The consequences of uncontrollable stress are sensitive to duration of prior wheel running

Greenwood, Benjamin N.; Foley, Teresa E.; Burhans, Dan; Maier, Steven F.; Fleshner, Monika

doi:10.1016/j.brainres.2004.11.037

Cited by 128 publications

(163 citation statements)

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Section: Serotonergic Gene Expression Following Chronic Crf Receptor mentioning

confidence: 99%

“…These peptides may respond differently under acute and chronic stress exposure than the serotonergic component. The internal anatomical complexity of the DRN has been more clearly appreciated recently (Rattray et al, 1999, Commons et al, 2003, Abrams et al, 2004, Abrams et al, 2005, Greenwood et al, 2005, Clark et al, 2006, and discrete changes in serotonergic gene expression in subregions of raphe could be sufficient to induce substantial behavioral changes.Of particular note, CRF receptor distribution in DRN is complex and varies by region (Day et al, 2004, Pernar et al, 2004. Recent reports have emphasized the discrete subregional nature of DRN response to both direct and indirect (via the basolateral amygala) exposure to CRF receptor ligands (Forster et al, 2006, Spiga et al, 2006.…”

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confidence: 99%

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Chronic low dose ovine corticotropin releasing factor or urocortin II into the rostral dorsal raphe alters exploratory behavior and serotonergic gene expression in specific subregions of the dorsal raphe

et al. 2007

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Corticotropin releasing factor (CRF) family peptides play key roles in integrating neural responses to stress. Both major CRF receptors have been pharmacologically identified in the dorsal raphe nucleus (DRN), a stress sensitive and internally heterogeneous nucleus supplying many forebrain regions with serotonergic input. Despite the involvement of chronic stress and serotonergic dysfunction in human mood and anxiety disorders, little is known about the effects of chronic CRF receptor activation on the DRN. We infused ovine CRF (1ng/hr), urocortin II (UCNII, 1ng/hr), or vehicle alone into rat DRN over 6 days. During infusion, animals were allowed to freely explore an open field for 15 minutes on each of two days, with the addition of a novel object on the second day. Following behavioral testing, 5-HT 1A , 5-HT 1B , serotonin transporter (SERT), and tryptophan hydroxylase-2 (Tph2) expression were examined through the DRN by in situ hybridization. Ovine CRF infusion resulted in significantly decreased novel object touches, climbs, as well as increased latency to first novel object contact. UCNII had a similar but less dramatic effect, decreasing only climbing behavior. Both ovine CRF and UCNII blunted the decrease in corner time expected on reexposure to the open field. Both peptides also produced regionally specific changes in gene expression: 5-HT 1A expression was increased 30% in the mid-rostral ventromedial DRN, while SERT was decreased by 30% in the mid-caudal shell dorsomedial DRN. There also appeared to be a shift in the relative level of Tph2 expression between the ventromedial and core dorsomedial DRN at the mid-rostral level. Changes in 5-HT 1A , SERT, and relative Tph2 mRNA abundance were correlated with novel object exploration. These findings suggest chronic intra-DRN administration of CRF agonists decreases exploratory behavior, while producing subregionally limited changes in serotonergic gene expression. These studies may be relevant to mechanisms underlying behavioral changes after chronic stress. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptDepression and anxiety disorders are among the leading causes of morbidity, mortality, and disability in the United States (Greenberg et al., 2003). They are often comorbid, and both are highly associated with chronic exposure to stress. Multiple lines of evidence suggest that chronic and inescapable stress produce long lasting effects on brain function and behavior that play a prominent role in the development, maintenance, and recurrence of both depression and a variety of anxiety disorders (Gulley and Nemeroff, 1993, Arborelius et al., 1999, Ressler and Nemeroff, 2000.Altered serotonin neurotransmission appears to be a central mechanism inducing both depressive (Maes and Meltzer, 1995) and anxiety disorders (Ressler and Nemeroff, 2000). The majority of serotonergic fibers to forebrain regions thought to be involved in mood and anxiety regulation arise from the dorsal raphe nucleus (DRN) and median raphe nucleus (MRN) ...

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Section: Serotonergic Gene Expression Following Chronic Crf Receptor mentioning

confidence: 99%

mentioning

confidence: 99%

Chronic low dose ovine corticotropin releasing factor or urocortin II into the rostral dorsal raphe alters exploratory behavior and serotonergic gene expression in specific subregions of the dorsal raphe

et al. 2007

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“…Exercise has many stress-buffering effects (Fleshner, 2005) and it is possible that the antidepressant properties of exercise are mediated through resistance against the effects of stress on hippocampal BDNF. Indeed, voluntary wheel running in rats can prevent the development of depressive-like behaviors in animal models of depression that depend on exposure to stress (Dishman, 1997b, Solberg et al, 1999, Moraska and Fleshner, 2001, Greenwood et al, 2005a, Zheng et al, 2006. For example, we have reported that wheel running prevents behavioral consequences of inescapable tail shock stress (IS), or learned helplessness (LH; .…”

Section: Introductionmentioning

confidence: 99%

“…Our approach employed stress, wheel running, acute administration of the selective serotonin (5-HT) reuptake inhibitor (SSRI) fluoxetine, or intra-DG microinjections of BDNF as means to manipulate levels of BDNF in the hippocampus. We hypothesized that 1) IS would decrease hippocampal BDNF in a time course consistent with LH behaviors, which are maximal 24 hours post-IS but are gone 72 hours post-IS , 2) 6 weeks, but not 3 weeks, of wheel running would prevent the IS-induced suppression of BDNF because 6 weeks, but not 3 weeks, of wheel running prevents LH (Greenwood et al, 2005a), 3) BDNF suppression in the hippocampus of physically active animals would restore LH in these animals following IS, and 4) increasing BDNF levels in the hippocampus of sedentary rats by microinjecting BDNF into the DG would prevent LH. We also examined BDNF levels in the prefrontal cortex (PFC), because this area is known to be involved in behavioral responses to stress (Vermetten andBremner, 2002, Amat et al, 2005) and to demonstrate stress-induced changes in BDNF opposite to those observed in the hippocampus , Lee et al, 2006.…”

Section: Introductionmentioning

confidence: 99%

Learned helplessness is independent of levels of brain-derived neurotrophic factor in the hippocampus

et al. 2007

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Reduced levels of brain-derived neurotrophic factor (BDNF) in the hippocampus have been implicated in human affective disorders and behavioral stress responses. The current studies examined the role of BDNF in the behavioral consequences of inescapable stress, or learned helplessness. Inescapable stress decreased BDNF mRNA and protein in the hippocampus of sedentary rats. Rats allowed voluntary access to running wheels for either 3 or 6 weeks prior to exposure to stress were protected against stress-induced reductions of hippocampal BDNF protein.The observed prevention of stress-induced deceases in BDNF, however, occurred in a time course inconsistent with the prevention of learned helplessness by wheel running, which is evident following 6 weeks, but not 3 weeks, of wheel running. BDNF suppression in physically active rats was produced by administering a single injection of the selective serotonin reuptake inhibitor fluoxetine (10 mg/ kg) just prior to stress. Despite reduced levels of hippocampal BDNF mRNA following stress, physically active rats given the combination of fluoxetine and stress remained resistant against learned helplessness. Sedentary rats given both fluoxetine and stress still demonstrated typical learned helplessness behaviors. Fluoxetine by itself reduced BDNF mRNA in sedentary rats only, but did not affect freezing or escape learning 24 hours later. Finally, bilateral injections of BDNF (1 μg) into the dentate gyrus prior to stress prevented stress-induced reductions of hippocampal BDNF but did not prevent learned helplessness in sedentary rats.These data indicate that learned helplessness behaviors are independent of the presence or absence of hippocampal BDNF because blocking inescapable stress-induced BDNF suppression does not always prevent learned helplessness, and learned helplessness does not always occur in the presence of reduced BDNF. Results also suggest that the prevention of stress-induced hippocampal BDNF suppression is not necessary for the protective effect of wheel running against learned helplessness.

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“…[4,8]). In particular, this has been studied for the case of mood regulation mechanisms in depressions, among others by using an animal model for human learned helplessness; e.g., [15,16,17,18,25]. It turns out that the extent of learned helplessness can substantially decrease when more physical activity is undertaken.…”

Section: Introductionmentioning

confidence: 99%

Computational Modeling and Analysis of the Role of Physical Activity in Mood Regulation and Depression

Both

Hoogendoorn

Klein

et al. 2010

Neural Information Processing. Theory and Algorithms

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Abstract. Physical activity is often considered an important factor in handling mood regulation and depression. This paper presents a computational model of this role of physical activity in mood regulation. It is shown on the one hand how a developing depression can go hand in hand with a low level of physical activity, and on the other hand, how Exercise Therapy is able to reverse this pattern and make the depression disappear. Simulation results are presented, and properties are formally verified against these simulation runs.

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The consequences of uncontrollable stress are sensitive to duration of prior wheel running

Cited by 128 publications

References 83 publications

Chronic low dose ovine corticotropin releasing factor or urocortin II into the rostral dorsal raphe alters exploratory behavior and serotonergic gene expression in specific subregions of the dorsal raphe

Chronic low dose ovine corticotropin releasing factor or urocortin II into the rostral dorsal raphe alters exploratory behavior and serotonergic gene expression in specific subregions of the dorsal raphe

Learned helplessness is independent of levels of brain-derived neurotrophic factor in the hippocampus

Computational Modeling and Analysis of the Role of Physical Activity in Mood Regulation and Depression

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