartment chamber. However, β-adrenoceptor antagonists attenuated the restraint- and ICV CRF-induced changes in defensive withdrawal, suggesting that β-adrenergic receptors may also be involved in stress-related responses. To determine whether the β-adrenergic antagonist effect was limited to rats tested in the defensive withdrawal model, we studied the effects of L-propranolol in two other behavioral models. Propranolol pretreatment (2.5 mg/kg, IP) prevented the restraint-induced changes in the behavior of mice observed in the multicompartment chamber and the elevated plus-maze. It also decreased the plasma corticosterone response measured in restrained mice after plus-maze testing. To investigate further the role of central β-adrenergic receptors in defensive withdrawal, the effects of the β-adrenereceptor agonist isopoproterenol were tested. Isoproterenol (0.3–10 μg, ICV) produced a dose-dependent increase in defensive withdrawal, statistically ssgnificant after 3 and 10 μg. Propranolol prevented the isoproterenol-induced defensive withdrawal, suggesting that the effect of isoproterenol resulted from stimulation of β-adrenergic receptors. These results support earlier data suggesting the involvement of CNS β-adrenergic receptors in stress-related behavioral changes and suggest that β-adrenergic agonists exert anxiolytic effects that differ from those of the benzodiazepines.