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Prefrontal Cortex Traumatic Brain Injury Produces Greater Neurobehavioral Dysfunction and Delayed Behavioral Recovery Versus TBI Localized to the Sensorimotor Cortex
Author(s) -
Mayeux Jacques,
Katz Paige,
Gilpin Nicholas,
Molina Patricia
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.840.10
Subject(s) - traumatic brain injury , prefrontal cortex , medicine , neuroinflammation , psychology , anesthesia , psychiatry , cognition , inflammation
Traumatic Brain Injury (TBI) is an increasingly prevalent health concern that accounts for 30% of all injury‐related deaths in the US with treatment costs surpassing $16 billion. Post‐TBI, individuals often report increases in alcohol drinking. Alcohol can exacerbate post‐TBI neuroinflammation and prolong the recovery period, so it is of great clinical and public health interest to study mechanisms driving this behavior. Hypothesis We predict that TBI localized to the prefrontal cortex (PFC), a brain area that controls alcohol drinking, will result in greater behavioral dysfunction and increased drinking compared to TBI localized to the sensorimotor cortex (SMC). Methods: Male Wistar rats were trained to self‐administer alcohol prior to receiving TBI by fluid percussion to the PFC or SMC. Following TBI, apnea, respiratory rate, and righting reflex were measured, and neurobehavioral scores (NBS) and neurological severity scores (NSS) were calculated as quantitative measures of behavioral dysfunction. In addition, alcohol self‐administration was measured post‐TBI. Results: Physiological outcomes were worse in PFC TBI compared to SMC TBI. PFC TBI also produced greater neurobehavioral dysfunction than SMC TBI as evidenced by increased NBS/NSS scores. Both PFC and SMC TBI increased alcohol drinking in the early post‐injury recovery period. Conclusions PFC TBI in rats produces more severe neurobehavioral disruption that may be clinically relevant to post‐TBI alcohol drinking. The role of the post‐TBI neuroinflammatory milieu in driving escalated drinking is the focus of current studies. Support T‐32 AA007577, F30 AA022838.