Spatio–temporal dynamics of brain activated regions during drinking behavior in rats

Tabuchi, Eiichi; Yokawa, Takashi; Mallick, Hrudananda; Inubushi, Toshiro; Kondoh, Takashi; Ono, Taketoshi; Torii, Kunio

doi:10.1016/s0006-8993(02)03173-6

Cited by 34 publications

(25 citation statements)

References 44 publications

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“…LH neurons encode sensory stimuli (Norgren, 1970; Yamamoto et al, 1989), including reward-associated cues (Nakamura et al, 1987). LH neurons also fire during both feeding (Burton et al, 1976; Schwartzbaum, 1988) and drinking (Tabuchi et al, 2002). However, making sense of the remarkable functional heterogeneity observed in the LH has been a major challenge in the field.…”

Section: Introductionmentioning

confidence: 99%

Decoding Neural Circuits that Control Compulsive Sucrose Seeking

Nieh

Matthews

Allsop

et al. 2015

Cell

327

249

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The lateral hypothalamic (LH) projection to the ventral tegmental area (VTA) has been linked to reward processing, but the computations within the LH-VTA loop that give rise to specific aspects of behavior have been difficult to isolate. We show that LH-VTA neurons encode the learned action of seeking a reward, independent of reward availability. In contrast, LH neurons downstream of VTA encode reward-predictive cues and unexpected reward omission. We show that inhibiting the LH-VTA pathway reduces “compulsive” sucrose-seeking, but not food consumption in hungry mice. We reveal that the LH sends excitatory and inhibitory input onto VTA dopamine (DA) and GABA neurons, and that the GABAergic projection drives feeding-related behavior. Our study overlays information about the type, function and connectivity of LH neurons and identifies a neural circuit that selectively controls compulsive sugar consumption, without preventing feeding necessary for survival, providing a potential target for therapeutic interventions for compulsive-overeating disorder.

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Section: Introductionmentioning

confidence: 99%

Decoding Neural Circuits that Control Compulsive Sucrose Seeking

Nieh

Matthews

Allsop

et al. 2015

Cell

327

249

View full text Add to dashboard Cite

show abstract

“…Because the hedonic/rewarding properties of sucrose, saccharin, or sex appear sufficient to dampen subsequent stress responses, we hypothesized that brain reward regions, such as the BLA, are likely to mediate these effects. Neuronal activity in the amygdala, including the BLA, is altered in humans and other animals while they are engaging in pleasurable behaviors, including eating ap- petizing foods (20)(21)(22)(23). The amygdala is also activated in humans and other animals during stress (24,25), and the BLA subregion is implicated in neuroendocrine and behavioral stress responses (26)(27)(28).…”

Section: Rewarding Properties Of Palatable Food Dampen Collective Stressmentioning

confidence: 99%

Pleasurable behaviors reduce stress via brain reward pathways

Ulrich‐Lai¹,

Christiansen²,

Ostrander³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

187

194

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Individuals often eat calorically dense, highly palatable "comfort" foods during stress for stress relief. This article demonstrates that palatable food intake (limited intake of sucrose drink) reduces neuroendocrine, cardiovascular, and behavioral responses to stress in rats. Artificially sweetened (saccharin) drink reproduces the stress dampening, whereas oral intragastric gavage of sucrose is without effect. Together, these results suggest that the palatable/rewarding properties of sucrose are necessary and sufficient for stress dampening. In support of this finding, another type of natural reward (sexual activity) similarly reduces stress responses. Ibotenate lesions of the basolateral amygdala (BLA) prevent stress dampening by sucrose, suggesting that neural activity in the BLA is necessary for the effect. Moreover, sucrose intake increases mRNA and protein expression in the BLA for numerous genes linked with functional and/or structural plasticity. Lastly, stress dampening by sucrose is persistent, which is consistent with long-term changes in neural activity after synaptic remodeling. Thus, natural rewards, such as palatable foods, provide a general means of stress reduction, likely via structural and/or functional plasticity in the BLA. These findings provide a clearer understanding of the motivation for consuming palatable foods during times of stress and influence therapeutic strategies for the prevention and/or treatment of obesity and other stress-related disorders.corticosterone | anxiety-related behavior | synaptophysin | cAMP response element-binding protein | calcium/calmodulin-dependent protein kinase T he obesity epidemic is fueled by the easy availability of palatable, calorically dense foods amid an ever-escalating level of daily stress (1-3). Humans and rodents increase palatable food consumption when stressed (3-6), and the term "comfort food" is commonly used to signify possible stress-dampening properties of certain foods (particularly calorically dense foods containing high amounts of carbohydrates and/or fats). Indeed, comfort food intake in humans is linked with improved emotional states (7), and a high-carbohydrate diet is associated with reduced resting and stress-evoked cortisol levels (8-11).Stress (a real or perceived threat to homeostasis or well-being) typically evokes both physiological and emotional responses (reviewed in ref. 12). The physiological responses include activation of the hypothalamic-pituitary-adrenocortical (HPA) axis and the sympathetic branch of the autonomic nervous system. Activation of the sympathetic nervous system has numerous effects, including increases in heart rate and blood pressure. Activation of the HPA axis results in elevations in circulating adrenocorticotropic hormone (ACTH) and glucocorticoids (e.g., cortisol in humans and corticosterone in rats). Glucocorticoids have widespread action on numerous physiological processes, including mobilization of stored energy and maintenance of vascular tone. Perceived stressors also engage emotional respons...

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“…Despite fMRI studies being feasible in awake, behaving rats (e.g. investigation of drinking behaviour: Tabuchi et al 2002), such experiments have not yet been performed systematically, and phMRI studies in rats have involved comparisons between the effect of a drug versus baseline and have not investigated the pharmacological modulation of behaviour. However, phMRI responses to a pharmacological challenge alone have been investigated in the rat and human brain.…”

Section: Comparison Of Phmri Responses Between Preclinical Species Anmentioning

confidence: 99%