***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: In the prefrontal cortex of subjects with schizophrenia , markers of the synthesis and re-uptake of GABA appear to be selectively altered in a subset of interneurons that includes ch and elier cells . Determining the effect of these disturbances in presynaptic GABA markers on inhibitory signaling requires knowledge of the status of GABA(A ) receptors at the postsynaptic targets of ch and elier cells , the axon initial segments ( AIS ) of pyramidal neurons . Because the alpha(2 ) subunit of the GABA(A ) receptor is preferentially localized at pyramidal neuron AIS , we quantified alpha(2 ) subunit immunoreactive AIS in tissue sections containing prefrontal cortex area 46 from 14 matched triads of subjects with schizophrenia , subjects with major depression and control subjects . Systematic , r and om sampling revealed that the mean number of alpha(2)-labeled AIS per mm(2 ) in subjects with schizophrenia was significantly ( P = 0.007 ) increased by 113 % compared to control subjects and non-significantly increased compared to subjects with major depression . Furthermore , within subjects with schizophrenia , the density of alpha(2)-labeled AIS was negatively correlated ( r = -0.49 , P = 0.038 ) with the density of ch and elier axon terminals immunoreactive for the GABA membrane transporter . These data suggest that GABA(A ) receptors are up-regulated at pyramidal neuron AIS in response to deficient GABA neuro-transmission at ch and elier axon terminals in schizophrenia . Thus , disturbances in inhibition at the ch and elier neuron-pyramidal neuron synapse may be a critical component of prefrontal cortical dysfunction in schizophrenia BACKGROUND The role of the inhibitory neurotransmitter gamma aminobutyric acid ( GABA ) in schizophrenia has previously been investigated using postmortem material . Recently , using single photon emission tomography ( SPET ) with the selective benzodiazepine antagonist 123I-Iomazenil as the radiolig and , we have demonstrated an in vivo relationship between reduced GABAA/benzodiazepine receptor binding and the severity of positive symptomatology in schizophrenia . The present study aim ed to build on this using the same in vivo scanning techniques , and relating findings to cognitive functioning . METHODS Ten nonpsychiatric control subjects and 15 schizophrenic patients , matched for age and h and edness , were scanned . A battery of neuropsychologic tests was also administered . RESULTS Correlational analysis revealed a pattern of increased correlations between GABAA/benzodiazepine receptor binding and task performance , in the schizophrenic group compared to the control group . CONCLUSIONS Findings are preliminary but suggest a relationship between reduced GABAA/benzodiazepine receptor binding and poorer cognitive functioning , involving memory and visual attention processes , in the schizophrenic group but not in the control group . A role for GABA in the pathophysiology of schizophrenia is suggested . Limitations of the present study and suggestions for future research are discussed 
    Output:
    
There were insufficient PET/SPECT receptor availability studies for meta-analyses , but a systematic review did not suggest replicable group differences in regional GABAA/BZR availability .
The current literature does not reveal consistent alterations in in vivo GABA neuroimaging measures in schizophrenia , as might be hypothesized from animal models and postmortem data .