Kim, Jeongyeon Song, Beomjong Hong, Ingie Kim, Jihye Lee, Junuk Park, Sungmo Eom, Jae Yong Lee, C. Justin Lee, Sukwon Choi, Sukwoo 2024-01-20T19:01:23Z 2024-01-20T19:01:23Z 2021-09-05 2010-07-14 0270-6474 https://pubs.kist.re.kr/handle/201004/131257 It is believed that memory reactivation transiently renders consolidated memory labile and that this labile or deconsolidated memory is reconsolidated in a protein synthesis-dependent manner. The synaptic correlate of memory deconsolidation upon reactivation, however, has not been fully characterized. Here, we show that 3,5-dihydroxyphenylglycine (DHPG), an agonist for group I metabotropic glutamate receptors (mGluRI), induces synaptic depotentiation only at thalamic input synapses onto the lateral amygdala (T-LA synapses) where synaptic potentiation is consolidated, but not at synapses where synaptic potentiation is not consolidated. Using this mGluRI-induced synaptic depotentiation (mGluRI-depotentiation) as a marker of consolidated synapses, we found that mGluRI-depotentiation correlated well with the state of memory deconsolidation and reconsolidation in a predictable manner. DHPG failed to induce mGluRI-depotentiation in slices prepared immediately after reactivation when the reactivated memory was deconsolidated. DHPG induced mGluRI-depotentiation 1 h after reactivation when the reactivated memory was reconsolidated, but it failed to do so when reconsolidation was blocked by a protein synthesis inhibitor. To test the memory-specificity of mGluRI-depotentiation, conditioned fear was acquired twice using two discriminative tones (2.8 and 20 kHz). Under this condition, mGluRI-depotentiation was fully impaired in slices prepared immediately after reactivation with both tones, whereas mGluRI-depotentiation was partially impaired immediately after reactivation with the 20 kHz tone. Consistently, microinjection of DHPG into the LA 1 h after reactivation reduced fear memory retention, whereas DHPG injection immediately after reactivation failed to do so. Our findings suggest that, upon memory reactivation, consolidated T-LA synapses enter a temporary labile state, displaying insensitivity to mGluRI-depotentiation. English SOC NEUROSCIENCE LONG-TERM POTENTIATION RIBOTOXIC STRESS-RESPONSE ACTIVATED PROTEIN-KINASE LATERAL AMYGDALA INPUT SYNAPSES RECONSOLIDATION DEPOTENTIATION EXTINCTION REVERSAL LTP Reactivation of Fear Memory Renders Consolidated Amygdala Synapses Labile Article 10.1523/JNEUROSCI.0940-10.2010 1 JOURNAL OF NEUROSCIENCE, v.30, no.28, pp.9631 - 9640 JOURNAL OF NEUROSCIENCE 30 28 9631 9640 scie scopus 000279899100030 2-s2.0-77954752887 Neurosciences Neurosciences & Neurology Article LONG-TERM POTENTIATION RIBOTOXIC STRESS-RESPONSE ACTIVATED PROTEIN-KINASE LATERAL AMYGDALA INPUT SYNAPSES RECONSOLIDATION DEPOTENTIATION EXTINCTION REVERSAL LTP