Anxiolytic and sedative drugs: Sleep modulation and memory implications

Sleep plays a crucial role in cognitive processes, particularly in memory consolidation, with Non-Rapid Eye Movement (NREM) and Rapid Eye Movement (REM) sleep phases playing distinct roles. Different classes of anxiolytics and sedatives influence sleep architecture and, consequently, memory function, with varying effects on learning, synaptic plasticity, and neurophysiological activity. While some drugs promote sedation and anxiolysis via GABAergic modulation, others act on serotonergic, dopaminergic, or orexinergic pathways, producing divergent effects on memory function. Rodent studies indicate that many compounds affect REM sleep and hippocampus-dependent memory, particularly those targeting the GABA-A system (benzodiazepines, Z-drugs). On the other hand, melatonin receptor agonists and dual orexin receptor antagonists appear to exert a more selective influence on sleep without severely disrupting memory function. Additionally, cannabinoids and opioids compounds modulate memory consolidation in complex ways, often depending on dose, receptor selectivity and interaction with sleep deprivation. The role of endocannabinoid system modulation in cognition remains an area of active investigation, with potential implications for novel therapeutic strategies. Understanding the diverse effects of these pharmacological agents on sleep and memory is essential for advancing knowledge in neuropharmacology and cognitive neuroscience, as well as for interpreting the diverse effects of these compounds. This review explores how psychoactive agents, either traditionally classified as hypnotics or commonly prescribed for their sedative or anxiolytic effects, affect sleep-dependent memory processes. To ensure consistency we limit our analysis to studies employing doses that produce clear hypnotic or sedative effects, focusing on the interplay between sleep modulation and cognitive outcomes.