Central administration of ghrelin alters emotional responses in rats: behavioural, electrophysiological and molecular evidence

Hansson, Caroline; Haage, David; Taube, Magdalena; Egecioglu, Emil; Salomé, Nicolas; Dickson, Suzanne L.

doi:10.1016/j.neuroscience.2011.02.002

Cited by 96 publications

(64 citation statements)

References 69 publications

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“…Chronic icv ghrelin treatment increases depression and anxiety related behaviors in male rats (Hansson et al, 2011), and the PVN appears to be an area particularly sensitive to the anxiogenic effects of ghrelin (Currie et al, 2012), possibly mediated through changes in AVP (Poretti et al, 2015). Serum ghrelin levels in humans are elevated in patients with major depression, and responders to treatments for depression and panic disorder have lower ghrelin levels than non-responders (Ishitobi et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Early life social stress induced changes in depression and anxiety associated neural pathways which are correlated with impaired maternal care

et al. 2015

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Exposures to various types of early life stress can be robust predictors of the development of psychiatric disorders, including depression and anxiety. The objective of the current study was to investigate the roles of the translationally relevant targets of central vasopressin, oxytocin, ghrelin, orexin, glucocorticoid, and the brain-derived neurotrophic factor (BDNF) pathway in an early chronic social stress (ECSS )based rodent model of postpartum depression and anxiety. The present study reports novel changes in gene expression and extracellular signal related kinase (ERK) protein levels in the brains of ECSS exposed rat dams that display previously reported depressed maternal care and increased maternal anxiety. Decreases in oxytocin, orexin, and ERK proteins, increases in ghrelin receptor, glucocorticoid and mineralocorticoid receptor mRNA levels, and bidirectional changes in vasopressin underscore related work on the adverse long-term effects of early life stress on neural activity and plasticity, maternal behavior, responses to stress, and depression and anxiety-related behavior. The differences in gene and protein expression and robust correlations between expression and maternal care and anxiety support increased focus on these targets in animal and clinical studies of the adverse effects of early life stress, especially those focusing on depression and anxiety in mothers and the transgenerational effects of these disorders on offspring.

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Section: Discussionmentioning

confidence: 99%

Early life social stress induced changes in depression and anxiety associated neural pathways which are correlated with impaired maternal care

et al. 2015

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“…A recent experiment investigating the role of ghrelin in the limbic system demonstrated that chronic intraventricular injections of ghrelin caused rats to display increased anxiety and depressive behaviors. In addition, the mRNA expression of 5-HT1A in the amygdaloid nucleus increased, and the electrical activity of neurons in the dorsal raphe nucleus was inhibited, which might explain the deterioration of the mood of rodents [24]. An experiment in which mice with genetic deletions in the ghrelin receptor gene (GHSR KO) were exposed to chronic stressors provided additional confirmation that ghrelin is an important factor in mediating stressor-provoked metabolic and serotonin changes.…”

Section: Interactions Between Ghrelin and The Serotonergic Systemmentioning

confidence: 97%

A review on the effect of the photoperiod and melatonin on interactions between ghrelin and serotonin

Kirsz

Zieba

2012

General and Comparative Endocrinology

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“…Lutter and colleagues [47], however, reported a decrease in anxiety- and depression-like behaviour in mice after peripheral ghrelin injection as well as after starvation. Given the chronicity of mood disorders in humans, the recent finding that chronic central ghrelin treatment of rats increases anxiety- and depression-like behaviour may be especially relevant [48]. …”

Section: Ghrelin Leptin and A Link Between Stress Reward And Appetitementioning

confidence: 99%

Neural Substrates Underlying Interactions between Appetite Stress and Reward

Menzies¹,

Skibicka²,

Dickson³

et al. 2012

Obes Facts

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Neurobiological mechanisms that normally control food intake and energy expenditure can be overcome by environmental cues and by stress. Of particular importance is the influence of the mesolimbic reward pathway. In genetically susceptible individuals, problematic over-eating likely reflects a changing balance in the control exerted by homeostatic versus reward circuits that are strongly influenced by environmental factors such as stress. Both stress and activation of the reward pathway have been shown to increase food intake and promote a preference for palatable, high-energy foods. Recent research has focused on the important role of circulating and central neuropeptides that powerfully regulate the brain response to food cues. For example, ghrelin has a potent positive effect on the motivational aspects of food intake, and central oxytocin may be involved in satiety. Thus, the decision to eat, or indeed to over-eat, involves a complex integrated neurobiology that includes brain centres involved in energy balance, reward and stress and their regulation by metabolic and endocrine factors.

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Central administration of ghrelin alters emotional responses in rats: behavioural, electrophysiological and molecular evidence

Cited by 96 publications

References 69 publications

Early life social stress induced changes in depression and anxiety associated neural pathways which are correlated with impaired maternal care

Early life social stress induced changes in depression and anxiety associated neural pathways which are correlated with impaired maternal care

A review on the effect of the photoperiod and melatonin on interactions between ghrelin and serotonin

Neural Substrates Underlying Interactions between Appetite Stress and Reward

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