Biochemical and Neurotransmitters Changes Associated with Tramadol in Streptozotocin-Induced Diabetes in Rats

Ezzeldin, Essam; Souror, Wafaa A. H.; El-Nahhas, Toqa; Soudi, Abdel Nasser M. M.; Shahat, Abdelaaty A.

doi:10.1155/2014/238780

Cited by 46 publications

(36 citation statements)

References 32 publications

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“…Changes in neurotransmitter concentrations in STZ-diabetic rats have also been reported by Ezzeldin et al, 11 who demonstrated altered levels of dopamine, noradrenaline (NA), and serotonin (5-hydroxytryptamine; 5-HT) in several brain regions, including the cerebral cortex, hypothalamus and brain stem. These findings suggest that changes in various neurotransmitters may play a role in the pathophysiology of comorbid depression in DM.…”

supporting

confidence: 63%

Depression‐related behavioural and neuroendocrine changes in the Spontaneously Diabetic Torii (SDT) fatty rat, an animal model of type 2 diabetes mellitus

Sakimura

Maekawa

Sasagawa

et al. 2018

Clin Exp Pharma Physio

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Depression is one of the most common psychiatric diseases and is commonly comorbid with type 1 or 2 diabetes mellitus (DM). However, the pathophysiology underlying the depressive state in DM remains poorly understood. Animal models are useful tools to investigate the association between depression and DM. In the present study we investigated whether the Spontaneously Diabetic Torii (SDT) fatty rat, a novel animal model of type 2 DM, shows depression-related features. We assessed depression-like behaviour, hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis, and neurotransmitter levels in the brain. Behaviour was evaluated using a forced swimming test, and the HPA axis was evaluated with changes in plasma corticosterone levels after a swimming stress exposure or dexamethasone challenge. In addition, serotonin (5-hydroxytryptamine; 5-HT), noradrenaline, glutamate and γ-aminobutyric acid (GABA) concentrations in the frontal cortex, hippocampus and brain stem were measured. In the forced swimming test, SDT fatty rats exhibited increased duration of immobility compared with control Sprague-Dawley (SD) rats. Moreover, basal corticosterone levels were significantly elevated in SDT fatty compared with control SD rats. However, there were no stress-induced increases or changes in dexamethasone-induced suppression of corticosterone in SDT fatty compared with control SD rats. Furthermore, there were significant changes in 5-HT concentrations in the prefrontal cortex, and in GABA and glutamate concentrations in the hippocampus in SDT fatty compared with controls. The results of the present study suggest that the SDT fatty rat may be an appropriate model for diabetes with comorbid depression associated with neurotransmitter impairments and aberrant basal HPA hyperactivity.

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supporting

confidence: 63%

Depression‐related behavioural and neuroendocrine changes in the Spontaneously Diabetic Torii (SDT) fatty rat, an animal model of type 2 diabetes mellitus

Sakimura

Maekawa

Sasagawa

et al. 2018

Clin Exp Pharma Physio

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“…While some researchers found reduced release of norepinephrine in the spinal cord in diabetic rats [116] , others have described opposite findings [117] . There is also evidence of diminished norepinephrine levels in supra spinal areas, such as brainstem and thalamus, but higher concentration in the cortex of diabetic animals [118] . Additionally, impaired spinal opioidinduced release of serotonin (5HT) has been demonstrated in diabetic rats, and this finding may be related to opioid hyporesponsiveness in experimental DNP [119] .…”

Section: Brain Plasticitymentioning

confidence: 97%

Diabetic neuropathic pain: Physiopathology and treatment

Schreiber

Nones

Reis

et al. 2015

WJD

353

267

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Diabetic neuropathy is a common complication of both type 1 and type 2 diabetes, which affects over 90% of the diabetic patients. Although pain is one of the main symptoms of diabetic neuropathy, its pathophysiological mechanisms are not yet fully known. It is widely accepted that the toxic effects of hyperglycemia play an important role in the development of this complication, but several other hypotheses have been postulated. The management of diabetic neuropathic pain consists basically in excluding other causes of painful peripheral neuropathy, improving glycemic control as a prophylactic therapy and using medications to alleviate pain. First line drugs for pain relief include anticonvulsants, such as pregabalin and gabapentin and antidepressants, especially those that act to inhibit the reuptake of serotonin and noradrenaline. In addition, there is experimental and clinical evidence that opioids can be helpful in pain control, mainly if associated with first line drugs. Other agents, including for topical application, such as capsaicin cream and lidocaine patches, have also been proposed to be useful as adjuvants in the control of diabetic neuropathic pain, but the clinical evidence is insufficient to support their use. In conclusion, a better understanding of the mechanisms underlying diabetic neuropathic pain will contribute to the search of new therapies, but also to the improvement of the guidelines to optimize pain control with the drugs currently available.

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“…High plasma levels of 5-HT have been reported in patients with T2DM, although its potential effect on insulin secretion is unclear. The release of 5-HT from activated platelets is enhanced, decreasing intraplatelet 5-HT content and resulting in increased plasma levels of 5-HT in patients with diabetes [ 44 ].…”

Section: 5-ht In Diabetes and Diabetic Complicationsmentioning

confidence: 99%

Serotonin and Its Receptor as a New Antioxidant Therapeutic Target for Diabetic Kidney Disease

Huang

et al. 2017

Journal of Diabetes Research

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Diabetic kidney disease (DKD) is a widespread chronic microvascular complication of diabetes mellitus (DM), affects almost 30–50% of patients, and represents a leading cause of death of DM. Serotonin or 5-hydroxytryptamine (5-HT) is a multifunctional bioamine that has crucial roles in many physiological pathways. Recently, emerging evidence from experimental and clinical studies has demonstrated that 5-HT is involved in the pathogenesis of diabetic vascular complications. The 5-HT receptor (5-HTR) antagonists exert renoprotective effects by suppressing oxidative stress, suggesting that 5-HTR can be used as a potential target for treating DKD. In this review, therefore, we summarize the published information available for the involvement of 5-HT and 5-HTR antagonists in the pathogenesis of various diabetic complications with a particular focus of DKD. We conclude that 5-HTR is a potential therapeutic target for treating DKD, as it has been successfully applied in animal models and has currently being investigated in randomized and controlled clinical trials.

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Biochemical and Neurotransmitters Changes Associated with Tramadol in Streptozotocin-Induced Diabetes in Rats

Cited by 46 publications

References 32 publications

Depression‐related behavioural and neuroendocrine changes in the Spontaneously Diabetic Torii (SDT) fatty rat, an animal model of type 2 diabetes mellitus

Depression‐related behavioural and neuroendocrine changes in the Spontaneously Diabetic Torii (SDT) fatty rat, an animal model of type 2 diabetes mellitus

Diabetic neuropathic pain: Physiopathology and treatment

Serotonin and Its Receptor as a New Antioxidant Therapeutic Target for Diabetic Kidney Disease

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