Changes in dopamine transporter expression in the midbrain following traumatic brain injury: an immunohistochemical and<i>in situ</i>hybridization study in a mouse model

Shimada, Ryo; Abe, Keiichi; Furutani, Rui; Kibayashi, Kazuhiko

doi:10.1179/1743132813y.0000000289

Cited by 36 publications

(25 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A variety of studies had reported that reduced extracellular dopamine levels may result in depressionlike behavior. Nevertheless, none has reported the delayed effect of the dopaminergic level as revealed by our data [48][49][50]. Interestingly, amantadine treatment demonstrated an intense effect on behavioral modification after the acute phase (3 days) of surgery [ Fig.…”

Section: Discussionmentioning

confidence: 51%

Amantadine preserves dopamine level and attenuates depression-like behavior induced by traumatic brain injury in rats

Tan

Tang

et al. 2015

Behavioural Brain Research

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 51%

Amantadine preserves dopamine level and attenuates depression-like behavior induced by traumatic brain injury in rats

Tan

Tang

et al. 2015

Behavioural Brain Research

View full text Add to dashboard Cite

“…Dysfunctional DAergic signaling may explain many of the persistent cognitive deficits observed with TBI (see review, Bales et al 10 ). Decreased DA transporter (DAT) levels in the prefrontal cortex and striatum 11 have been confirmed in a rat model after TBI 12 , suggesting compensatory action by DA neurons to increase DA signaling post-TBI. In severe levels of injury associated with the controlled cortical impact (CCI) model of experimental TBI, tyrosine hydroxylase (TH), a rate-limiting enzyme in the synthesis of DA is upregulated in presynaptic terminals in the frontal cortex 13 and in the striatum 10,14 .…”

Section: Introductionmentioning

confidence: 97%

Posttraumatic Brain Injury Cognitive Performance Is Moderated by Variation Within ANKK1 and DRD2 Genes

Failla

Ricker

et al. 2015

Journal of Head Trauma Rehabilitation

View full text Add to dashboard Cite

Objective As dopamine neurotransmission impacts cognition, we hypothesized variants in the linked dopamine D2 receptor (DRD2) and ankyrin repeat and kinase domain (ANKK1) genes might account for some individual variability in cognitive recovery post-TBI. Participants Prospective cohort of 108 survivors of severe TBI, recruited consecutively from a level 1 trauma center. Design We examined relationships between DRD2 genetic variation and functional recovery at 6 and 12 months post-TBI. Main Measures Cognitive performance was evaluated using 8 neuropsychological tests targeting different cognitive domains. An overall cognitive composite was developed based on normative data. We also assessed functional cognition, depression status, and global outcome. Subjects were genotyped for 6 DRD2 tagging single nucleotide polymorphisms and Taq1A within ANKK1. Results ANKK1 Taq1A heterozygotes performed better than homozygotes across several cognitive domains at both time-points post-injury. When adjusting for age, GCS, and education, the Taq1A (ANKK1) and rs6279 (DRD2) variants were associated with overall composite scores at 6 months post-TBI (p=0.0468, 0.0430, respectively). At 12 months, only Taq1A remained a significant genetic predictor of cognition (p=0.0128). Following multiple comparisons correction, there were no significant associations between examined genetic variants and functional cognition, depression status, and global outcome. Conclusion These data suggest genetic variation within DRD2 influences cognitive recovery post-TBI. Understanding genetic influences on dopaminergic systems post-TBI may impact current treatment paradigms.

show abstract

“…Because DAT plays an important role in maintenance of DA homeostasis, the decreased expression of DAT after TBI may also result in altered DA neurotransmission in the brain. 72 TBI-induced DA neurotransmission deficits were also attributable to deficits in TH activity. TBI reduces striatal TH activity and potassium-evoked DA release in rats at 1 wk after injury.…”

Section: Secondary Insults After Tbi (Related To Dopamine Suppression)mentioning

confidence: 96%

“…DAT plays an important role in recycling DA (DA) from the synapse and maintaining DA homeostasis, so the decreased expression of DAT after TBI may result in altered DA neurotransmission in the brain. 72 Neural plasticity and neurogenesis effects of environmental enrichment (EE) in neurodegenerative diseases like PD have been studied. 95,96 The restoration of monoamine (DA and serotonin) transporter function after EE has also been documented.…”

Section: Secondary Insults Related To the Dopamine Systemmentioning

confidence: 99%

Impact of traumatic brain injury on dopaminergic transmission

et al. 2017

View full text Add to dashboard Cite

Brain trauma is often associated with severe morbidity and is a major public health concern. Even when injury is mild and no obvious anatomic disruption is seen, many individuals suffer disabling neuropsychological impairments such as memory loss, mood dysfunction, substance abuse, and adjustment disorder. These changes may be related to subtle disruption of neural circuits as well as functional changes at the neurotransmitter level. In particular, there is considerable evidence that dopamine (DA) physiology in the nigrostriatal and mesocorticolimbic pathways might be impaired after traumatic brain injury (TBI). Alterations in DA levels can lead to oxidative stress and cellular dysfunction, and DA plays an important role in central nervous system inflammation. Therapeutic targeting of DA pathways may offer benefits for both neuronal survival and functional outcome after TBI. The purpose of this review is to discuss the role of DA pathology in acute TBI and the potential impact of therapies that target these systems for the treatment of TBI.

show abstract

Changes in dopamine transporter expression in the midbrain following traumatic brain injury: an immunohistochemical andin situhybridization study in a mouse model

Abstract: These findings indicated that TBI induced changes in DAT expression in the RRF. Because the DAT pumps dopamine (DA) out of the synapse back into the cytosol and maintains DA homeostasis, the decreased expression of DAT after TBI may result in decreased DA neurotransmission in the brain.

Cited by 36 publications

References 32 publications

Amantadine preserves dopamine level and attenuates depression-like behavior induced by traumatic brain injury in rats

Amantadine preserves dopamine level and attenuates depression-like behavior induced by traumatic brain injury in rats

Posttraumatic Brain Injury Cognitive Performance Is Moderated by Variation Within ANKK1 and DRD2 Genes

Impact of traumatic brain injury on dopaminergic transmission

Contact Info

Product

Resources

About