Appetitive Operant Behavior and Free-Feeding in Rats Exposed to Acute Stress

Youngblood, Bradley D.; Ryan, Donna H.; Harris, Ruth B. S.

doi:10.1016/s0031-9384(97)00245-x

Cited by 13 publications

(7 citation statements)

References 22 publications

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“…Although it is known that stress influences feeding behavior, the effect of stress on gustatory response in the taste system has not been investigated (23,24,75,91,98,102). The BNST is believed to be involved in modulating behavioral responses to stress (26).…”

Section: Discussionmentioning

confidence: 99%

Efferent projection from the bed nucleus of the stria terminalis suppresses activity of taste-responsive neurons in the hamster parabrachial nuclei

Li¹,

Cho²

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Although the reciprocal projections between the bed nucleus of the stria terminalis (BNST) and the gustatory parabrachial nuclei (PbN) have been demonstrated neuroanatomically, there is no direct evidence showing that the projections from the PbN to the BNST carry taste information or that descending inputs from the BNST to the PbN modulate the activity of PbN gustatory neurons. A recent electrophysiological study has demonstrated that the BNST exerts modulatory influence on taste neurons in the nucleus of the solitary tract (NST), suggesting that the BNST may also modulate the activity of taste neurons in the PbN. In the present study, we recorded from 117 taste-responsive neurons in the PbN and examined their responsiveness to electrical stimulation of the BNST bilaterally. Thirteen neurons (11.1%) were antidromically invaded from the BNST, mostly from the ipsilateral side (12 cells), indicating that a subset of taste neurons in the PbN project their axons to the BNST. The BNST stimulation induced orthodromic responses on most of the PbN neurons: 115 out of 117 (98.3%), including all BNST projection units. This descending modulation on the PbN gustatory neurons was exclusively inhibitory. We also confirmed that activation of this efferent inhibitory projection from the BNST reduces taste responses of PbN neurons in all units tested. The BNST is part of the neural circuits that involve stress-associated feeding behavior. It is also known that brain stem gustatory nuclei, including the PbN, are associated with feeding behavior. Therefore, this neural substrate may be important in the stress-elicited alteration in ingestive behavior.

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Section: Discussionmentioning

confidence: 99%

Efferent projection from the bed nucleus of the stria terminalis suppresses activity of taste-responsive neurons in the hamster parabrachial nuclei

Li¹,

Cho²

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Chronic caloric restriction blocks the ability of restraint stress to suppress food intake in rats (Youngblood et al 1997), whereas restraint stress is robustly hypophagic in ad libitum (ad lib)-fed rats (Krahn et al 1986). Caloric deficit also is sufficient to decrease hypophagic responses to an acute inflammatory event (Lennie et al 1995) or to systemic administration of CCK (McMinn et al 2000), indicating that caloric deficit reduces the ability of both cognitive and visceral stressors to suppress food intake.…”

Section: Emotional and Behavioral Stress Responsesmentioning

confidence: 99%

Interoceptive modulation of neuroendocrine, emotional, and hypophagic responses to stress

Maniscalco

Rinaman

2017

Physiology & Behavior

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Periods of caloric deficit substantially attenuate many centrally mediated responses to acute stress, including neural drive to the hypothalamic-pituitary-adrenal (HPA) axis, anxiety-like behavior, and stress-induced suppression of food intake (i.e., stress hypophagia). It is posited that this stress response plasticity supports food foraging and promotes intake during periods of negative energy balance, even in the face of other internal or external threats, thereby increasing the likelihood that energy stores are repleted. The mechanisms by which caloric deficit alters central stress responses, however, remain unclear. The caudal brainstem contains two distinct populations of stress-recruited neurons [i.e., noradrenergic neurons of the A2 cell group that co-express prolactin-releasing peptide (PrRP+ A2 neurons), and glucagon-like peptide 1 (GLP-1) neurons] that also are responsive to interoceptive feedback about feeding and metabolic status. A2/PrRP and GLP-1 neurons have been implicated anatomically and functionally in the central control of the HPA axis, anxiety-like behavior, and stress hypophagia. The current review summarizes a growing body of evidence that caloric deficits attenuate physiological and behavioral responses to acute stress as a consequence of reduced recruitment of PrRP+ A2 and hindbrain GLP-1 neurons, accompanied by reduced signaling to their brainstem, hypothalamic, and limbic forebrain targets.

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“…Although, chronic variable stress paradigms often decrease consumption of a weak sucrose solution, which has been attributed to stressinduced anhedonia (9,44,45), results from such studies vary (46,47), and the concentrations of the sucrose solutions are low (e.g. 1-2%), having little taste or metabolic impact.…”

Section: Feedforward Effects Of Stressmentioning

confidence: 99%

Chronic Stress Promotes Palatable Feeding, which Reduces Signs of Stress: Feedforward and Feedback Effects of Chronic Stress

Pecoraro¹,

Reyes²,

Gómez³

et al. 2004

Endocrinology

513

382

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We suggested a new model of the effects of glucocorticoids (GCs) exerted during chronic stress, in which GCs directly stimulate activities in the brain while indirectly inhibiting activity in the hypothalamo-pituitary-adrenal (HPA) axis through their metabolic shifts in energy stores in the periphery. This study is an initial test of our model. In a 2 x 2 design, we provided ad lib access to calorically dense lard and sucrose (comfort food) + chow or chow alone, and repeatedly restrained half of the rats in each group for 5 d (3 h/d). We measured caloric intake, body weight, caloric efficiency, ACTH, corticosterone (B), and testosterone during the period of restraint and leptin, insulin, and fat depot weights, as well as hypothalamic corticotropin-releasing factor mRNA at the end of the period. We hypothesized that chronically restrained rats would exhibit a relative increase in comfort food ingestion and that these rats would have reduced HPA responses to repeated restraint. Although total caloric intake was reduced in both groups of restrained rats, compared with controls, the proportion of comfort food ingested increased in the restrained rats compared with their nonrestrained controls. Moreover, caloric efficiency was rescued in the stressed, comfort food group. Furthermore, ACTH and B responses to the repeated restraint bouts were reduced in the rats with access to comfort food. Corticotropin-releasing factor mRNA was reduced in control rats eating comfort food compared with those eating chow, but there were no differences between the stressed groups. The results of this experiment tend to support our model of chronic effects of stress and GCs, showing a stressor-induced preference for comfort food, and a comfort-food reduction in activity of the HPA axis.

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Appetitive Operant Behavior and Free-Feeding in Rats Exposed to Acute Stress

Cited by 13 publications

References 22 publications

Efferent projection from the bed nucleus of the stria terminalis suppresses activity of taste-responsive neurons in the hamster parabrachial nuclei

Efferent projection from the bed nucleus of the stria terminalis suppresses activity of taste-responsive neurons in the hamster parabrachial nuclei

Interoceptive modulation of neuroendocrine, emotional, and hypophagic responses to stress

Chronic Stress Promotes Palatable Feeding, which Reduces Signs of Stress: Feedforward and Feedback Effects of Chronic Stress

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