Sucrose withdrawal induces depression and anxiety-like behavior by Kir2.1 upregulation in the nucleus accumbens

Kim, Seonil; Shou, Jiayi; Abera, Sinedu; Ziff, Edward B.

doi:10.1016/j.neuropharm.2017.11.041

Cited by 92 publications

(53 citation statements)

References 55 publications

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“…Neurochemically, morphine withdrawal is accompanied by a decrease in accumbens DA release with a simultaneous ACh increase ( 147 , 149 , 157 ). An equal response was observed when sugar experienced rats were injected naloxone or sugar deprived ( 200 – 202 ), confirming the involvement of the endogenous opioid system in the development of sugar dependency.…”

Section: Can Sugar Be Addictive?supporting

confidence: 53%

“…Hence, it is sensible to look for signs of opiate withdrawal in rats made dependent on sugar or palatable food ( 199 ). Injection of naloxone in sugar-dependent rats generated several of the opiate withdrawal symptoms and anxiety-like response on the plus-maze ( 200 , 201 ). Similarly, sugar deprivation (analogous to spontaneous drug withdrawal) produced signs of opiate withdrawal including anxiety-like behaviors ( 200 , 202 ).…”

Section: Can Sugar Be Addictive?mentioning

confidence: 99%

“…Injection of naloxone in sugar-dependent rats generated several of the opiate withdrawal symptoms and anxiety-like response on the plus-maze ( 200 , 201 ). Similarly, sugar deprivation (analogous to spontaneous drug withdrawal) produced signs of opiate withdrawal including anxiety-like behaviors ( 200 , 202 ). Only recently have withdrawal symptoms been elucidated in humans meeting criteria for FA by way of predictive reference resetting (allostasis) controlled by the rostral anterior cingulate cortex and the dorsal lateral prefrontal cortex ( 203 ).…”

Section: Can Sugar Be Addictive?mentioning

confidence: 99%

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Sugar Addiction: From Evolution to Revolution

2018

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The obesity epidemic has been widely publicized in the media worldwide. Investigators at all levels have been looking for factors that have contributed to the development of this epidemic. Two major theories have been proposed: (1) sedentary lifestyle and (2) variety and ease of inexpensive palatable foods. In the present review, we analyze how nutrients like sugar that are often used to make foods more appealing could also lead to habituation and even in some cases addiction thereby uniquely contributing to the obesity epidemic. We review the evolutionary aspects of feeding and how they have shaped the human brain to function in “survival mode” signaling to “eat as much as you can while you can.” This leads to our present understanding of how the dopaminergic system is involved in reward and its functions in hedonistic rewards, like eating of highly palatable foods, and drug addiction. We also review how other neurotransmitters, like acetylcholine, interact in the satiation processes to counteract the dopamine system. Lastly, we analyze the important question of whether there is sufficient empirical evidence of sugar addiction, discussed within the broader context of food addiction.

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Section: Can Sugar Be Addictive?supporting

confidence: 53%

Section: Can Sugar Be Addictive?mentioning

confidence: 99%

Section: Can Sugar Be Addictive?mentioning

confidence: 99%

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Sugar Addiction: From Evolution to Revolution

2018

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“…Therefore, the opposite relationships between BSV and anxiety level may indicate that (1) moderate anxiety is associated with the most stable brain state and the best performance, and (2) increased BSV in subjects with high anxiety and low anxiety may be related to distinctive brain states, leading to different performances. Considering that (1) the dopaminergic system is closely associated with both anxiety and BSV (68, 69), (2) the non-linear relationship between dopaminergic system and behavioral performance (70), and (3) the quadratic relationship between anxiety and behavioral performance (66), the opposite BSV-anxiety relationship may reflect different neural dynamical configurations mediated by the dopaminergic system in patients with GAD and healthy people. Furthermore, the negative correlation between the HC group and GAD group suggests that the neuropsychological association in HC and patients with GAD may be driven by the same mechanism rather than independent from each other.…”

Section: Discussionmentioning

confidence: 99%

Altered Brain Signal Variability in Patients With Generalized Anxiety Disorder

Wang

et al. 2019

Front. Psychiatry

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Generalized anxiety disorder (GAD) is characterized by a chronic, continuous symptom of worry and exaggerated startle response. Although functional abnormality in GAD has been widely studied using functional magnetic resonance imaging (fMRI), the dynamic signatures of GAD are not fully understood. As a vital index of brain function, brain signal variability (BSV) reflects the capacity of state transition of neural activities. In this study, we recruited 47 patients with GAD and 38 healthy controls (HCs) to investigate whether or not BSV is altered in patients with GAD by measuring the standard deviation of fMRI signal of each voxel. We found that patients with GAD exhibited decreased BSV in widespread regions including the visual network, sensorimotor network, frontoparietal network, limbic system, and thalamus, indicating an inflexible brain state transfer pattern in these systems. Furthermore, the correlation between BSV and trait anxiety score was prone to be positive in patients with GAD but negative in HCs. The opposite relationships between BSV and anxiety level in the two groups indicate that the brain with moderate anxiety level may stay in the most stable rather than in the flexible state. As the first study of BSV in GAD, we revealed extensively decreased BSV in patients with GAD similar to that in other mental disorders but with a non-linear relationship between BSV and anxiety level indicating a novel neurodynamic mechanism of the anxious brain.

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“…a mutation to glutamine (TPN-Q) was introduced to prevent this oxidation [20]. In addition, a computer simulation study showed that the I8R mutation of TPN-Q (TPN-RQ) possibly increased the affinity to Kir2.1 [21], which was also reported to be involved in depression-like behavior [22]. Likewise, peptide engineering studies have successfully created peptides with higher affinity and/or specificity using mutations and shortening of amino acids.…”

Section: Introductionmentioning

confidence: 99%

Antidepressive effect of an inward rectifier K+ channel blocker peptide, tertiapin-RQ

2020

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Renal outer medullary K+ channel, ROMK (Kir1.1, kcnj1) is expressed in the kidney and brain, but its role in the central nervous system remains unknown. Recent studies suggested an involvement of the ROMK channel in mental diseases. Tertiapin (TPN) is a European honey bee venom peptide and is reported to selectively block the ROMK channel. Here, we have chemically synthesized a series of mutated TPN peptides, including TPN-I8R and -M13Q (TPN-RQ), reported previously, and examined their blocking activity on the ROMK channel. Among 71 peptides tested, TPN-RQ was found to block the ROMK channel most effectively. Whole-cell patch-clamp recordings showed the essential roles of two disulfide bonds and the circular structure for the blockade activity. To examine the central role, we injected TPN-RQ intracerebroventricularly and examined the effects on depression- and anxiety-like behaviors in mice. TPN-RQ showed an antidepressive effect in tail-suspension and forced swim tests. The injection of TPN-RQ also enhanced the anxiety-like behavior in the elevated plus-maze and light/dark box tests and impaired spontaneous motor activities in balance beam and wheel running tests. Administration of TPM-RQ suppressed the anti-c-Fos immunoreactivity in the lateral septum, without affecting immunoreactivity in antidepressant-related nuclei, e.g. the dorsal raphe nucleus and locus coeruleus. TPN-RQ may exert its antidepressive effects through a different mechanism from current drugs.

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Sucrose withdrawal induces depression and anxiety-like behavior by Kir2.1 upregulation in the nucleus accumbens

Cited by 92 publications

References 55 publications

Sugar Addiction: From Evolution to Revolution

Sugar Addiction: From Evolution to Revolution

Altered Brain Signal Variability in Patients With Generalized Anxiety Disorder

Antidepressive effect of an inward rectifier K+ channel blocker peptide, tertiapin-RQ

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