Endogenous opioids (EO) effects related to sensory information modulat
ion and epileptogenesis are described. Based on the hypothesis of EO p
laying this modulator or ''filter'' role, previous experiments in the
visual pathway are described in which naloxone (opiate antagonist) pro
duced an amplitude increment of the visual evoked potentials (VEP) in
the temporal lobe amygdala. The VEP amplitude increment was also obser
ved by means of brief low-intensity, repeated electrical stimulation (
kindling procedure) of some limbic and visual structures. Again, this
increment was intensified by the administration of naloxone. Previous
works related to the effects of opioid antagonist administration alone
or during the development of the amygdaloid kindling in encephale iso
le preparations and intact free moving cats without anesthesia, are re
viewed. In both cases, naloxone facilitated the epileptogenesis. Anoth
er sensibilization model documented is the application of the kindling
method to the interneuron pathways of the presynaptic inhibition that
have properties corresponding to a complex circuitry. The plasticity
phenomena becomes evident in the spinal cord trhough the post-tetanic
potentiation and habituation processes. We found that the short and re
peated stimulation of the aferent cutaneous and muscular nerves produc
ed progresively amplitude increase of the polisynaptic reflexes. The p
reviously intensified reflexes by the afferent repetitive stimulation
were further enhanced by naloxone administration.