Abstracts

Rationale: Nitric oxide (NO) has been identified as a source of free-radical oxidants and has been implicated in the pathophysiology of several brain disorders. NO is associated with a variety of brain functions including synaptic plasticity and glutamate neurotoxicity. An abnormal neural plasticity has been suggested to be involved in pathologic processes such as epilepsy and schizophrenia. We investigated NOS expression in hippocampi of mesial temporal lobe epilepsy patients with no psychiatric comorbidities (TLE, n=16) and with interictal psychosis (TLE+P, n=14) or major depression (TLE+D, n=19). Methods: Hippocampi (n=49) were surgically obtained from medically intractable TLE patients and compared to autopsy controls (n=6) with no pre-mortem neurological disorders. Specimens were equally treated and submitted to hematoxilin-eosin and imunohistochemistry for Neu-N and nNOS. Positive immunoreactivity was estimated using an image analysis system software (ImageJ). Results: All epileptic groups had decreased neuron densities in all hippocampal subfields when compared to autopsy controls but no differences were found among epileptic groups. TLE patients had increased nNOS immunureactivity, and it was lower in the psychosis group in all hippocampal subfields, except CA1, CA2 and parasubiculum. Conclusions: We found differential expression of nNOS among epileptic groups with and without psychiatric comorbidities. These findings suggest that differential modulation of NO signaling pathways may underlie epilepsy and comorbid manifestation of psychiatric symptoms.