P. Degortari et al., CHANGES IN TRH AND ITS DEGRADING ENZYME PYROGLUTAMYL PEPTIDES-II, DURING THE DEVELOPMENT OF AMYGDALOID KINDLING, Brain research, 679(1), 1995, pp. 144-150
Pyroglutamyl peptidase II (PPII) is a neuronal ectoenzyme responsible
for thyrotropin releasing hormone (TRH) degradation at the synaptic cl
eft. PPII, heterogeneously distributed in different brain regions and
adenohypophysis, is regulated under various endocrine conditions where
TRH is involved in thyrotropin or prolactin regulation but only at th
e adenohypophyseal level. TRH can downregulate PPII activity in cultur
ed adenohypophyseal cells. TRH present in extrahypothalamic brain area
s has been postulated to serve as a neuromodulator and levels of this
peptide increase in amygdala, hippocampus and cortex after electrical
stimulation (kindling or electroshock). To study whether brain PPII co
uld be regulated in conditions that stimulate TRHergic neurons, TRH an
d PPII activity were determined during the development of amygdaloid k
indling in the rat. TRH levels increased from stage II to V in amygdal
a and hippocampus in the ipsi- and contralateral side to stimulation.
In n. accumbens a decrease, compared to sham was observed at stage II,
but levels raised through stage V. In contrast, PPII activity was inc
reased at stage II, in amygdala of both sides and in hippocampus, fron
tal cortex, n. accumbens and hypothalamus of the contralateral side; l
evels decreased at stage V to sham values in most structures (except a
mygdala and hippocampus where the activity was 30% below controls). Th
ese results suggest that PPII activity in the central nervous system c
an be regulated in conditions known to affect TRHergic neurons.