***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Little is known about the acute effects of antidepressant treatments on brain glutamate and gamma-amino-butyric acid ( GABA ) levels , and their association with clinical response . Using proton magnetic resonance spectroscopy ( 1H-MRS ) we examined longitudinally the effects of citalopram on glutamine/glutamate ratios and GABA levels in the pregenual anterior cingulate cortex ( pgACC ) of individuals with major depressive disorder ( MDD ) . We acquired 1H-MRS scans at baseline and at days 3 , 7 , and 42 of citalopram treatment in nineteen unmedicated individuals with MDD . Ten age- and sex-matched non-depressed comparison individuals were scanned once . The association between 1 ) baseline metabolites and 2 ) change in metabolites from baseline to each time point and clinical response ( change in Montgomery-Åsberg Depression Rating Scale ( MADRS ) score from baseline to day 42 ) was assessed by longitudinal regression analysis using generalized estimating equations . Contrary to our hypotheses , no significant associations emerged between glutamate metabolites and clinical response ; however , greater increases ( or smaller decreases ) in pgACC GABA levels from baseline to days 3 and 7 of citalopram treatment were significantly associated with clinical response . These findings suggest that an acute change in GABA levels in pgACC predicts , and possibly mediates , later clinical response to citalopram treatment in individuals with MDD Increasing interest surrounds potential neuroprotective or neurotrophic actions of antidepressants . While growing evidence points to important early clinical and neuropsychological effects of antidepressants , the time-course of any effect on neuronal integrity is unclear . This study used magnetic resonance spectroscopy to assess effects of short-term treatment with escitalopram on N-acetyl-aspartate ( NAA ) , a marker of neuronal integrity . Thirty-nine participants with major depression were r and omly assigned to receive either 10 mg escitalopram or placebo daily in a double-blind , parallel group design . On the seventh day of treatment , PRESS data were obtained from a 30 × 30 × 20 mm voxel placed in medial frontal cortex . Age and gender-matched healthy controls who received no treatment were also scanned . Levels of NAA were significantly higher in patients treated with escitalopram than in either placebo-treated patients ( p<0.01 ) or healthy controls ( p<0.01 ) . Our findings are consistent with the proposition that antidepressant treatment in depressed patients can produce early changes in neuronal integrity The dorsolateral prefrontal cortex ( DLPFC ) plays an essential role in mood regulation and integration of cognitive functions that are abnormal in major depressive disorder ( MDD ) . Few neuroimaging studies have evaluated the still maturing DLPFC in depressed children and adolescents . We conducted single voxel proton magnetic resonance spectroscopy ( (1)H MRS ) of the left DLPFC in 14 depressed children and adolescents ( 13.3 + /- 2.3 years old , 10 males ) and 22 matched healthy controls ( 13.6 + /- 2.8 years old , 13 males ) . Depressed subjects had significantly lower levels of glycerophosphocholine plus phosphocholine ( GPC + PC ; or choline-containing compounds ) and higher myo-inositol levels in the left DLPFC compared to healthy controls . In the depressed subjects , we found significant inverse correlations between glutamate levels and both duration of illness and number of episodes . In healthy controls there was a significant direct correlation between age and glutamine levels , which was not present in the patient group . Lower GPC + PC levels in pediatric MDD may reflect lower cell membrane content per volume in the DLPFC . Increased myo-inositol levels in MDD may represent a disturbed secondary messenger system . GPC + PC and myo-inositol abnormalities further demonstrate the involvement of DLPFC in pediatric MDD BACKGROUND A growing body of pre clinical research suggests that brain glutamate systems may be involved in the pathophysiology of major depression and the mechanism of action of antidepressants . This is the first placebo-controlled , double-blinded trial to assess the treatment effects of a single dose of an N-methyl-D-aspartate ( NMDA ) receptor antagonist in patients with depression . METHODS Seven subjects with major depression completed 2 test days that involved intravenous treatment with ketamine hydrochloride ( .5 mg/kg ) or saline solutions under r and omized , double-blind conditions . RESULTS Subjects with depression evidence d significant improvement in depressive symptoms within 72 hours after ketamine but not placebo infusion ( i.e. , mean 25-item Hamilton Depression Rating Scale scores decreased by 14 + /- SD 10 points vs. 0 + /- 12 points , respectively during active and sham treatment ) . CONCLUSIONS These results suggest a potential role for NMDA receptor-modulating drugs in the treatment of depression Previous research has revealed that major depression is accompanied by disorders in excitatory amino acids , e.g. glutamate and aspartate , and alterations in serum levels of other amino acids , e.g. serine , glycine and taurine . The aim of the present study was to examine serum levels of aspartate , asparagine , glutamate , glutamine , serine , glycine , threonine , histidine , alanine , taurine and arginine in major depression patients with treatment‐resistant depression ( TRD ) . No significant differences in the serum concentrations of any of the above amino acids could be found between patients with and without TRD and normal controls . Non‐responders to treatment with antidepressants during a period of 5 weeks were characterized by significantly lower serum levels of aspartate , asparagine , serine , threonine and taurine . A 5‐week period of treatment with antidepressants significantly reduced the serum levels of aspartate , glutamate and taurine , and significantly increased the serum concentrations of glutamine . The results suggest that alterations in serum levels of aspartate , asparagine , serine , threonine and taurine may predict the subsequent response to treatment with antidepressants , and that the latter may modulate serum levels of excitatory amino acids and taurine 
    Output:
    
Overall , decreased levels of glutamatergic metabolites in the medial frontal cortex are linked with the pathophysiology of depression .
These findings are in line with the hypothesis that depression may be associated with abnormal glutamatergic neurotransmission