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BNIP3L\/NIX, a mitophagy receptor, has been linked to neurological disorders, yet its specific function in the brain remains unclear. We found BNIP3L highly expressed in basolateral amygdala (BLA) neurons. Selective deletion of\n                    <jats:italic>bnip3l<\/jats:italic>\n                    in BLA glutamatergic neurons (BLA\n                    <jats:sup>GLU<\/jats:sup>\n                    ) impaired contextual fear memory, accompanied by reduced neuronal excitation and mitochondrial respiration. Notably, fear conditioning did not invariably activate mitophagy in BLA\n                    <jats:sup>GLU<\/jats:sup>\n                    neurons. Overexpression of both wild\u2010type and a mitophagy\u2010deficient mutant (BNIP3L\n                    <jats:sup>\u0394LIR<\/jats:sup>\n                    ) in BLA\n                    <jats:sup>GLU<\/jats:sup>\n                    neurons was sufficient to rescue the contextual fear memory deficits in\n                    <jats:italic>bnip3l<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice, suggesting a non\u2010mitophagy role. Instead, we detected a prompt mitochondrial fission in BLA\n                    <jats:sup>GLU<\/jats:sup>\n                    neurons after foot\u2010shock conditioning, an effect abolished by\n                    <jats:italic>bnip3l<\/jats:italic>\n                    deletion. Inhibition of Drp1 with Mdivi\u20101 disrupted memory formation, whereas optogenetic activation of Drp1 restored neuronal excitation and rescued memory deficits in\n                    <jats:italic>bnip3l<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. These data indicated an essential role of BNIP3L\u2010mediated mitochondrial fission in modulating contextual fear memory. Mechanistically, BNIP3L and Drp1 competitively interact with AMPK, leading to reduced Drp1 phosphorylation and increased Drp1 accumulation on mitochondria, thereby promoting mitochondrial fission. Taken together, the present study revealed a previously uncharacterized, non\u2010mitophagy\u2010dependent role for BNIP3L in contextual fear memory conditioning.\n                  <\/jats:p>","DOI":"10.1002\/advs.202517585","type":"journal-article","created":{"date-parts":[[2026,1,25]],"date-time":"2026-01-25T08:48:46Z","timestamp":1769330926000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["A Non\u2010Mitophagy Activity of BNIP3L\/NIX in Amygdala Glutamatergic Neurons is Essential for Contextual Fear Memory Formation"],"prefix":"10.1002","volume":"13","author":[{"given":"Xingxian","family":"Zhang","sequence":"first","affiliation":[{"name":"Institute of Pharmacology &amp; Toxicology Zhejiang Key Laboratory of Neuropsychopharmacology State Key Laboratory of Advanced Drug Delivery and Release Systems College of Pharmaceutical Sciences Zhejiang University  Hangzhou 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