Learning and Generalization in Schizophrenia: Effects of Disease and Antipsychotic Drug Treatment

Shohamy, Daphna; Mihalakos, Perry; Chin, R; Thomas, Binu P.; Wagner, Anthony D.; Tamminga, Carol A.

doi:10.1016/j.biopsych.2009.10.025

Cited by 31 publications

(36 citation statements)

References 38 publications

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“…By contrast, prior studies with the computer-based acquired equivalence task have reported much better performance particularly in control groups, with control groups often averaging at or below 10–15% errors on generalization pairs (20, 21, 34), although one prior study using an Australian sample found error rates of about 31% in healthy elderly subjects (41). These prior studies did not include separate reward- and punishment-based trials; rather, on each trial the subject received explicit reward (feedback and point gain) for a correct response or explicit punishment (feedback and point loss) for an incorrect response.…”

Section: Discussionmentioning

confidence: 74%

“…Patients symptomatic for early (AD) show similar deficits on generalization, although they also show slower learning than age-matched controls, consistent with a more diffuse pattern of accumulating brain pathology in early AD (19). Disrupted generalization on acquired equivalence tasks is also seen in other psychopathologies that commonly involve hippocampal-region volume reductions, including schizophrenia (20, 21) and post-traumatic stress disorder (22). …”

Section: Introductionmentioning

confidence: 99%

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Learning and generalization from reward and punishment in opioid addiction

Myers

Rego

Haber

et al. 2017

Behavioural Brain Research

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This study adapts a widely-used acquired equivalence paradigm to investigate how opioid-addicted individuals learn from positive and negative feedback, and how they generalize this learning. The opioid-addicted group consisted of 33 participants with a history of heroin dependency currently in a methadone maintenance program; the control group consisted of 32 healthy participants without a history of drug addiction. All participants performed a novel variant of the acquired equivalence task, where they learned to map some stimuli to correct outcomes in order to obtain reward, and to map other stimuli to correct outcomes in order to avoid punishment; some stimuli were implicitly “equivalent” in the sense of being paired with the same outcome. On the initial training phase, both groups performed similarly on learning to obtain reward, but as memory load grew, the control group outperformed the addicted group on learning to avoid punishment. On a subsequent testing phase, the addicted and control groups performed similarly on retention trials involving previously-trained stimulus-outcome pairs, as well as on generalization trials to assess acquired equivalence. Since prior work with acquired equivalence tasks has associated stimulus-outcome learning with the nigrostriatal dopamine system, and generalization with the hippocampal region, the current results are consistent with basal ganglia dysfunction in the opioid-addicted patients. Further, a selective deficit in learning from punishment could contribute to processes by which addicted individuals continue to pursue drug use even at the cost of negative consequences such as loss of income and the opportunity to engage in other life activities.

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Section: Discussionmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Learning and generalization from reward and punishment in opioid addiction

Myers

Rego

Haber

et al. 2017

Behavioural Brain Research

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“…According to recent findings in humans, memory generalization does not rely solely on inferential processes that take place during retrieval, but also relies on integrative and constructive processes already at the time of encoding (Shohamy and Wagner, 2008). Such processes have been associated with functional coupling of the hippocampus and midbrain: phasic dopaminergic firing in response to novel stimuli is thought to trigger reactivations of related or overlapping representations of prior memories and thus result in updating through integration of new information into existing memory (Kumaran and Duzel, 2008;Shohamy and Wagner, 2008;Shohamy et al, 2010). It is therefore possible that the overgeneralization of memory representations that results in a positive response bias is caused by stress-induced tonic activation of this circuit.…”

Section: Discussionmentioning

confidence: 99%

Understanding Low Reliability of Memories for Neutral Information Encoded under Stress: Alterations in Memory-Related Activation in the Hippocampus and Midbrain

Qin¹,

Hermans²,

Marle³

et al. 2012

J. Neurosci.

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Exposure to an acute stressor can lead to unreliable remembrance of intrinsically neutral information, as exemplified by low reliability of eyewitness memories, which stands in contrast with enhanced memory for the stressful incident itself. Stress-sensitive neuromodulators (e.g., catecholamines) are believed to cause this low reliability by altering neurocognitive processes underlying memory formation. Using event-related functional magnetic resonance imaging, we investigated neural activity during memory formation in 44 young, healthy human participants while incidentally encoding emotionally neutral, complex scenes embedded in either a stressful or neutral context. We recorded event-related pupil dilation responses as an indirect index of phasic noradrenergic activity. Autonomic, endocrine, and psychological measures were acquired to validate stress manipulation. Acute stress during encoding led to a more liberal response bias (more hits and false alarms) when testing memory for the scenes 24 h later. The strength of this bias correlated negatively with pupil dilation responses and positively with stress-induced heart rate increases at encoding. Acute stress, moreover, reduced subsequent memory effects (SMEs; items later remembered vs forgotten) in hippocampus and midbrain, and in pupil dilation responses. The diminished SMEs indicate reduced selectivity and specificity in mnemonic processing during memory formation. This is in line with a model in which stress-induced catecholaminergic hyperactivation alters phasic neuromodulatory signaling in memory-related circuits, resulting in generalized (gist-based) processing at the cost of specificity. Thus, one may speculate that loss of specificity may yield less discrete memory representations at time of encoding, thereby causing a more liberal response bias when probing these memories.

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“…In schizophrenia, dysregulation of dopamine in the hippocampus does seem linked to mnemonic dysfunction, suggesting that restoring “normal” levels is advantageous (Shohamy et al, 2010). These results suggest similar dynamics for dopamine in the medial temporal lobes and the basal ganglia, yet many questions remain regarding the mechanisms of dopamine action in the medial temporal lobes; findings of distinct dopamine receptor distribution in the basal ganglia vs. the medial temporal lobes suggest possibly distinct modes of action in these regions (see Shohamy & Adcock, 2010 for detail).…”

Section: Interactions Between the Basal Ganglia And Other Brain Symentioning

confidence: 99%

The role of the basal ganglia in learning and memory: Insight from Parkinson’s disease

Foerde

Shohamy

2011

Neurobiology of Learning and Memory

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110

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It has long been known that memory is not a single process. Rather, there are different kinds of memory that are supported by distinct neural systems. This idea stemmed from early findings of dissociable patterns of memory impairments in patients with selective damage to different brain regions. These studies highlighted the role of the basal ganglia in non-declarative memory, such as procedural or habit learning, contrasting it with the known role of the medial temporal lobes in declarative memory. In recent years, major advances across multiple areas of neuroscience have revealed an important role for the basal ganglia in motivation and decision making. These findings have led to new discoveries about the role of the basal ganglia in learning and highlighted the essential role of dopamine in specific forms of learning. Here we review these recent advances with an emphasis on novel discoveries from studies of learning in patients with Parkinson's disease. We discuss how these findings promote the development of current theories away from accounts that emphasize the verbalizability of the contents of memory and towards a focus on the specific computations carried out by distinct brain regions. Finally, we discuss new challenges that arise in the face of accumulating evidence for dynamic and interconnected memory systems that jointly contribute to learning.

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Learning and Generalization in Schizophrenia: Effects of Disease and Antipsychotic Drug Treatment

Cited by 31 publications

References 38 publications

Learning and generalization from reward and punishment in opioid addiction

Learning and generalization from reward and punishment in opioid addiction

Understanding Low Reliability of Memories for Neutral Information Encoded under Stress: Alterations in Memory-Related Activation in the Hippocampus and Midbrain

The role of the basal ganglia in learning and memory: Insight from Parkinson’s disease

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