Diet-induced obesity promotes depressive-like behaviour that is associated with neural adaptations in brain reward circuitry
TL;DR: It is suggested that increases in striatal BDNF and CREB activity are well implicated in depressive behaviour and reward, and may mediate the effects of high-fat feeding and DIO to promote negative emotional states and depressive-like symptomology.
Abstract: Diet-induced obesity promotes depressive-like behaviour that is associated with neural adaptations in brain reward circuitry
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TL;DR: This report summarizes and builds upon some of the key concepts in the symposium “The Microbiome: Development, Stress, and Disease” within the context of how microbiota might influence the neurobiology of stress.
637 citations
Cites background from "Diet-induced obesity promotes depre..."
...…that adult C57Bl6 mice consuming a diet containing 58% of calories as trans-fat for 12 weeks develop depressive-like behaviours, including increased immobility in the forced swim task and reduced time spent in open areas of the elevated-plus maze and open field tests (Sharma and Fulton, 2013)....
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TL;DR: Intervention studies which suggest that the restoration of insulin activity in the hippocampus may be an effective strategy to alleviate the cognitive decline associated with T2DM and AD are discussed.
Abstract: Clinical studies suggest a link between type 2 diabetes mellitus (T2DM) and insulin resistance (IR) and cognitive dysfunction, but there are significant gaps in our knowledge of the mechanisms underlying this relationship. Animal models of IR help to bridge these gaps and point to hippocampal IR as a potential mediator of cognitive dysfunction in T2DM, as well as in Alzheimer disease (AD). This Review highlights these observations and discusses intervention studies which suggest that the restoration of insulin activity in the hippocampus may be an effective strategy to alleviate the cognitive decline associated with T2DM and AD.
392 citations
TL;DR: The effect of acute and chronic inflammation on BDNF levels in the most common psychiatric and neurodegenerative disorders is focused on and some light is shed on the possible biological mechanisms that may influence this effect.
Abstract: Brain-derived neurotrophic factor (BDNF) is one of the most studied neurotrophins in the healthy and diseased brain. As a result, there is a large body of evidence that associates BDNF with neuronal maintenance, neuronal survival, plasticity, and neurotransmitter regulation. Patients with psychiatric and neurodegenerative disorders often have reduced BDNF concentrations in their blood and brain. A current hypothesis suggests that these abnormal BDNF levels might be due to the chronic inflammatory state of the brain in certain disorders, as neuroinflammation is known to affect several BDNF-related signaling pathways. Activation of glia cells can induce an increase in the levels of pro- and antiinflammatory cytokines and reactive oxygen species, which can lead to the modulation of neuronal function and neurotoxicity observed in several brain pathologies. Understanding how neuroinflammation is involved in disorders of the brain, especially in the disease onset and progression, can be crucial for the development of new strategies of treatment. Despite the increasing evidence for the involvement of BDNF and neuroinflammation in brain disorders, there is scarce evidence that addresses the interaction between the neurotrophin and neuroinflammation in psychiatric and neurodegenerative diseases. This review focuses on the effect of acute and chronic inflammation on BDNF levels in the most common psychiatric and neurodegenerative disorders and aims to shed some light on the possible biological mechanisms that may influence this effect. In addition, this review will address the effect of behavior and pharmacological interventions on BDNF levels in these disorders.
377 citations
TL;DR: The previously published literature is analyzed for factors which are known to influence animal behavior in the FST, and consideration of these factors in planning experiments may result in more consistent FST results.
318 citations
TL;DR: An overview of complex nature of food intake where various biological factors link mood, food intake, and brain signaling that engages both peripheral and central nervous system signaling pathways in a bi-directional manner in obesity is provided.
Abstract: Food is a potent natural reward and food intake is a complex process. Reward and gratification associated with food consumption leads to dopamine (DA) production, which in turn activates reward and pleasure centers in the brain. An individual will repeatedly eat a particular food to experience this positive feeling of gratification. This type of repetitive behavior of food intake leads to the activation of brain reward pathways that eventually overrides other signals of satiety and hunger. Thus, a gratification habit through a favorable food leads to overeating and morbid obesity. Overeating and obesity stems from many biological factors engaging both central and peripheral systems in a bi-directional manner involving mood and emotions. Emotional eating and altered mood can also lead to altered food choice and intake leading to overeating and obesity. Research findings from human and animal studies support a two-way link between three concepts, mood, food, and obesity. The focus of this article is to provide an overview of complex nature of food intake where various biological factors link mood, food intake, and brain signaling that engages both peripheral and central nervous system signaling pathways in a bi-directional manner in obesity.
296 citations
Cites background or result from "Diet-induced obesity promotes depre..."
...…foods can provide some relief from negative emotions and mood states, chronic consumption of calorically-rich foods ultimately leads to obesity which in turn promotes vulnerability to depression and anxiety (Novick et al., 2005; Simon et al., 2006; Kloiber et al., 2007; Sharma and Fulton, 2013)....
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...…preference for palatable food is often seen in humans (Souquet and Rowland, 1989; Epel et al., 2004; Pecoraro et al., 2004; Christiansen et al., 2011; Gibson, 2012; Merali et al., 2013; Sharma et al., 2013; Sharma and Fulton, 2013; Meye and Adan, 2014; Park et al., 2014; Rho et al., 2014)....
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...…and obesity is often associated with depression and anxiety in humans which has also been reported in animal models (Novick et al., 2005; Simon and Von Korff, 2006; Kloiber et al., 2007; Singh et al., 2007, 2009; Akubuiro et al., 2013; Patterson and Abizaid, 2013; Sharma and Fulton, 2013)....
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TL;DR: The mouse procedure is more rapid and less costly than that with rats and is thus more suitable for the primary screening of antidepressant drugs, suggesting that the procedure is selectively sensitive to antidepressant treatments.
Abstract: A depressed state can be induced in mice by forcing them to swim in a narrow cylinder from which they cannot escape. After a brief period of vigorous activity the mice adopt a characteristic immobile posture which is readily identifiable. Immobility was reduced by tricyclic antidepressants, monoamine oxidase inhibitors and atypical antidepressants, as well as by electroconvulsive shock. Psychostimulants also reduced immobility but in contrast to antidepressants caused marked motor stimulation. Immobility was not affected by minor or major tranquilisers. These findings, closely parallel to those we have previously reported in rats, suggest that the procedure is selectively sensitive to antidepressant treatments. The mouse procedure is, however, more rapid and less costly than that with rats and is thus more suitable for the primary screening of antidepressant drugs.
3,277 citations
TL;DR: A neurobiologic understanding of depression also requires identification of the genes that make individuals vulnerable or resistant to the syndrome, and advances will fundamentally improve the treatment and prevention of depression.
2,768 citations
TL;DR: Progress in identifying candidate mechanisms of addiction is reviewed, including molecular and cellular mechanisms that underlie long-term associative memories in several forebrain circuits (involving the ventral and dorsal striatum and prefrontal cortex) that receive input from midbrain dopamine neurons.
Abstract: Addiction is a state of compulsive drug use; despite treatment and other attempts to control drug taking, addiction tends to persist. Clinical and laboratory observations have converged on the hypothesis that addiction represents the pathological usurpation of neural processes that normally serve reward-related learning. The major substrates of persistent compulsive drug use are hypothesized to be molecular and cellular mechanisms that underlie long-term associative memories in several forebrain circuits (involving the ventral and dorsal striatum and prefrontal cortex) that receive input from midbrain dopamine neurons. Here we review progress in identifying candidate mechanisms of addiction.
2,406 citations
TL;DR: It is shown that viral-mediated, mesolimbic dopamine pathway–specific knockdown of brain-derived neurotrophic factor is required for the development of experience-dependent social aversion in mice experiencing repeated aggression.
Abstract: Mice experiencing repeated aggression develop a long-lasting aversion to social contact, which can be normalized by chronic, but not acute, administration of antidepressant. Using viral-mediated, mesolimbic dopamine pathway-specific knockdown of brain-derived neurotrophic factor (BDNF), we showed that BDNF is required for the development of this experience-dependent social aversion. Gene profiling in the nucleus accumbens indicates that local knockdown of BDNF obliterates most of the effects of repeated aggression on gene expression within this circuit, with similar effects being produced by chronic treatment with antidepressant. These results establish an essential role for BDNF in mediating long-term neural and behavioral plasticity in response to aversive social experiences.
1,873 citations
TL;DR: It is proposed that the NAc and VTA contribute importantly to the pathophysiology and symptomatology of depression and may even be involved in its etiology.
1,859 citations