scholarly journals A Selective Depolarisation-Induced Increase in Excitatory Amino Acid Neurotransmitter Release in Rat Medial Prefrontal Cortex Using a Microdialysis Model of Traumatic Brain Injury

2005 ◽  
pp. 393-404 ◽  
Author(s):  
Aoife Smyth ◽  
Michael D. Gilchrist ◽  
William T. O'Connor
Keyword(s):  
Traumatic Brain Injury ◽  
Prefrontal Cortex ◽  
Amino Acid ◽  
Brain Injury ◽  
Medial Prefrontal Cortex ◽  
Neurotransmitter Release ◽  
Excitatory Amino Acid

Relationship between apoE4 allele and excitatory amino acid levels after traumatic brain injury

2003 ◽  
Vol 31 (9) ◽  
pp. 2371-2379 ◽  
Author(s):  
Mary E. Kerr ◽  
M. Ilyas Kamboh ◽  
Kim Yookyung ◽  
Marilyn F. Kraus ◽  
Ava M. Puccio ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Amino Acid ◽  
Brain Injury ◽  
Excitatory Amino Acid ◽  
Apoe4 Allele ◽  
Amino Acid Levels

The expression of excitatory amino acid transporter 2 in traumatic brain injury

2002 ◽  
Vol 130 (2-3) ◽  
pp. 83-89 ◽  
Author(s):  
Kazuya Ikematsu ◽  
Ryouichi Tsuda ◽  
Toshikazu Kondo ◽  
Ichiro Nakasono
Keyword(s):  
Traumatic Brain Injury ◽  
Amino Acid ◽  
Brain Injury ◽  
Excitatory Amino Acid ◽  
Amino Acid Transporter ◽  
Excitatory Amino Acid Transporter ◽  
Acid Transporter

Excitatory amino acids in cerebrospinal fluid following traumatic brain injury in humans

1993 ◽  
Vol 79 (3) ◽  
pp. 369-372 ◽  
Author(s):  
Andrew J. Baker ◽  
Richard J. Moulton ◽  
Vernon H. MacMillan ◽  
Peter M. Shedden
Keyword(s):  
Amino Acids ◽  
Traumatic Brain Injury ◽  
Cerebrospinal Fluid ◽  
Amino Acid ◽  
Brain Injury ◽  
Excitatory Amino Acids ◽  
Excitatory Amino Acid ◽  
Neuronal Damage ◽  
Control Group ◽  
Injured Patients

✓ Evidence from models of traumatic brain injury implicates excitotoxicity as an integral process in the ultimate neuronal damage that follows. Concentrations of the excitatory amino acid glutamate were serially measured in the cerebrospinal fluid (CSF) of patients with traumatic brain injuries and in control patients for comparison. The purpose of the study was to determine whether glutamate concentrations were significantly elevated following traumatic brain injury and, if so, whether they were elevated in a time frame that would allow the use of antagonist therapy. Cerebrospinal fluid was sampled fresh from ventricular drains every 12 hours and analyzed using high-performance liquid chromatography for the excitatory amino acids. The peak concentrations of glutamate in the CSF of the 12 brain-injured patients ranged from 14 to 474 µM and were significantly higher than those in the three control patients, 4.9 to 17 µM (Mann-Whitney U-test, p < 0.02). Glutamate concentrations in five of the eight patients who were still being sampled on Day 3 were beyond the control group range. The implication of this study is that severely head-injured patients are exposed to high concentrations of a neurotoxic amino acid for days following injury and thus may benefit from antagonist intervention.

scholarly journals Aggression, DRD1 polymorphism, and lesion location in penetrating traumatic brain injury

CNS Spectrums ◽  
2014 ◽  
Vol 19 (5) ◽  
pp. 382-390 ◽  
Author(s):  
Matteo Pardini ◽  
Frank Krueger ◽  
Colin A. Hodgkinson ◽  
Vanessa Raymont ◽  
Maren Strenziok ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Prefrontal Cortex ◽  
Brain Injury ◽  
Dopamine Receptor ◽  
Medial Prefrontal Cortex ◽  
Dopaminergic System ◽  
Lateral Prefrontal Cortex ◽  
Lesion Location ◽  
Comt Val158met ◽  
The Relationship

ObjectiveThis study evaluated whether structural brain lesions modulate the relationship between pathological aggression and the dopaminergic system in traumatic brain injury (TBI). While converging evidence suggests that different areas of the prefrontal cortex modulate dopaminergic activity, to date no evidence exists of a modulation of endogenous dopaminergic tone by lesion localization in penetrating TBI (pTBI).MethodsThis study included 141 male Caucasian veterans who suffered penetrating pTBI during their service in Vietnam and 29 healthy male Caucasian Vietnam veterans. Participants were genotyped for 3 functional single nucleotide polymorphisms (SNPs): dopamine receptor D1 (DRD1) rs686, dopamine receptor D2 (DRD2) rs4648317, and catechol-O-methyltransferase (COMT) Val158Met. Patients underwent brain CT scans and were divided into medial prefrontal cortex, lateral prefrontal cortex, and posterior cortex lesion groups. Long-term aggression levels were evaluated with the agitation/aggression subscale of the Neuropsychiatric Inventory.ResultsOur data showed that carriers of more transcriptionally active DRD1 alleles compared to noncarriers demonstrated greater aggression levels due to medial prefrontal cortex lesions but reduced aggression levels due to lateral prefrontal cortex lesions independently of DRD2 rs4648317 or COMT Val158Met genotypes.ConclusionsOur results suggest that the relationship between pTBI-related aggression and the dopaminergic system is modulated by lesion location. Potentially lesion location could represent an easy-to-use, widely available, para-clinical marker to help in the development of an individualized therapeutic approach to pTBI-related pathological aggression.

scholarly journals Repeated blast mild traumatic brain injury and oxycodone self-administration produce interactive effects on neuroimaging outcomes

2020 ◽  
Author(s):  
Matthew J. Muelbl ◽  
Breanna Glaeser ◽  
Alok S. Shah ◽  
Rachel Chiariello ◽  
Natalie N. Nawarawong ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Prefrontal Cortex ◽  
Brain Injury ◽  
Functional Connectivity ◽  
Medial Prefrontal Cortex ◽  
Drug Exposure ◽  
Interactive Effect ◽  
Interactive Effects ◽  
Self Administration ◽  
Drug Seeking

AbstractTraumatic brain injury (TBI) and drug addiction are common comorbidities, but it is unknown if the neurological sequelae of TBI contribute to this relationship. We have previously reported elevated oxycodone seeking after drug self-administration in rats that received repeated blast TBI (rbTBI). TBI and exposure to drugs of abuse can each change structural and functional neuroimaging outcomes, but it is unknown if there are interactive effects of injury and drug exposure. To determine the effects of TBI and oxycodone exposure, we subjected rats to rbTBI and oxycodone self-administration and measured drug seeking and several neuroimaging measures. We found interactive effects of rbTBI and oxycodone on fractional anisotropy (FA) in the nucleus accumbens (NAc), and that FA in the medial prefrontal cortex (mPFC) was correlated with drug seeking. We also found an interactive effect of injury and drug on widespread functional connectivity and regional homogeneity of the BOLD response, and that interhemispheric functional connectivity in the infralimbic medial prefrontal cortex positively correlated with drug seeking. In conclusion, rbTBI and oxycodone self-administration had interactive effects on structural and functional MRI measures, and correlational effects were found between some of these measures and drug seeking. These data support the hypothesis that TBI and opioid exposure produce neuroadaptations that contribute to addiction liability.

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