Animal Models of Learning, Memory & Cognition

Introduction & memory taxonomy

• Learning = an experience-dependent change in behaviour; memory = retention and later expression of that change. Cognition is the broader information-processing set (attention, executive function, working memory, recognition) in which learning & memory sit.
• Why animal models? They permit invasive manipulation (lesions, drugs, electrophysiology, genetics) impossible in humans, allow drug timing to dissect distinct memory phases, and are the mandatory preclinical step before human cognition-enhancer trials.
• They are the methodological substrate behind every nootropic / anti-Alzheimer / antiamnesic claim — clinical drugs (donepezil, memantine, piracetam) appear only as the standards / positive controls against which test compounds are run.
• Performance varies with species, strain, sex, age and environment — each both a controllable variable and a confounder; environmental enrichment acts via epigenetic modification.
• Operational memory taxonomy — the dimensions a screen actually manipulates:
  • STM vs LTM — distinguished only by the retention interval: minutes (STM) vs ≥24 h (LTM); the same apparatus (e.g. step-down) tests either by when the retention trial is run.
  • Working vs reference memory — working = trial-unique (which arms already visited); reference = constant across trials (which arms are always baited).
  • Memory phases dissected by drug timing — acquisition (drug pre-training), consolidation (immediately post-training), retrieval (pre-retention test), plus reconsolidation & extinction; drug timing is the core design lever.
  • Declarative (hippocampus-dependent, e.g. spatial mazes) vs non-declarative (e.g. cerebellar eyeblink conditioning, habituation) — anatomical dissociation decides which paradigm fits which clinical target.