midazolam intra-basolateral amygdala (BLA) infusion prior to stress attenuated the enhancement of fear memory
thus suggesting the involvement of a stress-induced reduction of the GABAergic transmission in BLA in the stress-induced
enhancing effect.
We therefore evaluate the relative contribution of these two neurobiological processes to the fear memory resulting from the above-mentioned interaction. Intra-dorsal hippocampus (DH) infusions of either the antisense Zif268 or the inhibitor of the protein degradation (Clasto-Lactacystin b-Lactone), suggested to be involved in the retrieval-dependent destabilization
process, did not affect the resulting contextual memory. In contrast, the knockdown of hippocampal BDNF mitigated the stress-induced facilitating influence on fear retention. In addition, the retrieval experience elevated BDNF level in DH at 60 min after recall exclusively in stressed animals. These findings suggest the involvement of a hippocampal BDNF sensitive mechanism in the stress-promoting influence on the fear memory following retrieval. process, did not affect the resulting contextual memory. In contrast, the knockdown of hippocampal BDNF mitigated the stress-induced facilitating influence on fear retention. In addition, the retrieval experience elevated BDNF level in DH at 60 min after recall exclusively in stressed animals. These findings suggest the involvement of a hippocampal BDNF sensitive mechanism in the stress-promoting influence on the fear memory following retrieval. process, did not affect the resulting contextual memory. In contrast, the knockdown of hippocampal BDNF mitigated the stress-induced facilitating influence on fear retention. In addition, the retrieval experience elevated BDNF level in DH at 60 min after recall exclusively in stressed animals. These findings suggest the involvement of a hippocampal BDNF sensitive mechanism in the stress-promoting influence on the fear memory following retrieval.
We therefore evaluate the relative contribution of these two neurobiological processes to the fear memory resulting from
the above-mentioned interaction. Intra-dorsal hippocampus (DH) infusions of either the antisense Zif268 or the inhibitor of
the protein degradation (Clasto-Lactacystin b-Lactone), suggested to be involved in the retrieval-dependent destabilization
process, did not affect the resulting contextual memory. In contrast, the knockdown of hippocampal BDNF mitigated the stress-induced facilitating influence on fear retention. In addition, the retrieval experience elevated BDNF level in DH at 60 min after recall exclusively in stressed animals. These findings suggest the involvement of a hippocampal BDNF sensitive mechanism in the stress-promoting influence on the fear memory following retrieval.
process, did not affect the resulting contextual memory. In contrast, the knockdown of hippocampal BDNF mitigated the
stress-induced facilitating influence on fear retention. In addition, the retrieval experience elevated BDNF level in DH at 60
min after recall exclusively in stressed animals. These findings suggest the involvement of a hippocampal BDNF sensitive
mechanism in the stress-promoting influence on the fear memory following retrieval.
process, did not affect the resulting contextual memory. In contrast, the knockdown of hippocampal BDNF mitigated the
stress-induced facilitating influence on fear retention. In addition, the retrieval experience elevated BDNF level in DH at 60
min after recall exclusively in stressed animals. These findings suggest the involvement of a hippocampal BDNF sensitive
mechanism in the stress-promoting influence on the fear memory following retrieval.
We therefore evaluate the relative contribution of these two neurobiological processes to the fear memory resulting from
the above-mentioned interaction. Intra-dorsal hippocampus (DH) infusions of either the antisense Zif268 or the inhibitor of
the protein degradation (Clasto-Lactacystin b-Lactone), suggested to be involved in the retrieval-dependent destabilization
process, did not affect the resulting contextual memory. In contrast, the knockdown of hippocampal BDNF mitigated the stress-induced facilitating influence on fear retention. In addition, the retrieval experience elevated BDNF level in DH at 60 min after recall exclusively in stressed animals. These findings suggest the involvement of a hippocampal BDNF sensitive mechanism in the stress-promoting influence on the fear memory following retrieval.
process, did not affect the resulting contextual memory. In contrast, the knockdown of hippocampal BDNF mitigated the
stress-induced facilitating influence on fear retention. In addition, the retrieval experience elevated BDNF level in DH at 60
min after recall exclusively in stressed animals. These findings suggest the involvement of a hippocampal BDNF sensitive
mechanism in the stress-promoting influence on the fear memory following retrieval.
process, did not affect the resulting contextual memory. In contrast, the knockdown of hippocampal BDNF mitigated the
stress-induced facilitating influence on fear retention. In addition, the retrieval experience elevated BDNF level in DH at 60
min after recall exclusively in stressed animals. These findings suggest the involvement of a hippocampal BDNF sensitive
mechanism in the stress-promoting influence on the fear memory following retrieval.
We therefore evaluate the relative contribution of these two neurobiological processes to the fear memory resulting from
the above-mentioned interaction. Intra-dorsal hippocampus (DH) infusions of either the antisense Zif268 or the inhibitor of
the protein degradation (Clasto-Lactacystin b-Lactone), suggested to be involved in the retrieval-dependent destabilization
process, did not affect the resulting contextual memory. In contrast, the knockdown of hippocampal BDNF mitigated the stress-induced facilitating influence on fear retention. In addition, the retrieval experience elevated BDNF level in DH at 60 min after recall exclusively in stressed animals. These findings suggest the involvement of a hippocampal BDNF sensitive mechanism in the stress-promoting influence on the fear memory following retrieval.
process, did not affect the resulting contextual memory. In contrast, the knockdown of hippocampal BDNF mitigated the
stress-induced facilitating influence on fear retention. In addition, the retrieval experience elevated BDNF level in DH at 60
min after recall exclusively in stressed animals. These findings suggest the involvement of a hippocampal BDNF sensitive
mechanism in the stress-promoting influence on the fear memory following retrieval.
process, did not affect the resulting contextual memory. In contrast, the knockdown of hippocampal BDNF mitigated the
stress-induced facilitating influence on fear retention. In addition, the retrieval experience elevated BDNF level in DH at 60
min after recall exclusively in stressed animals. These findings suggest the involvement of a hippocampal BDNF sensitive
mechanism in the stress-promoting influence on the fear memory following retrieval.
process, did not affect the resulting contextual memory. In contrast, the knockdown of hippocampal BDNF mitigated the
stress-induced facilitating influence on fear retention. In addition, the retrieval experience elevated BDNF level in DH at 60
min after recall exclusively in stressed animals. These findings suggest the involvement of a hippocampal BDNF sensitive
mechanism in the stress-promoting influence on the fear memory following retrieval.
