Discrimination Deficits Research Articles

Visual self-face and self-body recognition in a left-brain-damaged prosopagnosic patient.

The present case study describes the patient N.G., who reported prosopagnosia along with difficulty in recognising herself in the mirror following a left-sided temporo-occipital hemispheric stroke. The neuropsychological and experimental investigation revealed only a mild form of apperceptive prosopagnosia, without visual agnosia, primarily caused by an impaired visual processing of face-parts and body parts but not of full faces. Emotional expressions did not modulate her face processing. On the other hand, N.G. showed a marked impairment of visual self-recognition, as assessed with visual matching-to-sample tasks, both at the level of body-part and face-part processing and at a full-face level, featured by a deficit in the perceptual discrimination of her own face and body, as compared to the others' face and body. N.G.'s lesion mapping showed damage to the left inferior occipito-temporal cortex, affecting the inferior occipital gyrus and compromising long-range connections between the occipital/temporo-occipital areas and the anterior fronto-temporal areas. Overall, the present case report documents that visual processing of the person's own face may be selectively compromised by a left-sided hemispheric lesion disconnecting extra-striate body- and face-selective visual areas to self-representation regions. Moreover, others' (full) face processing may be preserved, as compared with the impaired ability to discriminate others' body and face parts.

Amyloid-β deposition in basal frontotemporal cortex is associated with selective disruption of temporal mnemonic discrimination.

Cerebral amyloid-beta (Aβ) accumulation, a hallmark pathology of Alzheimer's disease (AD), precedes clinical impairment by two to three decades. However, it is unclear whether Aβ contributes to subtle memory deficits observed during the preclinical stage. The heterogenous emergence of Aβ deposition may selectively impact certain memory domains, which rely on distinct underlying neural circuits. In this context, we tested whether specific domains of mnemonic discrimination, a neural computation essential for episodic memory, exhibit specific deficits related to early Aβ deposition. We tested 108 cognitively unimpaired human older adults (66% female) who underwent 18F-florbetapir positron emission tomography (Aβ-PET), and a control group of 35 young adults, on a suite of mnemonic discrimination tasks taxing object, spatial, and temporal domains. We hypothesized that Aβ pathology would be selectively associated with temporal discrimination performance due to Aβ's propensity to accumulate in the basal frontotemporal cortex, which supports temporal processing. Consistent with this hypothesis, we found a dissociation in which generalized age-related deficits were found for object and spatial mnemonic discrimination, while Aβ-PET levels were selectively associated with deficits in temporal mnemonic discrimination. Further, we found that higher Aβ-PET levels in medial orbitofrontal and inferior temporal cortex, regions supporting temporal processing, were associated with greater temporal mnemonic discrimination deficits, pointing to the selective vulnerability of circuits related to temporal processing early in AD progression. These results suggest that Aβ accumulation within basal frontotemporal regions may disrupt temporal mnemonic discrimination in preclinical AD, and may serve as a sensitive behavioral biomarker of emerging AD progression.

Deciphering the impairment of perimenopausal insomnia on visual search from a neurocognitive processing perspective.

Perimenopausal insomnia (PMI) is associated with observable performance impairments in visual search tasks. This study examines how various cognitive processing stages contribute to search performance delays in PMI compared to healthy controls (HCs). We recruited 76 participants diagnosed with PMI and 63 HCs. Event-related potentials (ERPs) were recorded as participants engaged in a visual search task, reporting the orientation of a color popout target within an array of ellipses. We analyzed group differences in behavioral performance and ERP components across cognitive processing stages. Compared to HCs, PMI patients exhibited behavioral response delays, although accuracy was not different between groups. Electrophysiological analyses revealed group differences across several ERP components. Firstly, the N1 component's amplitude increased bilaterally, suggesting enhanced visual sensory processing. Secondly, a slower and smaller N2pc indicated reduced attentional orienting. Thirdly, a decreased SPCN amplitude pointed to deficits in target discrimination. Fourthly, an increased amplitude of the stimulus-locked LRP, with unchanged latency, suggested heightened neural inputs for maintaining motor initiation speed. Fifthly, prolonged response-locked LRP latency indicated slower motor execution. Finally, these changes in ERP components, along with significant correlations between LRP components and insomnia symptoms, suggest potential neural biomarkers for PMI. Our findings provide high-temporal-resolution insights into the neurocognitive disruptions associated with PMI, highlighting how sleep disturbances affect cognitive processing in visual tasks. These insights enhance our understanding of PMI and contribute to discussions on neural mechanisms driving behavioral performance in various conditions.

Effect of Pitch Discrimination-Based Rehabilitation on Diagnostic Indices of Dichotic Digit Test, monaural Selective Auditory Attention Test, and Pitch Pattern Test in Children Suspected of Auditory Processing Disorder with Pitch Discrimination Deficits

Effect of Pitch Discrimination-Based Rehabilitation on Diagnostic Indices of Dichotic Digit Test, monaural Selective Auditory Attention Test, and Pitch Pattern Test in Children Suspected of Auditory Processing Disorder with Pitch Discrimination Deficits

Digital cognitive assessments as low-burden markers for predicting future cognitive decline and tau accumulation across the Alzheimer's spectrum.

Digital cognitive assessments, particularly those that can be done at home, present as low burden biomarkers for participants and patients alike, but their effectiveness in diagnosis of Alzheimer's or predicting its trajectory is still unclear. Here, we assessed what utility or added value these digital cognitive assessments provide for identifying those at high risk for cognitive decline. We analyzed >500 ADNI participants who underwent a brief digital cognitive assessment and Aβ/tau PET scans, examining their ability to distinguish cognitive status and predict cognitive decline. Performance on the digital cognitive assessment were superior to both cortical Aβ and entorhinal tau in detecting mild cognitive impairment and future cognitive decline, with mnemonic discrimination deficits emerging as the most critical measure for predicting decline and future tau accumulation. Digital assessments are effective in identifying at-risk individuals, supporting their utility as low-burden tools for early Alzheimer's detection and monitoring.

A maturational frequency discrimination deficit may explain developmental language disorder.

Auditory perceptual deficits are widely observed among children with developmental language disorder (DLD). Yet, the nature of these deficits and the extent to which they explain speech and language problems remain controversial. In this study, we hypothesize that disruption to the maturation of the basilar membrane may impede the optimization of the auditory pathway from brainstem to cortex, curtailing high-resolution frequency sensitivity and the efficient spectral decomposition and encoding of natural speech. A series of computational simulations involving deep convolutional neural networks that were trained to encode, recognize, and retrieve naturalistic speech are presented to demonstrate the strength of this account. These neural networks were built on top of biologically truthful inner ear models developed to model human cochlea function, which-in the key innovation of the present study-were scheduled to mature at different rates over time. Delaying cochlea maturation qualitatively replicated the linguistic behavior and neurophysiology of individuals with language learning difficulties in a number of ways, resulting in (a) delayed language acquisition profiles, (b) lower spoken word recognition accuracy, (c) word finding and retrieval difficulties, (d) "fuzzy" and intersecting speech encodings and signatures of immature neural optimization, and (e) emergent working memory and attentional deficits. These simulations illustrate many negative cascading effects that a primary maturational frequency discrimination deficit may have on early language development and generate precise and testable hypotheses for future research into the nature and cost of auditory processing deficits in children with language learning difficulties. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Maladaptation of dentate gyrus mossy cells mediates contextual discrimination deficit after traumatic stress

Fear overgeneralization is a maladaptive response to traumatic stress that is associated with the inability to discriminate between threat and safety contexts, a hallmark feature of post-traumatic stress disorder (PTSD). However, the neural mechanisms underlying this deficit remain unclear. Here, we show that traumatic stress exposure impairs contextual discrimination between threat and safety contexts in the learned helplessness (LH) model. Mossy cells (MCs) in the dorsal hippocampus are suppressed in response to traumatic stress. Bidirectional manipulation of MC activity in the LH model reveals that MC inhibition is causally linked to impaired contextual discrimination. Mechanistically, MC inhibition increases the number of active granule cells in a given context, significantly overlapping context-specific ensembles. Our study demonstrates that maladaptive inhibition of MCs after traumatic stress is a substantial mechanism underlying fear overgeneralization with contextual discrimination deficit, suggesting a potential therapeutic target for cognitive symptoms of PTSD.

Social Interaction in Adolescent Rats with Neonatal Ethanol Exposure: Impact of Sex and CE-123, a Selective Dopamine Reuptake Inhibitor.

Children with fetal alcohol spectrum disorders (FASDs) demonstrate deficits in social functioning that contribute to early withdrawal from school and delinquency, as well as the development of anxiety and depression. Dopamine is involved in reward, motivation, and social behavior. Thus, we evaluated whether neonatal ethanol exposure (in an animal model of FASDs) has an impact on social recognition memory using the three-chamber social novelty discrimination test during early and middle adolescence in male and female rats, and whether the modafinil analog, the novel atypical dopamine reuptake inhibitor CE-123, can modify this effect. Our study shows that male and female rats neonatally exposed to ethanol exhibited sex- and age-dependent deficits in social novelty discrimination in early (male) and middle (female) adolescence. These deficits were specific to the social domain and not simply due to more general deficits in learning and memory because these animals did not exhibit changes in short-term recognition memory in the novel object recognition task. Furthermore, early-adolescent male rats that were neonatally exposed to ethanol did not show changes in the anxiety index but demonstrated an increase in locomotor activity. Chronic treatment with CE-123, however, prevented the appearance of these social deficits. In the hippocampus of adolescent rats, CE-123 increased BDNF and decreased its signal transduction TrkB receptor expression level in ethanol-exposed animals during development, suggesting an increase in neuroplasticity. Thus, selective dopamine reuptake inhibitors, such as CE-123, represent interesting drug candidates for the treatment of deficits in social behavior in adolescent individuals with FASDs.

Contribution of internal noise and calculation efficiency to face discrimination deficits in older adults

Classification images (CIs) measured in a face discrimination task differ significantly between older and younger observers. These age differences are consistent with the hypothesis that older adults sample diagnostic face information less efficiently, or have higher levels of internal noise, compared to younger adults. The current experiments assessed the relative contributions of efficiency and internal noise to age differences in face discrimination using the external noise masking and double-pass response consistency paradigms. Experiment 1 measured discrimination thresholds for faces embedded in several levels of static white noise, and the resulting threshold-vs.-noise curves were used to estimate calculation efficiency and equivalent input noise: older observers had lower efficiency and higher equivalent input noise than younger observers. Experiment 2 presented observers with two identical sequences of faces embedded in static white noise to measure the association between response accuracy and response consistency and estimate the internal:external (i/e) noise ratio for each observer. We found that i/e noise ratios did not differ significantly between groups. These results suggest that age differences in face discrimination are due to differences in calculation efficiency and additive internal noise, but not to age differences in multiplicative internal noise.

Clinical correlates of pareidolias and color discrimination deficits in idiopathic REM sleep behavior disorder and Parkinson's disease.

Visuoperceptual dysfunction is common in Parkinson's disease (PD) and is also reported in its prodromal phase, isolated REM sleep behavior disorder (iRBD). We aimed to investigate color discrimination ability and complex visual illusions known as pareidolias in patients with iRBD and PD compared to healthy controls, and their associating clinical factors. 46 iRBD, 43 PD, and 64 healthy controls performed the Farnsworth-Munsell 100 hue test and noise pareidolia tests. Any relationship between those two visual functions and associations with prodromal motor and non-motor manifestations were evaluated, including MDS-UPDRS part I to III, Cross-Cultural Smell Identification Test, sleep questionnaires, and comprehensive neuropsychological assessment. iRBD and PD patients both performed worse on the Farnsworth-Munsell 100 hue test and had greater number of pareidolias compared to healthy controls. No correlations were found between the extent of impaired color discrimination and pareidolia scores in either group. In iRBD patients, pareidolias were associated with frontal executive dysfunction, while impaired color discrimination was associated with visuospatial dysfunction, hyposmia, and higher MDS-UPDRS-III scores. Pareidolias in PD patients correlated with worse global cognition, whereas color discrimination deficits were associated with frontal executive dysfunction. Color discrimination deficits and pareidolias are frequent but does not correlate with each other from prodromal to clinically established stage of PD. The different pattern of clinical associates with the two visual symptoms suggests that evaluation of both color and pareidolias may aid in revealing the course of neurodegeneration in iRBD and PD patients.

Pro-social and pro-cognitive effects of LIT-001, a novel oxytocin receptor agonist in a neurodevelopmental model of schizophrenia

Social and cognitive dysfunctions are the most persistent symptoms of schizophrenia. Since oxytocin (OXT) is known to play a role in social functions and modulates cognitive processes, we investigated the effects of a novel, nonpeptide, selective OXT receptor agonist, LIT-001, in a neurodevelopmental model of schizophrenia. Administration of methylazoxymethanol acetate (MAM; 22 mg/kg) on the 17th day of rat pregnancy is known to cause developmental disturbances of the brain, which lead to schizophrenia-like symptomatology in the offspring. Here, we examined the effects of acutely administered LIT-001 (1, 3, and 10 mg/kg) in MAM-exposed males and females on social behaviour, communication and cognition. We report that MAM-treated adult male and female rats displayed reduced social behaviour, ultrasonic communication and novel object recognition test performance. LIT-001 partially reversed these deficits, increasing the total social interaction time and the number of ‘positive’, highly-modulated 50 kHz ultrasonic calls in male rats. The compound ameliorated MAM-induced deficits in object discrimination in both sexes. Present results confirm the pro-social activity of LIT-001 and demonstrate its pro-cognitive effects following acute administration.

Loss of oxytocin receptors in hilar mossy cells impairs social discrimination

Hippocampal oxytocin receptor (OXTR) signaling is crucial for discrimination of social stimuli to guide social recognition, but circuit mechanisms and cell types involved remain incompletely understood. Here, we report a role for OXTR-expressing hilar mossy cells (MCs) of the dentate gyrus in social stimulus discrimination by regulating granule cell (GC) activity. Using a Cre-loxP recombination approach, we found that ablation of Oxtr from MCs impairs discrimination of social, but not object, stimuli in adult male mice. Ablation of MC Oxtr increases spontaneous firing rate of GCs, synaptic excitation to inhibition ratio of MC-to-GC circuit, and GC firing when temporally associated with the lateral perforant path inputs. Using mouse hippocampal slices, we found that bath application of OXTR agonist [Thr4,Gly7]-oxytocin causes membrane depolarization and increases MC firing activity. Optogenetic activation of MC-to-GC circuit ameliorates social discrimination deficit in MC OXTR deficient mice. Together, our results uncover a previously unknown role of MC OXTR signaling for discrimination of social stimuli and delineate a MC-to-GC circuit responsible for social information processing.

'A human face and voice': transgender patient-educator and medical student perspectives on gender-diversity teaching

BackgroundTransgender and gender diverse (TGD) people face many obstacles in accessing health care, including discrimination, institutional bias, and clinician knowledge deficits. We developed a clinical skills and education module on gender-affirming care for pre-clinical medical students, in collaboration with a TGD-led civil society organisation. The module consisted of an educational session followed by preceptor-facilitated small group tutorials, led by TGD patient-educators (n = 22) who used their lived experience to explore medical history-taking and broader issues related to TGD healthcare with students (n = 199). This study aimed to explore the views of students and TGD patient-educators on the structure, delivery and impact of the module.MethodsAnalysis of responses of TGD patient-educators and students to the module (2020 and 2021), in post-intervention surveys using open-ended questions for TGD patient-educators (18 responses from 22 educators) and free text comments as part of a quantitative survey for medical students (89 responses).ResultsResponses from students and patient-educators to the session were highly positive. Students and patient-educators emphasised that the teaching session succeeded through elevating the centrality of shared experience and creating a safe space for learning and teaching. Safety was experienced by patient-educators through the recognition of their own expertise in a medical environment, while students reported a non-judgemental teaching space which allowed them to explore and redress recognised limitations in knowledge and skill. Patient-educators described their motivation to teach as being driven by a sense of responsibility to their community. Preceptor attitudes may function as a barrier to the effectiveness of this teaching, and further attention should be paid to supporting the education of clinical facilitators in TGD health.ConclusionThe experiences of TGD patient-educators and medical students in this study suggest that this model of teaching could serve as a transferable template for TGD health and the inclusion of other historically marginalised groups in medical education.

A detailed examination of pitch discrimination deficits associated with auditory verbal hallucinations in schizophrenia.

Individuals with schizophrenia spectrum disorders (SSD) and a history of experiencing auditory verbal hallucinations (AVH) exhibit poor pitch discrimination relative to those with an SSD but no AVH history. The present study extended this research, asking if a lifetime history, and the current presence, of AVH exacerbated the pitch discrimination challenges that are seen in SSD. Participants completed a pitch discrimination task, where the tones presented differed in pitch by either 2%, 5%, 10%, 25% or 50%. Pitch discrimination accuracy, sensitivity, reaction time (RT) and intra-individual RT variability (IIV) were examined in individuals with SSD and AVHs (AVH+; n=46), or without AVHs (AVH-; n=31), and healthy controls (HC; n=131). Secondary analyses split the AVH+ group into state (i.e., actively experiencing AVH; n=32) and trait hallucinators (i.e., a history of, but not actively experiencing, AVH; n=16). Relative to HC, significantly poorer accuracy and sensitivity was detected in individuals with SSD at 2% and 5% pitch deviants, and in hallucinators at 10%; however, no significant differences in accuracy, sensitivity, RT nor IIV were found between AVH+ and AVH- groups. No differences between state and trait hallucinators were observed. A general SSD deficit drove the current findings. The findings may inform future research into the auditory processing capabilities of AVH+ individuals.

Mnemonic discrimination deficits in multidimensional schizotypy.

Current developmental psychopathology models indicate that schizophrenia can be understood as the most extreme expression of a multidimensional continuum of symptoms and impairment referred to as schizotypy. In nondisordered adults, schizotypy predicts risk for developing schizophrenia-spectrum psychopathology. Schizophrenia is associated with disruptions in detecting subtle differences between objects, which is linked to hippocampal dysfunction. These disruptions have been shown in the Mnemonic Similarity Task (MST) when patients are less likely to reject lures that are similar but not identical to studied objects, and instead mistake them for studied items. This pattern of errors may be a behavioral manifestation of impaired pattern separation, a key episodic memory ability associated with hippocampal integrity and overreliance on pattern completion. We examined whether multidimensional schizotypy is associated with such deficits in nondisordered young adults. Participants (n = 230) were assessed for positive, negative, and disorganized schizotypy and completed the MST and a perceptual discrimination task. MST performance showed that a combination of elevated negative and disorganized schizotypy was associated with decreased rejections of similar lures because they were mistakenly identified as studied items. These deficits were not observed in traditional recognition measures within the same task, nor in perceptual discrimination, suggesting that mnemonic discrimination deficits assessed by MST were selective and did not reflect generalized deficits. These findings extend the results obtained in schizophrenia patients and support a multidimensional model of schizophrenia-spectrum psychopathology.

Impaired mnemonic discrimination in children and adolescents at risk for schizophrenia

People with schizophrenia and their high-risk, first-degree relatives report widespread episodic memory impairments that are purportedly due, at least in part, to failures of mnemonic discrimination. Here, we examined the status of mnemonic discrimination in 36 children and adolescents (aged 11–17 years) with and without familial risk for schizophrenia by employing an object-based recognition task called the Mnemonic Similarity Task (MST). The MST assesses the ability to discriminate between studied images and unstudied images that are either perceptually similar to studied images or completely novel. We compared 16 high-risk, unaffected first-degree relatives of people with schizophrenia, bipolar disorder, and/or schizoaffective disorder to 20 low-risk, control participants. High-risk participants showed worse mnemonic discrimination than low-risk participants, with no difference in recognition memory or perceptual discrimination. Our findings demonstrate that mnemonic discrimination deficits previously observed in people with schizophrenia are also present in their young, high-risk, first-degree relatives.

Interactions between early adversity and the serotonin system determine lifespan immune responses in the hippocampus

Early Life Adversity (ELA) is a major risk factor for psychiatric disorders, but the neurobiological mechanisms that mediate the long-lasting effects of ELA are largely unknown. One candidate process implicated in stress-induced psychiatric disorders that is also increased by ELA, is neuroinflammation. Reducing neuroinflammation may thus be a promising new strategy to rescue the impact of ELA on brain function and mental health. To test this hypothesis, we exposed mice to ELA (limited bedding and nesting material from postnatal day (PND)3 to PND10). We then tested their behavior in a fear discrimination task and collected brains at PND35 (adolescence), PND56 (adulthood), and at 18 months of age (old age). While ELA did not alter adolescent behavior, we find that ELA causes fear discrimination deficits in female mice from adulthood (PND56; n=12, p=0.009) that last into old age (18 months; n=5, p=0.02). At the neurobiological level, we used immunohistochemistry for CD68+/Iba1+ to determine the number of activated microglia. We found a strong and long-lasting increase in the number of activated microglia in the hippocampus of ELA-exposed mice in adulthood and in old age (n=6; p<0.001). We then used a transgenic mouse line to increase hippocampal serotonin (5-HT) by knockdown of the 5-HT1A autoreceptor, and found that adolescent 5-HT1A knockdown can rescue ELA effects on fear discrimination and neuroinflammation later on. Our findings provide new insight into the potential of targeting the 5-HT system to prevent the neuroinflammatory and behavioral deficits resulting from ELA.

Reversal of memory and autism-related phenotypes in Tsc2+/- mice via inhibition of Nlgn1.

Tuberous sclerosis complex (TSC) is a rare monogenic disorder co-diagnosed with high rates of autism and is caused by loss of function mutations in the TSC1 or TSC2 genes. A key pathway hyperactivated in TSC is the mammalian/mechanistic target of rapamycin complex 1 (mTORC1), which regulates cap-dependent mRNA translation. We previously demonstrated that exaggerated cap-dependent translation leads to autism-related phenotypes and increased mRNA translation and protein expression of Neuroligin 1 (Nlgn1) in mice. Inhibition of Nlgn1 expression reversed social behavior deficits in mice with increased cap-dependent translation. Herein, we report elevated translation of Nlgn1 mRNA and an increase in its protein expression. Genetic or pharmacological inhibition of Nlgn1 expression in Tsc2 +/- mice rescued impaired hippocampal mGluR-LTD, contextual discrimination and social behavior deficits in Tsc2 +/- mice, without correcting mTORC1 hyperactivation. Thus, we demonstrate that reduction of Nlgn1 expression in Tsc2 +/- mice is a new therapeutic strategy for TSC and potentially other neurodevelopmental disorders.

Deficits in odor discrimination versus odor identification in patients with schizophrenia and negative correlations with GABAergic and DNA methyltransferase mRNAs in lymphocytes.

People with schizophrenia have been reported to show deficits in tests of olfactory function. DNA methylation and GABAergic input have been implicated in biochemical processes controlling odor in animal studies, but this has not been investigated in human studies. In a study of measures of DNA methylation and GABAergic mRNAs in lymphocytes, we also measured odor identification and discrimination with the Sniffin' Sticks battery in 58 patients with chronic schizophrenia (CSZ) and 48 controls. mRNAs in lymphocytes were assessed by qPCR using TaqManTM probes. Cognition was assessed by the MATRICS battery (Measurement and Treatment Research to Improve Cognition in Schizophrenia) in CSZ and controls, and symptoms in CSZ were assessed by PANSS scale (Positive and Negative Symptom Scale). The relationships of odor deficits with mRNA, cognition, and symptoms were explored by correlation analysis. Variables which significantly differentiated CSZ from controls were explored by logistic regression. Overall, CSZ showed significantly (P≤.001) lower scores on odor discrimination compared to controls, with a moderate effect size, but no difference in odor identification. Deficits in odor discrimination, which has not been standardly assessed in many prior studies, strongly differentiated CSZ from controls. In logistic regression analysis, odor discrimination, but not odor identification, was a significant variable predicting schizophrenia versus control class membership. This is the first study to report relationship between odor deficits and DNA methylation and GABAergic mRNAs in blood cells of human subjects. There were negative correlations of odor identification with DNA methylation enzymes mRNAs and significant negative correlations with odor discrimination and GABAergic mRNAs. Lower odor scores were significantly associated with lower cognitive scores on the MATRICS battery in CSZ but not control subjects. In CSZ, lower odor scores were significantly associated with negative symptom scores, while higher odor identification scores were associated with PANNS Excitement factor. Odor discrimination was a more powerful variable than odor identification in discriminating CSZ from controls and should be used more regularly as an odor measure in studies of schizophrenia. The substantive meaning of the negative correlations of odor discrimination and GABAergic mRNA variables in peripheral lymphocytes of CSZ needs more investigation and comparison with results in neural tissue.

Lesions to Caudomedial Nidopallium Impair Individual Vocal Recognition in the Zebra Finch.

Many social animals can recognize other individuals by their vocalizations. This requires a memory system capable of mapping incoming acoustic signals to one of many known individuals. Using the zebra finch, a social songbird that uses songs and distance calls to communicate individual identity (Elie and Theunissen, 2018), we tested the role of two cortical-like brain regions in a vocal recognition task. We found that the rostral region of the Cadomedial Nidopallium (NCM), a secondary auditory region of the avian pallium, was necessary for maintaining auditory memories for conspecific vocalizations in both male and female birds, whereas HVC (used as a proper name), a premotor areas that gates auditory input into the vocal motor and song learning pathways in male birds (Roberts and Mooney, 2013), was not. Both NCM and HVC have previously been implicated for processing the tutor song in the context of song learning (Sakata and Yazaki-Sugiyama, 2020). Our results suggest that NCM might not only store songs as templates for future vocal imitation but also songs and calls for perceptual discrimination of vocalizers in both male and female birds. NCM could therefore operate as a site for auditory memories for vocalizations used in various facets of communication. We also observed that new auditory memories could be acquired without intact HVC or NCM but that for these new memories NCM lesions caused deficits in either memory capacity or auditory discrimination. These results suggest that the high-capacity memory functions of the avian pallial auditory system depend on NCM.SIGNIFICANCE STATEMENT Many aspects of vocal communication require the formation of auditory memories. Voice recognition, for example, requires a memory for vocalizers to identify acoustical features. In both birds and primates, the locus and neural correlates of these high-level memories remain poorly described. Previous work suggests that this memory formation is mediated by high-level sensory areas, not traditional memory areas such as the hippocampus. Using lesion experiments, we show that one secondary auditory brain region in songbirds that had previously been implicated in storing song memories for vocal imitation is also implicated in storing vocal memories for individual recognition. The role of the neural circuits in this region in interpreting the meaning of communication calls should be investigated in the future.