Stress, Brain Adenosine Signaling, and Fatigue-Related Behavioral Processes

Plumb, Traci N.; Sterlace, Sarah R.; Cavanaugh, Kelly A.; Minor, Thomas R.

doi:10.1007/978-1-4614-3903-5_25

Cited by 8 publications

(8 citation statements)

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“…Perhaps the benefit of post-stress glucose is independent of hippocampal processing and is instead simply derived from its ability to prevent metabolic exhaustion. Fear is an intensely catabolic state and rapidly challenges brain metabolic homeostasis [ 2 , 8 , 9 , 10 , 19 , 46 ]. Under these circumstances, adenosine is released to inhibit further activity in an effort to prevent cell death.…”

Section: Discussionmentioning

confidence: 99%

“…All rats are then tested 24 h later for escape-performance in a shuttle box. Rats that receive inescapable shock show a profound, exaggerated fear response and shuttle-escape deficits during testing [ 8 , 9 , 10 ]. This transition to an unresponsive, depression-like state is referred to as conservation-withdrawal [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

“…A number of findings suggest that metabolic homeostasis is challenged by exposure to uncontrollable, traumatic stress [ 8 , 9 , 10 , 12 , 13 ]. Minor and Saade (1997) hypothesized that simply treating rats with glucose following traumatic stress would restore energy homeostasis and eliminate the helplessness effect [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

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Post-Stress Fructose and Glucose Ingestion Exhibit Dissociable Behavioral and Physiological Effects

et al. 2019

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An acute traumatic event can lead to lifelong changes in stress susceptibility and result in psychiatric disease such as Post-Traumatic Stress Disorder (PTSD). We have previously shown that access to a concentrated glucose solution for 24 h beginning immediately after trauma decreased stress-related pathology in the learned helplessness model of PTSD and comorbid major depression. The current study sought to investigate the peripheral physiological effects of post-stress glucose consumption. We exposed 128 male Sprague-Dawley rats to inescapable and unpredictable 1-milliamp electric tail shocks or simple restraint in the learned helplessness procedure. Rats in each stress condition had access to a 40% glucose solution, 40% fructose solution, or water. Blood and liver tissue were extracted and processed for assay. We assessed corticosterone, corticosteroid-binding globulin (CBG), glucose, and liver glycogen concentrations at various time points following stress. We found that rats given access to glucose following exposure to traumatic shock showed a transient rise in blood glucose and an increase in liver glycogen repletion compared to those that received water or fructose following exposure to electric shock. We also found that animals given glucose following shock exhibited reduced free corticosterone and increased CBG compared to their water-drinking counterparts. However, this difference was not apparent when glucose was compared to fructose. These data suggest that post-stress glucose prophylaxis is likely not working via modulation of the HPA axis, but rather may provide its benefit by mitigating the metabolic challenges of trauma exposure.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Post-Stress Fructose and Glucose Ingestion Exhibit Dissociable Behavioral and Physiological Effects

et al. 2019

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“…As testing progresses, inescapably shocked rats rapidly transition to an unresponsive, depression-like state, termed conservation-withdrawal . The transition to conservation-withdrawal is evident as a profound deficit in escape performance (Minor et al, 1994a,b; Plumb et al, 2013). Experience with inescapable shock also results in behavioral depression as defined by the forced swim task (Weiss et al, 1981) and sucrose preference (Christianson et al, 2008; but see Dess, 1992), disturbances in sleep (Adrien et al, 1991), exaggerated startle (Servatius et al, 1995), anorexia (Weiss, 1968; Dess et al, 1989), anhedonia (Zacharko and Anisman, 1991), anxiety as measured by decreased social interaction (Short and Maier, 1993) and the elevated plus maze (Steenbergen et al, 1989), reinstatement of drug seeking (Figueroa-Guzman et al, 2011) and attentional/cognitive deficits in rats (Jackson et al, 1980; Minor et al, 1984; Shors, 2004).…”

Section: Learned Helplessnessmentioning

confidence: 99%

“…Thus, the animal enters the test session in a state of conservation withdrawal, a behavior deemed to conserve energy resources. This behavior limits the animal's motivation to escape, and is mediated by adenosine signaling in the nucleus accumbens core (Minor et al, 1994a,b, 2001, 2006, 2008, 2010; Plumb et al, 2013). Furthermore, consumption of glucose following the trauma, which has been shown to replete energy reserves (Conoscenti et al, 2019), eliminates the negative behavioral consequences of stress (Minor and Saade, 1997; Conoscenti et al, 2017, 2019).…”

Section: Learned Helplessnessmentioning

confidence: 99%

Dissociation in Effective Treatment and Behavioral Phenotype Between Stress-Enhanced Fear Learning and Learned Helplessness

Conoscenti

Fanselow

2019

Front. Behav. Neurosci.

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Post-traumatic stress disorder (PTSD) is a debilitating disease with relatively high lifetime prevalence. It is marked by a high diversity of symptoms and comorbidity with other psychiatric disease. Furthermore, PTSD has a high level of origin and symptom heterogeneity within the population. These characteristics taken together make it one of the most challenging diseases to effectively model in animals. However, with relatively little headway made in developing effective disease interventions, PTSD remains as a high priority target for animal model study. Learned Helplessness (LH) is a procedure classically used to model depression, but has in recent years transitioned to use as a model of PTSD. Animals in this procedure receive 100 inescapable and unpredictable tailshocks or simple restraint without shock. The following day, the animals are tested in a shuttle box, where inescapably-shocked subjects exhibit exaggerated fear and profound deficit in escape performance. Stress-enhanced fear learning (SEFL) also uses an acute (single session) stressor for modeling PTSD in rodents. The SEFL procedure begins with exposure to 15 footshocks or simple context exposure without shock. Animals that initially received the 15 footshocks exhibit future enhanced fear learning. In this review, we will compare the behavior, physiology, and interventions of these two animal models of PTSD. Despite considerable similarity (a single session containing inescapable and uncontrollable shock) the two procedures produce a very divergent set of behavioral consequences.

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Temporal parameters of post-stress prophylactic glucose treatment in rats

Conoscenti

Hart

Smith

et al. 2017

Stress

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Acute trauma can lead to life-long changes in susceptibility to psychiatric disease, such as post-traumatic stress disorder (PTSD). Rats given free access to a concentrated glucose solution for 24 h beginning immediately after trauma failed to show stress-related pathology in the learned helplessness model of PTSD and comorbid major depression. We assessed effective dosing and temporal constraints of the glucose intervention in three experiments. We exposed 120 male Sprague-Dawley rats to 100, 1 mA, 3-15 s, inescapable and unpredictable electric tail shocks (over a 110-min period) or simple restraint in the learned helplessness procedure. Rats in each stress condition had access to a 40% glucose solution or water. We measured fluid consumption under 18-h free access conditions, or limited access (1, 3, 6, 18 h) beginning immediately after trauma, or 3-h access with delayed availability of the glucose solution (0, 1, 3, 6 h). We hypothesized that longer and earlier access following acute stress would improve shuttle-escape performance. Rats exposed to traumatic shock and given 18-h access to glucose failed to show exaggerated fearfulness and showed normal reactivity to foot shock during testing as compared to their water-treated counterparts. At least 3 h of immediate post-stress access to glucose were necessary to see these improvements in test performance. Moreover, delaying access to glucose for more than 3 h post-trauma yielded no beneficial effects. These data clearly identify limits on the post-stress glucose intervention. In conclusion, glucose should be administered almost immediately and at the highest dose after trauma.

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Stress, Brain Adenosine Signaling, and Fatigue-Related Behavioral Processes

Cited by 8 publications

References 106 publications

Post-Stress Fructose and Glucose Ingestion Exhibit Dissociable Behavioral and Physiological Effects

Post-Stress Fructose and Glucose Ingestion Exhibit Dissociable Behavioral and Physiological Effects

Dissociation in Effective Treatment and Behavioral Phenotype Between Stress-Enhanced Fear Learning and Learned Helplessness

Temporal parameters of post-stress prophylactic glucose treatment in rats

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