The mTOR pathway acts as a dynamic dial that shifts cellular priority between growth‑dependent plasticity and immediate survival responses. In aging CeA‑CRF neurons, chronic low‑grade mTOR activity locks the circuit into a maladaptive state: extinction memory consolidation fails because the anabolic burst needed for new synaptic proteins is missing, yet acute threat‑evoked CRF release is blunted, indicating a loss of phasic signaling flexibility. We hypothesize that restoring transient, high‑amplitude mTOR pulses—mimicking the natural peaks that occur during safety learning—will selectively revive translation of plasticity‑related mRNAs (e.g., Arc, Bdnf, Egr1) without globally elevating CRF synthesis, thereby rescuing fear extinction while preserving appropriate acute stress responses.

Mechanistically, mTORC1 controls the phosphorylation state of 4E‑BP1 and S6K1, which together regulate cap‑dependent translation and the activity of prohormone convertases that process CRF precursor. In aged CeA‑CRF neurons, we predict reduced 4E‑BP1 phosphorylation leads to preferential translation of mRNAs with simple 5′UTRs (housekeeping genes) and exclusion of those with complex, structured leaders that encode plasticity effectors. Simultaneously, diminished S6K1 activity lowers phosphorylation of PC1/2, impairing CRF peptide maturation and contributing to the observed blunted FOS/FOSB response to acute stress. Intermittent mTOR activation—achieved via timed rapamycin withdrawal, optogenetic stimulation of upstream Akt, or brief bouts of high‑intensity exercise—should transiently increase 4E‑BP1 and S6K1 phosphorylation, thereby shifting the translational repertoire toward plasticity proteins and restoring PC‑mediated CRF processing.

Testable predictions: (1) Aged rats receiving intermittent mTOR activation (e.g., rapamycin washout every 48 h for two weeks) will show increased p‑4E‑BP1 and p‑S6K1 levels in laser‑captured CeA‑CRF neurons compared with continuously rapamycin‑treated or vehicle controls. (2) These animals will exhibit normalized fear extinction retention in auditory fear conditioning, measured as reduced freezing during extinction recall, while preserving a normal increase in CRF‑FOS co‑expression after a novel acute stressor. (3) Pharmacological blockade of S6K1 (using PF‑4708671) during the mTOR pulse window will prevent the rescue of extinction, confirming that S6K1‑dependent translation—not merely global mTOR activity—is critical. (4) Ribosome profiling of CeA‑CRF neurons will reveal a specific increase in ribosome footprints on mRNAs with complex 5′UTRs (Arc, Bdnf, Synapsin1) after intermittent mTOR activation, without a commensurate rise in Crf transcript translation.

Falsification: If intermittent mTOR activation fails to improve extinction retention, does not alter p‑4E‑BP1/p‑S6K1 dynamics, or rescues extinction only alongside a maladaptive increase in baseline CRF release, the hypothesis would be refuted. Conversely, confirmation would support the notion that mTOR’s role in aging stress circuits is not a static suppressor but a rhythmic regulator whose phasic peaks are essential for the civilization‑mode plasticity that underlies adaptive fear extinction.