In the hippocampal formation many neuromodulators are possibly implied in the synaptic plasticity such as the long-term potentiation (LTP) induced by high-frequency stimulation (HFS) of afferent fibers. We investigated the involvement of locally synthesized neural 17-estradiol (nE2) in the induction of HFS-LTP in hippocampal slices from male rats by stimulating the Schaffer collateral fibers and recording the evoked field excitatory postsynaptic potential (fEPSP) in the CA1 region. We demonstrated that either the blockade of nE2 synthesis by the aromatase inhibitor letrozole, or the antagonism of E2 receptors (ERs) by ICI 182,780 did not prevent the induction of HFS-LTP, but reduced its amplitude by 60%, without influencing its maintenance. Moreover, letrozole and ICI 182,780 did not affect the first short-term post-tetanic component of LTP and the paired-pulse facilitation (PPF). These findings demonstrate that nE2 plays an important role in the induction phase of HFS-dependent LTP. Since the basal responses were not affected by the blocking agents, we suggest that the synthesis of nE2 is induced or enhanced by HFS through aromatase activation. In this context, the local production of nE2 seems to be a very effective mechanism to modulate the amplitude of LTP. © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.
Neural 17beta-estradiol facilitates long-term potentiation in the hippocampal CA1 region
GRASSI, Silvarosa;Tozzi, Alessandro;COSTA, CINZIA;SCARDUZIO, MARIANGELA;CALABRESI, PAOLO;PETTOROSSI, Vito Enrico
2011
Abstract
In the hippocampal formation many neuromodulators are possibly implied in the synaptic plasticity such as the long-term potentiation (LTP) induced by high-frequency stimulation (HFS) of afferent fibers. We investigated the involvement of locally synthesized neural 17-estradiol (nE2) in the induction of HFS-LTP in hippocampal slices from male rats by stimulating the Schaffer collateral fibers and recording the evoked field excitatory postsynaptic potential (fEPSP) in the CA1 region. We demonstrated that either the blockade of nE2 synthesis by the aromatase inhibitor letrozole, or the antagonism of E2 receptors (ERs) by ICI 182,780 did not prevent the induction of HFS-LTP, but reduced its amplitude by 60%, without influencing its maintenance. Moreover, letrozole and ICI 182,780 did not affect the first short-term post-tetanic component of LTP and the paired-pulse facilitation (PPF). These findings demonstrate that nE2 plays an important role in the induction phase of HFS-dependent LTP. Since the basal responses were not affected by the blocking agents, we suggest that the synthesis of nE2 is induced or enhanced by HFS through aromatase activation. In this context, the local production of nE2 seems to be a very effective mechanism to modulate the amplitude of LTP. © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
