Mild traumatic brain injury (mTBI) is the most common form of TBI (70-90%)(1) with anxiety disorders are found in 23% of mTBI cases. Studies report neurometabolic alterations following different severities and types of rodent TBI (2) using magnetic resonance spectroscopy (MRS) with scant evidences of studies relating anxiety-like behavior and metabolic alterations in mTBI. So, the present study aims to investigate the longitudinal neurometabolic alterations in anxiety modulating regions in a suitable experimental model of mTBI.68adult, male SDrats (250gms) were used during the study. mTBI was induced by freely dropping 450 gm(1cm diameter) brass rod from a height of 25cm above the sagittal midway of the rat brain(3). The experiment was done in 3phases with 4groups of rats viz; GpI:injury with anesthesia(IA), GpII:Injury only(IO),GpIII:anesthesia only (AO), GpIV:control(OO)(Fig1). In phaseI mTBI induced longitudinal neurometabolic alterations were studied using 1H-MRS prior to injury (D0) and at 4hr, day1 and day5 post injury(PI) in gpIA . In phII of the study, 1H-MRS was done at D5 in 4groups to analyse the effect of injury on metabolic alterations without/with interference of anesthesia used for imaging. Neurobehavioral analysis was done in phaseIII of the study in all 4groups at D5. 1H-MRS experiments were carried on a 7T(Biospec USR70/30) Bruker system. Based on anxiety modulating regions, the MRS voxels were localised in the cortex, hippocampus region and amygdala of the rat brain(Fig2). Due to poor SNR, amygdala could not be investigated in the study. The local field homogeneity in 1H-MRS acquisition was optimised using the FASTMAP sequence. Outer volume suppression combined with a point resolved spectroscopy (PRESS) sequence was used with TR/TE 2500/20 ms, 512 averages. The water signal was suppressed by variable power and optimised relaxation delay (VAPOR). A spectrum without water suppression was acquired using 16 averages. The line width of the water peak was between 9-12 Hz FWHM. MRS spectra were quantified offline using LCModel (Provencher 2001). Total creatine, tCr (sum of Cr and PCr) concentration was used as a normalising factor since no difference was observed in tCr between groups. Gross behavioral changes, locomotor activities and basal anxiety level parameters were studied using open field test (OFT) paradigm. The novel object recognition test (NORT) paradigm was used to measure short-term memory functions in the rodents. All the behavioral tests were conducted on the D5 PI, except for novel object recognition tests, which include 2-day paradigms and hence were completed 24 hr later, on D6.Results of phI of the study was analysed using repeated measures one way analysis of variance(ANOVA) with boneferroni confidence interval adjustment. Results of phII and III, were analysed using ANOVA with post-hoc boneferroni correction. p-value of ≤0.05 was considered to be significant. PhI showed statistically significant reduction in Tau/tCr levels in cortex at D5 PI in GpIA as compared to D0 (Fig3). PhII showed reduced Tau/tCr levels in gpIA and IO at D5 as compared to gpOO. AO didnot show any significant change in taurine levels indicating injury induced changes in taurine levels. tGlu/tCr levels were significantly decreased in group IA as compared to controls and AO group at D5 PI. tCho/tCr levels showed non-significant reduction in IA group as compared to gpOO. Group AO showed statistically increased tCho/tCr levels as compared to group IO at D5 imaging. GpIA didnot show any statistical difference in tNAA/tCr levels at any timepoint PI. Group AO showed significantly increased levels of tNAA/tCr as compared to gpsOO and IO at D5 (Fig3). Hippocampus did not show any metabolic alteration in any group/timepoint PI. PhaseIII showed locomotor hyperactivity in gpsIO and AO groups with respect to gpOO rats. Increased anxiety behaviour was observed in 3gps (IA,IO,AO) as compared to gpOO. NORT showed non-significantly changed discrimination ratio of gpIA, IO and AO as compared to gpOO(Fig4,5).mTBI has shown high extracellular K+concentration, leading to cytotoxic edema and progressive taurine release. Significantly decreased tGlu/tCr levels in gpIA at D5 PI suggests towards neuroprotective mechanism to overcome injury induced glutamate excitotoxicity. Interaction of taurine and glutamate alters physiological functions of the brain where taurine may activate both GABAA and glycine receptors to modulate anxiety behavior. Other metabolites showed variable results indicating anesthetic affect; which needs further histological/cellular investigation. This study presents neurometabolic basis of anxiety-like behavior in mTBI where acute reduction in cortical taurine levels is accompanied with anxiety-like behavior but normal cognition similar to symptoms of generalized anxiety disorder as seen in clinical TBI.