Serotonin 5-HT1A receptors modulate depression-related symptoms following mild traumatic brain injury in male adult mice

Kosari‐Nasab, Morteza; Shokouhi, Ghaffar; Azarfarin, Maryam; Amirkhiz, Maryam Bannazadeh; Abbasi, Mehran Mesgari; Salari, Ali-Akbar

doi:10.1007/s11011-018-0366-4

Cited by 29 publications

(10 citation statements)

References 56 publications

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“…These findings expand upon a growing body of evidence supporting the therapeutic efficacy of 5-HT receptor agonists for the treatment of neuropsychiatric disturbances, and our data concur with a limited number of systematic studies aimed at determining the effects of various forms of TBI on central 5-HT signaling. As noted earlier, several previous studies have provided evidence that targeting 5-HT 1A receptors post-injury is advantageous in preventing cognitive/learning deficits (Kline et al, 2002;Olsen et al, 2012;Cheng et al, 2016), neurodegeneration (Kline et al, 2004;Cheng et al, 2016), and despair-like behavior post-injury in rodent subjects (Kosari-Nasab et al, 2019). Although we failed to find in vivo evidence of altered 5-HT 1A function post-injury, a singular study has shown increased hippocampal 5-HT 1A receptor expression post-injury (Wilson and Hamm, 2002).…”

Section: Discussioncontrasting

confidence: 42%

“…These tracts, however, form altered spatial orientations (Jin et al, 2016;Kajstura et al, 2018), an effect with unknown implications on receptor expression/densities, neuronal network function, and behavior. Last, several studies have provided evidence that specifically targeting 5-HT 1A receptors post-injury may be advantageous in preventing cognitive/learning deficits (Kline et al, 2002;Olsen et al, 2012;Cheng et al, 2016), neurodegeneration (Kline et al, 2004;Cheng et al, 2016), and despair-like behavior postinjury in rodent subjects (Kosari-Nasab et al, 2019). It is currently clear that specific types of neurotrauma, including concussions, alter 5-HT signaling within the CNS (Jin et al, 2016;Kajstura et al, 2018); however, the extent to which 5-HT alterations impact psychiatric states, and ultimately behavior following neurotrauma, is currently not well characterized.…”

Section: Introductionmentioning

confidence: 99%

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Altered Serotonin 2A (5-HT2A) Receptor Signaling Underlies Mild TBI-Elicited Deficits in Social Dominance

et al. 2022

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Various forms of traumatic brain injury (TBI) are a leading cause of disability in the United States, with the generation of neuropsychiatric complications such as depression, anxiety, social dysfunction, and suicidality being common comorbidities. Serotonin (5-HT) signaling is linked to psychiatric disorders; however, the effects of neurotrauma on normal, homeostatic 5-HT signaling within the central nervous system (CNS) have not been well characterized. We hypothesize that TBI alters specific components of 5-HT signaling within the CNS and that the elucidation of specific TBI-induced alterations in 5-HT signaling may identify novel targets for pharmacotherapies that ameliorate the neuropsychiatric complications of TBI. Herein, we provide evidence that closed-head blast-induced mild TBI (mTBI) results in selective alterations in cortical 5-HT2A receptor signaling. We find that mTBI increases in vivo cortical 5-HT2A receptor sensitivity and ex vivo radioligand binding at time points corresponding with mTBI-induced deficits in social behavior. In contrast, in vivo characterizations of 5-HT1A receptor function revealed no effect of mTBI. Notably, we find that repeated pharmacologic activation of 5-HT2A receptors post-injury reverses deficits in social dominance resulting from mTBI. Cumulatively, these studies provide evidence that mTBI drives alterations in cortical 5-HT2A receptor function and that selective targeting of TBI-elicited alterations in 5-HT2A receptor signaling may represent a promising avenue for the development of pharmacotherapies for TBI-induced generation of neuropsychiatric disorders.

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Section: Discussioncontrasting

confidence: 42%

Section: Introductionmentioning

confidence: 99%

Altered Serotonin 2A (5-HT2A) Receptor Signaling Underlies Mild TBI-Elicited Deficits in Social Dominance

et al. 2022

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“…To investigate anhedonia-like behaviour (a depression symptom) in animals, 1 day after the last session of the swimming exercise, the animals were acclimated to two water bottles. Three days later, animals were deprived of food and water for 18 h. Then, mice were given two bottles including sucrose solution (2%) and water for 1 h. The percentage of sucrose preference was considered as an indicator of anhedonia-like behaviour (Kosari-Nasab et al, 2019). Before and after the test, the sucrose solution and water bottles were weighed, and the sucrose preference was calculated as the percentage of ingested sucrose solution relative to the total amount of liquid consumed (Majidi et al, 2016).…”

Section: Sucrose Preferencementioning

confidence: 99%

Swimming exercise decreases depression‐like behaviour and inflammatory cytokines in a mouse model of type 2 diabetes

Gilak-Dalasm

Peeri

Azarbayjani

2021

Experimental Physiology

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Clinical and experimental studies have shown that type 2 diabetes is associated with depression-related disorders. Inflammation has been identified as a common mechanism in both type 2 diabetes and depression. Several studies have suggested that swimming exercise might be able to reduce depression-related symptoms. The present study aimed to explore whether swimming exercise can decrease depressionlike behaviour in type 2 diabetic mice. To induce type 2 diabetes, male C57BL6 mice were treated with a high-fat diet and streptozocin. Type 2 diabetic animals were subjected to swimming exercise for 4 weeks. Then, depression-like behaviours were evaluated by sucrose preference, novelty-suppressed feeding, social interaction and tail suspension tests. We also measured levels of glucose, insulin and pro-inflammatory cytokines such as interleukin-1β and tumour necrosis factor-α in the serum of animals.The results indicated that type 2 diabetes significantly increased anhedonia-and depression-like behaviours in mice. We also found significant increases in glucose, insulin and inflammatory cytokines in diabetic mice. Moreover, swimming exercise reduced anhedonia-and depression-like behaviour in type 2 diabetic mice. Swimming exercise also decreased glucose and inflammatory cytokines in the serum of mice with type 2 diabetes. Collectively, this study demonstrates that swimming exercise decreased depression-like behaviour by reducing inflammation in type 2 diabetic mice.Further clinical studies are needed to validate these findings in patients with type 2 diabetes.

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“…As mentioned earlier, the imbalance of neurotransmitters seen in animal models of mild to moderate TBI, and the subcortical nuclei neurodegeneration seen in post-mortem studies in patients with a history of mild to moderate TBI, together suggests that neurotransmission systems are dysfunctional following mild to moderate TBI. [4][5][6][7][8][9][10][11][14][15][16] This in part might explain the increased risk of developing psychiatric sequelae such as depression, anxiety, and suicidal ideation after TBI. [58][59][60] Silver and colleagues showed that in addition to exacerbated depression, patients that have experienced mild TBI also undergo a decline in cognitive function.…”

Section: Cannabis Psychiatric Disorders and Tbimentioning

confidence: 99%

“…A long-standing hypothesis is that multiple neurotransmission systems including serotonergic, dopaminergic, noradrenergic, and cholinergic systems are perturbed after an event. [4][5][6][7][8][9] The evidence supporting this hypothesis mostly comes from mild to moderate TBI models in rodents [10][11][12][13] ; however, multiple other lines of evidence link neurotransmission system disturbances with mild to moderate TBI. For example, patients with Chronic Traumatic Encephalopathy (CTE), a neurodegenerative disease that has been associated with repetitive mild TBI, often present with similar neuropsychiatric and psychiatric symptoms to those with TBI.…”

Section: Introductionmentioning

confidence: 99%

Cannabis in the Treatment of Traumatic Brain Injury: A Primer for Clinicians

Ponnambalam

Lee

Lauwers

et al. 2019

Can. J. Neurol. Sci.

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ABSTRACT:Our clinical experience at a specialized brain injury clinic suggests that numerous patients with traumatic brain injury (TBI) are using cannabis to alleviate their symptoms. While this patient population often inquires about the evidence of using cannabis post-head injury for the neurosensory, neurocognitive, and neuropsychiatric sequelae, most health professionals have little to no knowledge of this evidence. Given the recent legalization of recreational cannabis in Canada, questions and guidance related to cannabis use following a TBI are likely to become more common. This article reviews the evidence for cannabis use in psychiatric disorders with or without TBI. Overall, we found that the evidence for the use of cannabis among TBI patients is sparse and that patients tend to have little knowledge of the proven benefits and diverse effects of cannabis use. We feel this paper can serve as a stepping stone for future studies that explore the impact of cannabis use in a TBI population and can guide clinicians in advising their patients.

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Serotonin 5-HT1A receptors modulate depression-related symptoms following mild traumatic brain injury in male adult mice

Cited by 29 publications

References 56 publications

Altered Serotonin 2A (5-HT2A) Receptor Signaling Underlies Mild TBI-Elicited Deficits in Social Dominance

Altered Serotonin 2A (5-HT2A) Receptor Signaling Underlies Mild TBI-Elicited Deficits in Social Dominance

Swimming exercise decreases depression‐like behaviour and inflammatory cytokines in a mouse model of type 2 diabetes

Cannabis in the Treatment of Traumatic Brain Injury: A Primer for Clinicians

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