Suppression of feeding and body weight by inescapable shock: Modulation by quinine adulteration, stress reinstatement, and controllability

Dess, Nancy K.; Minor, Thomas R.; Brewer, John I.

doi:10.1016/0031-9384(89)90224-2

Cited by 63 publications

(48 citation statements)

References 33 publications

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“…Although determining the mechanisms that lead to altered energy deposition and growth was not the primary focus of this study, we did evaluate factors known to influence these functions. Feed and metabolizable energy consumption were significantly reduced by repeated behavioral stress, and this response is consistent with the reduced feed or energy intake that results from other types of stress (18,33,34,37). On the other hand, feeding was enhanced during the recovery period after either one or three episodes of stress.…”

Section: Discussionsupporting

confidence: 76%

Energetic response to repeated restraint stress in rapidly growing mice

Laugero

Moberg

2000

American Journal of Physiology-Endocrinology and Metabolism

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There is a cost of stress that may result in the loss of normal biological function (e.g., growth). Repeated, and even single, applications of stressors have been shown to induce negative energy balance in rodents. However, here we addressed whether this energetic response changes during multiple stress exposure and whether there is complete recovery subsequent to the cessation of stress exposure. These questions were addressed in growing C57Bl/6 mice (31 day) by determining at different times the energetic and endocrine responses after the exposure to restraint (R) stress for 4 h applied once (R1), repeatedly over 3 days (R3), or repeatedly over 7 days (R7). Compared with control values, R elevated (P<0.05) plasma corticosterone and reduced plasma insulin-like growth factor I on all days of exposure to the stressor. Seven days, but not 1 or 3 days of R, decreased the net growth (126%, P<0.05) and deposition of fat (71%, P<0.05) and lean (60%, P<0.05) energy over the 7 days. Only R7 depressed the 7-day metabolizable energy intake (P<0.05), and R7, but not R1 or R3, increased the overall energy expenditure (10%, P<0.05). Our results demonstrate that repeated episodes of stress are energetically costly to the rapidly growing animal, but compensatory mechanisms mitigate this cost of repeated stress exposure and permit complete recovery of energy balance after the cessation of stress application.

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Section: Discussionsupporting

confidence: 76%

Energetic response to repeated restraint stress in rapidly growing mice

Laugero

Moberg

2000

American Journal of Physiology-Endocrinology and Metabolism

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“…In contrast, SAL animals exposed to the same footshock paradigm did in fact show a significant reduction in weight gain over the 10-day paradigm, as is typically observed in chronic stress protocols (Dess and Minor, 1989;DiasFerreira et al, 2009;Jankord and Herman, 2008). Indeed, the effects of stress on the HPA axis and the subsequent endocrine response are known to influence appetite as well as metabolic processes (McEwen, 2007).…”

Section: Discussionmentioning

confidence: 89%

Abnormal Stress Responsivity in a Rodent Developmental Disruption Model of Schizophrenia

Zimmerman

Bellaire

Ewing

et al. 2013

Neuropsychopharmacol

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Although numerous studies have implicated stress in the pathophysiology of schizophrenia, less is known about how the effects of stress interact with genetic, developmental, and/or environmental determinants to promote disease progression. In particular, it has been proposed that in humans, stress exposure in adolescence could combine with a predisposition towards increased stress sensitivity, leading to prodromal symptoms and eventually psychosis. However, the neurobiological substrates for this interaction are not fully characterized. Previous work in our lab has demonstrated that rats born to dams administered with the DNA-methylating agent methylazoxymethanol acetate (MAM) at gestational day 17 exhibit as adults behavioral and anatomical abnormalities consistent with those observed in patients with schizophrenia. Here, we examined behavioral and neuroendocrine responses to stress in the MAM model of schizophrenia. MAM-treated male rats were exposed to acute and repeated footshock stress at prepubertal, peripubteral, and adult ages. Ultrasonic vocalizations (USVs), freezing, and corticosterone responses were quantified. We found that juvenile MAM-treated rats emitted significantly more calls, spent more time vocalizing, emitted calls at a higher rate, and showed more freezing in response to acute footshock stress when compared with their saline (SAL) treated counterparts, and that this difference is not present in older animals. In addition, adolescent MAM-treated animals displayed a blunted HPA axis corticosterone response to acute footshock that did not adapt after 10 days of stress exposure. These data demonstrate abnormal stress responsivity in the MAM model of schizophrenia and suggest that these animals are more sensitive to the effects of stress in youth.

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“…These outcomes suggest that inescapably shocked rats not only experience more fear during pretreatment, but also begin the test task more afraid than do escapably shocked rats. Heightened fear at the time of testing is likely to alter the selection and processing of task-relevant stimuli Minor et al, 1988), reduce the capacity of endogenous vegetative processes to cope with the stressor (Anisman & Zacharko, 1986;Dess, Minor, & Brewer, 1989;Haracz et al, 1988;Weiss & Simson, 1985), and result in the perseveration of innately prepared or welltrained motor programs (Anisman & Zacharko, 1986).…”

Section: Discussionmentioning

confidence: 99%

Conditioned fear and neophobia following inescapable shock

Minor¹

1990

Animal Learning & Behavior

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Lick-suppression tests were used in seven experiments to assess the transsituational transfer of fear in the learned helplessness paradigm. Two sources of fear combined to suppress test drinking in inescapably shocked rats. A situational odor was strongly associated with shock pretreatments and mediated the transfer of conditioned fear during testing. Fear of the pretreatment odor was greater following inescapable shock than after escapable shock or restraint. This conditioned suppression was retained for at least 72 h after pretreatment. Neophobia was enhanced as a second, nonassociative reaction to inescapable shock. Unconditioned fear was augmented by a novel odor in the test context, but otherwise was weak and dissipated within 72 h. However, neophobia was necessary for differential conditioned suppression in inescapably shocked rats. The pretreatment odor elicited fear only when tested in a novel context. Initial habituation to the test apparatus reduced conditioned fear. These data provide additional evidence for odor-mediated transfer of helplessness. Conditioned fear and neophobia are discussed in relation to recent anxiety interpretations of the phenomenon.

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Suppression of feeding and body weight by inescapable shock: Modulation by quinine adulteration, stress reinstatement, and controllability

Cited by 63 publications

References 33 publications

Energetic response to repeated restraint stress in rapidly growing mice

Energetic response to repeated restraint stress in rapidly growing mice

Abnormal Stress Responsivity in a Rodent Developmental Disruption Model of Schizophrenia

Conditioned fear and neophobia following inescapable shock

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