Disturbance of serotonergic neurotransmission in patients with postmyocardial infarction and depression.

Metabolic brain disease

PubMedID: 23129293

Manjarrez-Gutiérrez G, Ramírez-Campillo R, Borrayo-Sánchez G, Hernández-Rodríguez J. Disturbance of serotonergic neurotransmission in patients with postmyocardial infarction and depression. Metab Brain Dis. 2013;28(1):15-20.
The objective of this study was to assess the hypothesis that patients who develop depression after myocardial infarction (MI) have a lower level of brain serotonergic neurotransmission through measurement of plasma free fraction of L-tryptophan and intensity-dependence auditory-evoked potentials (IDAEPs). A cross-sectional study was carried out in 74 adults after MI. Thirty-four patients suffered from depression and 40 patients did not demonstrate depressive symptoms. We measured the free fraction, bound and total plasma L-tryptophan, and neutral amino acids as well as recording IDAEPs. Patients who developed depression after MI showed a significantly lower level in the free fraction of L-tryptophan and in the ratios of free fraction of L-tryptophan/total L-tryptophan and free fraction of L-tryptophan/neutral amino acids. It is noteworthy that the slope of the amplitude/stimulus intensity functions (ASF slope) of the N1/P2 component was significantly higher post-MI in depressed patients. Higher ASF slope of the N1/P2 component associated with a low free fraction of L-tryptophan in plasma reflect a low brain serotonergic neurotransmission. These findings suggest an important deterioration of brain serotonergic activity as a pathophysiological mechanism in post-MI patients for the development of clinical depression. Therefore, we propose these biochemical and electrophysiological procedures as noninvasive clinical indicators of brain serotonergic activity in these patients.