Neurobiology of Learning and Memory

Statistical learning (SL) has been proposed to depend on the hippocampus, but traditional neuropsychological theories of long-term memory posit that the hippocampus is only necessary for explicit memory processes, not implicit memory processes. To reconcile these two accounts, we exposed 27 temporal lobe epilepsy (TLE) patients to a continuous speech stream containing embedded trisyllabic words, then tested their statistical knowledge using both implicit and explicit behavioural measures. TLE patients showed impairments on two explicit measures of SL alongside intact performance on an implicit measure of SL. These results suggest that the hippocampus may only be necessary for the explicit expression, but not the initial acquisition or implicit expression, of statistical knowledge.

Homeostatic mechanisms adjust synaptic strengths to regulate neuronal activity across wake-sleep cycles. Although sleep supports memory consolidation, limited research has explored how sleep-induced homeostatic changes influence memory outcomes in humans. The EEG-derived aperiodic slope (1/f) could be a candidate measure of homeostatic memory processes through its reflection of neural excitation-inhibition balance. In this study, 27 participants learned object-word pairs, and completed an immediate recognition test before either a nap or equivalent wakeful period. Resting-state EEG was recorded, both before and after learning and the interval, to derive changes in aperiodic slope values. A delayed recognition test then assessed whether changes in the aperiodic slope (i.e., homeostatic activity) across learning and the interval predicted memory accuracy and N400 amplitude, an index of stimulus expectancy and recognition. Our study found evidence to suggest homeostatic renormalisation, for the nap condition only, indicated by a shift towards inhibition across sleep which was inversely related to the slope change across learning. Although the aperiodic slope change across the nap and wake intervals did not predict delayed memory accuracy, a shift towards inhibition during learning was beneficial for memory accuracy, only in the nap condition. Similarly, a shift towards inhibition across learning, followed by a shift towards excitation in the nap condition, predicted reduced N400 amplitudes. This suggests that homeostatic renormalisation across the nap influenced model updating and stimulus expectancy. This study provides evidence for a link between synaptic homeostatic processes and memory consolidation, emphasising the importance of encoding-related aperiodic activity in this relationship.

Schema memory refers to generalized knowledge extracted from multiple related episodes. According to systems consolidation theory, such representations emerge during sleep through the transformation of hippocampus-dependent episodic memories into neocortical schema representations. Whether this process requires mature episodic memory expression during early development remains unclear. Here, we examined schema formation in infant rats with an immature hippocampus. At postnatal day (PD) 25, pups (n=24) were tested in an adapted object-place paradigm enabling abstraction of a spatial regularity across eight consecutive episodes. Following encoding, pups either slept or remained awake for two hours, and schema memory was tested 22 hours later. Control groups were exposed to pseudorandomized object configurations. Schema memory was expressed only after exposure to spatial regularities and only when sleep followed encoding. To directly assess episodic memory under comparable conditions, an additional group of pups (n=12) was tested in a standard single-episode object-place recognition (OPR) task with post-encoding sleep. At a 4-hours test, these pups did not show episodic object-place memory. These findings indicate that sleep supports schema memory formation during early life under conditions in which the expression of robust single-episode memory is not yet evident, suggesting that schema abstraction in infancy does not depend on fully developed hippocampal episodic representations.

How does the brain integrate experiences that are separated in time? The present study addressed this question using sensory preconditioning protocols in rats. In these protocols, rats integrate an A-B association (e.g., tone-light) formed in stage 1 with a B-shock association (e.g., light-shock) formed in stage 2 to generate fear responses (freezing) when tested with A alone in stage 3. Here we show that the mechanism of integration depends on the number, order and timing of events across the two stages of training. When the events are novel (low number of exposures) and the interval between stages 1 and 2 is short (24 hours), the A-B and B-shock associations are integrated through formation of a mediated A-shock association during stage 2. By contrast, when the events are more familiar (greater number of exposures), ordered in a particular way, and the interval between stages 1 and 2 is long (14-days), the A-B and B-shock associations are integrated through their chaining at the time of testing with A alone. Thus, number, order and time determine how distinct experiences are integrated in the brain. These findings are discussed with respect to theories of integration and information processing in the medial temporal lobe.

Propofol-induced general anesthesia and natural sleep are both associated with GABA-A-ergic inhibition and slow-wave activity. Whereas sleep actively supports memory consolidation, consolidation may be disrupted during anesthesia. Here, we compared EEG and memory data from 19 participants undergoing surgery under propofol-induced anesthesia with data from 17 participants taking a nap. In both groups, participants completed a hippocampus-dependent spatial memory task (Virtual Water Maze) and a procedural memory task (Mirror Tracing) before (pre) and after (post) an interval filled with either anesthesia or sleep. Performance declined from pre to post in the propofol group for both tasks, whereas it remained stable in the sleep group. Slow oscillations (SO) occurred during both non-REM sleep and propofol-induced anesthesia. However, only during non-REM sleep did SOs show increased spindle activity during the SO upstate. Together, these findings suggest that propofol anesthesia disrupts memory consolidation, most likely because SOs under anesthesia lack the spindle coupling that mediates the hippocampal-neocortical information transfer underlying systems memory consolidation.

Animals detect and evaluate signs of danger and safety in their environment to ensure survival, yet the neural mechanisms that distinguish safety learning from other forms of conditioned inhibition, remain poorly understood. Here, we directly compared fear and safety learning in male rats. Fear conditioned rats showed high freezing to the tone and the conditioning context, whereas safety conditioned rats showed significant tone-specific reduction in freezing. This safety cue could also generalize to a novel, previously unassociated threat context leading to suppressed freezing when presented demonstrating that inhibitory actions of safety cues are not tied to its original training environment but can modify fear expression across settings. Fear and safety learning also produced unique patterns of neuronal activation and glutamatergic receptor expression in the medial prefrontal cortex (mPFC), basolateral amygdala (BLA), and central amygdala (CeA), as measured by c-Fos immunohistochemistry and Western blotting. Fear conditioning induced greater Fos expression in the BLA and CeA, as well as elevated amygdalar NMDA receptor (GluN1) levels, whereas safety learning increased amygdalar PSD-95 and AMPA receptor (GluA1) expression. Both safety and fear learning increased mPFC Fos expression without affecting glutamatergic receptors levels. Finally, safety conditioning was associated with lower tone-evoked freezing than fear conditioned rats across early extinction sessions and was accompanied by distinct patterns of prefrontal and amygdala activation across extinction. Together, these findings suggest that safety learning engages neural and behavioral mechanisms distinct from fear learning and extinction, while modifying amygdala-prefrontal circuits towards more rapid fear suppression.

Self-directed learning allows learners to actively control their learning experience and has been shown to enhance memory compared with matched yoked learning. However, it remains unclear when and how active control modulates memory-related neural activity during learning and retrieval. We recorded electroencephalography (EEG) while participants encoded objects under active and yoked learning conditions and again during a delayed recognition test approximately 24 h later. We examined event-related potential (ERP) activity across earlier processing windows, including pre-stimulus slow potentials and early N2 activity, and later processing windows, including P300, late slow-wave, and post-stimulus slow-potential activity. We also examined encoding-retrieval similarity (ERS) between neural patterns during encoding and retrieval. Behaviorally, active control improved delayed recognition, with the advantage selectively expressed in detailed recognition. In the ERP analyses, earlier processing windows showed memory-related effects, with pre-stimulus slow-potential and N2 activity differentiating subsequently remembered from forgotten items, but were not modulated by active control. By contrast, active control modulated later memory-related ERP activity, with remembered-forgotten differences expressed during late stimulus-related and immediate post-stimulus processing only in the active condition. ERS showed a similar active-control modulation: memory-related encoding-retrieval pattern similarity was evident under active learning, but not under yoked learning, with this effect involving relatively late encoding and retrieval windows. Together, these findings support a constructive-processing account, suggesting that memory formation under active control depends more strongly on rich, detailed encoding representations that can be reinstated during retrieval.

Working memory has been considered a delay-dependent retention system, but variability in delay duration across species and tasks suggests that task-intrinsic factors may also contribute. Here, we investigated the effects of delay duration (75 s vs. 150 s) and task distance (0 m vs. 2 m) on working memory using a T-maze delayed alternation task with a movable home-cage apparatus in rats. At the 150-s delay, accuracy was 9% lower at 0 m than at 2 m (75% vs. 84%), with a similar numerical tendency observed at the 75-s delay (4% lower). A two-way repeated measures ANOVA revealed significant main effects of both task distance and delay duration, with no significant interaction (p = 0.217). Post hoc pairwise comparisons indicated that accuracy in the 0-m condition was significantly lower at 150 s than at 75 s (adjusted p = 0.038). At the 150-s delay, accuracy was also significantly lower in the 0-m condition than in the 2-m condition (adjusted p = 0.019). These results suggest that working memory retention is influenced not only by temporal constraints but also by task-intrinsic factors such as task distance, with the observed effects appearing independent and consistent with a two-factor framework.

The formation of long-term memory during sleep depends on the reactivation and redistribution of recently acquired mnemonic information during non-rapid eye movement (NREM) sleep. Animal studies suggest that hippocampal memory replay during slow-wave sleep is coordinated through the interaction of sharp-wave ripples, thalamocortical sleep spindles, and neocortical slow oscillations (SOs). However, direct evidence for the contribution of hippocampal network dynamics to sleep-dependent memory consolidation in humans remains limited. Here, we investigated sleep-dependent memory consolidation in patients (n=13) with transient global amnesia (TGA), a clinical syndrome associated with focal and transient lesions of the hippocampal CA1 region. Patients completed a verbal paired-associative learning task followed by nocturnal polysomnography and subsequent memory retrieval during the acute phase of TGA (acute condition) and again after clinical recovery (follow-up condition). Overnight memory consolidation was significantly impaired during the acute phase compared with the follow-up session. NREM EEG theta power (4-8 Hz) was reduced during the acute phase of TGA. Importantly, increases in theta power from the acute to the follow-up session predicted corresponding improvements in memory consolidation within individuals. In contrast, established NREM markers of sleep-dependent memory consolidation, including sleep spindle density, SO density, and SO-spindle coupling, did not differ between the acute and follow-up conditions. These findings suggest that transient hippocampal CA1 dysfunction disrupts sleep-related hippocampal network dynamics reflected in reduced NREM theta activity, which in turn is associated with impaired memory consolidation. Sleep-related theta oscillations may therefore represent a functional marker of hippocampal network integrity during sleep-dependent memory consolidation in humans.

Sleep supports the consolidation of newly acquired information, however its role in the formation of self-beliefs has not yet been examined. Here, we investigated whether sleep facilitates the retention, stabilization, revision and long-term maintenance of newly formed ability beliefs. Using a Sleep vs. Wake between-subjects design (N=54), participants completed the Learning Of Own Performance (LOOP) task, which allowed them to form new positive and negative ability self-beliefs based on mocked feedback at a first session, and to revise them when encountering contradictory feedback at a second session. Belief formation was followed by either a sleep or wake retention interval. Belief states were tested at four time points: immediately after belief formation, after the 12-h retention interval, following the revision phase and after three weeks. Participants successfully formed and revised self-beliefs using the LOOP task. Compared with wakefulness, sleep following belief formation did not affect belief retention across the 12-h interval, nor did it stabilize beliefs against their revision. However, after three weeks, participants who slept after belief formation showed a shift towards more positivity for the initially formed low ability self-beliefs. Contrary to our hypotheses, sleep did not enhance short-term retention or stabilization of newly formed self-beliefs. However, the more positively recalled ability self-belief associated with the initially low-performance condition suggest that sleep may facilitate a positive long-term shift.

Sleep is proposed to have a beneficial effect on the consolidation of memories and gist abstraction in adults. For children, gist abstraction is of special relevance to transform new information from social and emotional contexts into stable representations. This study investigated the effect of sleep on emotional and social recognition and gist abstraction on N=34 typically developing children assessed in a sleep and a wake condition. In an emotional memory task, reward-associated stimuli were presented, while a social memory task used face-stimuli to implement social acceptance or rejection from peers. Both paradigms relied on a hidden rule to be abstracted. In general, children were able to remember emotional and social stimuli and to abstract gist information. With respect to sleep, we found a beneficial effect of sleep on the recognition of emotional stimuli but no sleep-dependent enhancement for either social recognition or emotional or social gist abstraction. Overall, our results indicate, that sleep-dependent recognition might depend on the type of memory task. Furthermore, nighttime sleep as compared to daytime wakefulness has no differential influence on gist abstraction in children as assessed in our paradigms, contrasting previous results found in adults.

The cerebellar nuclei (CN) has demonstrated its influence on cognitive behavior via the cerebello-cortico circuit, yet the role of CN critical period mechanisms and how they may influence cognitive behavior, such as parvalbumin (PV) expressing interneurons enwrapped by perineuronal nets (PNNs), is still unclear. Therefore, we investigated the role of the lateral CN (LCN) PV cell calcium activity while animals performed a visual discrimination touchscreen cognitive task. All animals received the PV cell calcium indicator GCaMP6f at postnatal day 21 (P21). We targeted the LCN critical period by manipulating neural activity in male mice using the inhibitory Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) from postnatal day 21 to 35 or by injecting an Hapln1-AAV vector to selectively target LCN PNN development. After animals completed the visual discrimination task, cerebellar tissue was collected for viral recovery and antibody staining for PNN components, Hapln1 and aggrecan. Results revealed DREADD animals showed improved reversal learning, an increase in calcium response to learning-related activity and altered PNN expression (Hapln1 and aggrecan). Hapln1 treated animals displayed a decrease in final day acquisition performance, lower reversal performance compared to DREADD groups, a decrease in reversal calcium learning-related activity, and an increase in PNN expression (Hapln1). Together, these data provide further evidence of LCN mechanisms associated with learning as well as the importance of understanding region-specific critical periods of plasticity.

Background: Temporal lobe epilepsy surgery (TLS) is an effective treatment for drug-resistant focal epilepsy but is often associated with cognitive decline. A key unresolved question is how to distinguish average from severe memory loss and how these levels differentially affect everyday life. We addressed this question applying patient-derived norms of memory decline and conducting qualitative inter-views with patients experiencing expected or unexpectedly severe memory loss. Methods: Regression-based normative change criteria for postoperative verbal memory loss were derived from a single-center cohort of 806 patients. Two matched groups of four patients each were selected from the severe memory de-cline (SMD; below the 5th percentile) and average memory decline (AMD; 20th - 75th percentile) ranges. In-depth, semi-structured narrative interviews were analyzed using qualitative content analysis with a combined deductive-inductive ap-proach. Results: AMD narratives emphasized recovery, with surgery integrated into a con-tinuing sense of self. In contrast, SMD descriptions focused on persistent symp-toms, continued treatment, and illness despite meaningful seizure reduction. Pa-tients with SMD also reported limited information, insufficient psychological preparation or postoperative cognitive rehabilitation. Conclusions: Whereas AMD was generally manageable and successfully integrat-ed into everyday life, SMD disrupted identity, autonomy, and expected life trajecto-ries. Current surgical pathways appear to address these cognitive sequelae insufficiently. Improved expectation management, together with structured preoperative counseling and postoperative rehabilitation, may facilitate adaption to memory de-cline and improve long-term functioning and quality of life after surgery.

We recently reported that rats performed better at a task distance of 2 m than at 0 m in a T-maze delayed alternation paradigm using a movable home cage in the longer-delay condition (Takita & Ichitani, 2026). We simultaneously recorded local field potentials from the bilateral prefrontal cortex, intermediate hippocampus, and ventral hippocampus. Across task epochs, coherence and two cross-frequency measures (phase-locking value and modulation index [MI]) revealed differences between correct and error trials in prefrontal interactions with hippocampal subregions. Among these measures, only MI was affected by task distance during the pre-task delay epoch. MI was highest in 2-m error trials and lowest in correct trials. In 0-m error trials, MI transiently increased during arm entry to levels comparable to those in 2-m error trials before declining toward the levels observed in correct trials during the later post-task delay. These MI dynamics appeared to be consistent with distance-dependent differences in behavioral performance. In addition, normalized Correct-Error Indices calculated for each electrophysiological measure revealed differential contributions of prefrontal coupling with the intermediate and ventral hippocampus across task distances. These findings suggest the existence of distinct near and far working memory states underlying distance-dependent behavioral differences, with distinct yet complementary contributions of the intermediate and ventral hippocampus to prefrontal interactions.

The integration of separate memories sharing overlapping elements allows for inferring relationships between events that have never been experienced together. Recent findings indicate that stress impairs this process of mnemonic inference, which may have important implications for stress-related psychopathologies. However, the mechanisms underlying such impairments remain largely unknown. To elucidate the neuroendocrine mechanisms by which stress affects mnemonic inference, mice were first trained on two sets of auditory visual cue associations. Afterwards, one of the visual cues was paired with reward. Mnemonic inference was probed by examining reward seeking behavior in response to the auditory cues alone. Control mice successfully inferred the auditory cue outcome association, selectively seeking reward in response to the auditory cue associated with the rewarded visual cue. In contrast, systemic administration of the stress hormone corticosterone before testing impaired inference accuracy, leading mice to seek reward to both auditory cues. Corticosterone administration was accompanied by increased noradrenergic activity, and stimulation of noradrenergic signaling with yohimbine similarly disrupted inference accuracy. Conversely, the beta adrenoceptor antagonist propranolol prevented the corticosterone induced impairment, indicating that corticosterone effects depend on concurrent noradrenergic activation. At the neural level, the corticosterone induced mnemonic inference impairment was associated with enhanced GABAergic inhibition of pyramidal neurons in the hippocampal CA3 region. Furthermore, hippocampal administration of the GABAA receptor antagonist bicuculline prevented the corticosterone induced impairment in mnemonic inference. Together, these findings identify a glucocorticoid noradrenergic mechanism that disrupts mnemonic inference through enhanced GABAergic inhibition in hippocampal CA3, providing an account of how stress hormones impair inferential memory.

Targeted memory reactivation (TMR) during sleep can benefit recently acquired memories, but whether it can also influence memories after an initial period of consolidation remains unclear. Here, we tested whether auditory reactivation during non-rapid eye movement (NREM) sleep could strengthen declarative memories learned 24 h earlier. Twenty-six healthy young adults learned 30 sound word associations and returned the following day for a 90 min nap. During NREM sleep, participants in the Reactivation group received incomplete reminders consisting of the learned sound followed by the first syllable of the associated word, whereas the No-Reactivation group slept under the same conditions without memory related cues. Participants who received reminders showed significantly less forgetting, despite comparable training performance and sleep macroarchitecture. Across NREM sleep, reactivation was associated with greater slow oscillation and delta power, more slow oscillations and fast spindles, and greater slow oscillation spindle cooccurrence. The memory benefit remained significant after adjusting for NREM physiological measures and in sensitivity analyses restricted to overlapping physiological ranges between groups. Cue locked analyses revealed significant responses in the slow oscillation, delta, theta, and fast-spindle ranges, but the magnitude of these responses was not associated with memory change. These findings show that TMR during NREM sleep can benefit declarative memories after a 24 h consolidation interval and suggest that its effects extend beyond the immediate post-learning sleep period.

Hippocampal place cells encode spatial information within a theta-organized temporal framework paced by the medial septum (MS). Lesions or inactivation of the MS impair spatial learning and disrupt hippocampal theta rhythmicity, long-term potentiation, and plasticity-related gene expression, while often sparing spatially selective firing of CA1 neurons (but not CA3 neurons). Although many rodent studies argue against classical systems consolidation by showing persistent hippocampal dependence of spatial memories, other work has suggested that training structure, spaced vs. massed trials, can influence this dependence. To investigate this possibility, we used DREADD-based, reversible, inhibition of MS GABAergic neurons, some of which are known to project to hippocampus. DREADD activation reduced hippocampal theta power and spatial information encoded by hippocampal neurons while largely preserving overall neuronal firing. We then examined the effect of inhibition of medial septal GABAergic neurons on learning the correct goal arm in an 8-arm maze when the correct arm was randomly changed each day. On each day, the mice were given two forced-choice trials indicating the correct arm and then 5 free-choice trials (without correction) and were always started from an opaque cylinder in the maze center, in a random orientation, to eliminate possible use of a simple response strategy. When the correct goal arm varied randomly daily, MS cell inhibition severely and repeatedly impaired acquisition. In contrast, when the correct goal arm was subsequently fixed across days, performance was initially impaired but became resistant to DREADD activation over time. Once performance reached asymptote, the goal arm was switched to a new (random) position. In this case, learning was no longer impaired by DREADD activation. This generalization suggests that repeated fixed-goal training in the same environment induces a broader reorganization of the neural systems supporting spatial behaviour. One possibility is that mice develop a septal-independent task-solving strategy that supports both retrieval of established goal locations and acquisition of new ones within a stable environment. This transition could reflect the gradual adoption of a non-spatial strategy such as visual pattern recognition, or the use of a directional cue. Moving the most salient distal cue in the environment (a single room light) produced a substantial change in the visual configurations seen from the arm entry points, and disrupted performance; however, it did not produce a consistent directional shift relative to the cue, suggesting that the light contributed to an integrated visuo-spatial representation rather than serving as the reference frame origin. We conclude that the mice switched from a hippocampus/MS-dependent spatial strategy to a non-hippocampus-dependent visual pattern matching solution.

The vestibular system has been implicated in several aspects of self-representation, including bodily self-location, yet its role in episodic source and reality monitoring remains unclear. Moreover, symptoms of depersonalisation and derealisation (DPDR) have been associated with both vestibular dysfunction and altered source and reality monitoring. We tested whether noisy galvanic vestibular stimulation (nGVS) modulates source and reality monitoring during a word-encoding paradigm and whether this increased symptoms of DPDR. Sixty young adults (N = 30 active nGVS, N = 30 sham) encoded words that varied by context (spoken vs. imagined), agentic source (self vs. other), and valence (positive vs. threat) before completing source/reality judgments. Active nGVS reduced overall accuracy relative to sham on both reality and source monitoring. Across conditions, self-referential items were remembered with greater sensitivity compared to other-referential items, and spoken items were recalled with greater sensitivity than imagined items. We additionally show an interaction effect whereby active nGVS reduced accuracy specifically for imagined and threat-valenced items. Trait DPDR did not moderate the effects of stimulation, although higher trait DPDR was associated with a more liberal reality-monitoring response criterion. Results indicate that transient vestibular perturbation via nGVS can impair source monitoring for internalised and threatening stimuli and impairs cognitive distinctions between internally and externally generated events in general, supporting a role for vestibular input in maintaining self-other and reality boundaries in episodic memory.

It is estimated that approximately fifty percent of the population will encounter at least one traumatic event during their lifetime; however, only six percent develop Posttraumatic Stress Disorder (PTSD), a trauma-related disorder characterized by persistent alterations in affect and cognition, including an exaggerated fear response. It is well established that females (9.7%) are more than twice as likely as males (3.6%) to be diagnosed with PTSD. Nevertheless, a significant challenge remains in understanding how the severity of traumas experienced in childhood versus adulthood influences PTSD development across sexes. To address this challenge effectively, the adoption of preclinical animal models that accurately reflect these key characteristics is crucial. The Stress Enhanced Fear Learning (SEFL) paradigm in rodents encapsulates some of these complexities associated with PTSD, such as persistent fear sensitization following exposure to acute trauma. This study investigates how stress severity and developmental timing affect the long-term maintenance of SEFL in male and female rats. Juvenile and adult rats were initially subjected to no stress (control, context only), low stress (1 footshock), moderate stress (3 footshocks), or high stress (15 footshocks), followed by an extinction session either one day (recent) or sixty days (remote) later. Subsequently, to evaluate SEFL in a new context, all subjects received a single footshock and were tested the following day. Shortly after stress induction, all groups displayed SEFL. Although the effects persisted for sixty days in adult males and juvenile females, even at the lowest stress level, they were significantly reduced in juvenile males and adult females. These findings offer novel insights into sex-related differences in the persistence of SEFL and introduce new considerations regarding how the timing of developmental stressors influences future threat encoding and fear responses.

Source and reality monitoring enable individuals to distinguish the origins of remembered information, including whether information was self- or other-generated and whether it was perceived or imagined. Although the dorsolateral prefrontal cortex (dlPFC) and temporoparietal junction (TPJ) have been implicated in these processes, their independent causal contributions remain unclear. We investigated whether focal transcranial direct current stimulation (f-tDCS) of the left dlPFC and left TPJ differentially modulates source and reality monitoring. One hundred participants were randomly assigned to receive anodal or sham stimulation of the left dlPFC or TPJ before completing an episodic memory task manipulating agent (self, experimenter), context (spoken, imagined), and emotional valence (positive, negative). Discrimination sensitivity (d') and response criterion (c) were examined separately. For source monitoring, stimulation interacted with context and cortical region: anodal dlPFC stimulation was associated with a greater spoken-imagined difference in self-experimenter discrimination than sham stimulation, whereas no equivalent context-dependent effect emerged following TPJ stimulation. For reality monitoring, stimulation effects also differed by cortical target, with reduced spoken-imagined discrimination following anodal relative to sham TPJ stimulation and no significant effect of dlPFC stimulation. These effects were not accompanied by corresponding stimulation effects on response criterion. Independent of stimulation, source discrimination was substantially greater for spoken than imagined information, while reality-monitoring sensitivity was enhanced for self-generated relative to experimenter-generated negative information. Together, these findings provide evidence that the dlPFC and TPJ make dissociable contributions to source and reality monitoring, while highlighting the importance of contextual and affective features in determining how the origins of memories are evaluated.