Analysis of the effects of frontal lesions in monkey: II. Variations of delayed response.

Mishkin, Mortimer; Pribram, Karl H.

doi:10.1037/h0040592

Cited by 112 publications

(48 citation statements)

References 6 publications

(4 reference statements)

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“…This view originated from early discoveries of discrete language centers in the brain and has expanded to include current 'phrenology'-like assignment of specific cognitive processes to exact cortical locations. Behavioral correlations of discrete cortical lesions in human and animal studies, as well as neurophysiological findings of distinct integrative representations in different subregions, have supported this modular view of cognitive processing (Mishkin and Pribram, 1955;Goldman and Rosvold, 1970;Stuss and Benson, 1984;Passingham et al, 2000). The other is the connectionist view that emphasizes parallel distributed neural networks in mediation of complex cognitive processes (Edelman and Mouncastle, 1978;Goldman-Rakic, 1988;Damasio, 1989;Mesulam, 1990;Fuster, 2003).…”

Section: Introductionmentioning

confidence: 81%

Divergent Plasticity of Prefrontal Cortex Networks

Moghaddam

Homayoun

2007

Neuropsychopharmacol

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The 'executive' regions of the prefrontal cortex (PFC) such as the dorsolateral PFC (dlPFC) and its rodent equivalent medial PFC (mPFC) are thought to respond in concert with the 'limbic' regions of the PFC such as the orbitofrontal (OFC) cortex to orchestrate behavior that is consistent with context and expected outcome. Both groups of regions have been implicated in behavioral abnormalities associated with addiction and psychiatric disorders, in particular, schizophrenia and mood disorders. Theories about the pathophysiology of these disorders, however, incorporate abnormalities in discrete PFC regions independently of each other or assume they are one and the same and, thus, bunch them under umbrella of 'PFC dysfunction.' Emerging data from animal studies suggest that mPFC and OFC neurons display opposing patterns of plasticity during associative learning and in response to repeated exposure to psychostimulants. These data corroborate clinical studies reporting different patterns of activation in OFC versus dlPFC in individuals with schizophrenia or addictive disorders. These suggest that concomitant but divergent engagement of discrete PFC regions is critical for learning stimulus-outcome associations, and the execution of goal-directed behavior that is based on these associations. An atypical interplay between these regions may lead to abnormally high or low salience assigned to stimuli, resulting in symptoms that are fundamental to many psychiatric and addictive disorders, including attentional deficits, improper affective response to stimuli, and inflexible or impulsive behavior.

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Section: Introductionmentioning

confidence: 81%

Divergent Plasticity of Prefrontal Cortex Networks

Moghaddam

Homayoun

2007

Neuropsychopharmacol

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“…This task is sensitive to dmPFC lesion (Aggleton et al, 1995;Divac, 1971;Jacobsen, 1936;Mishkin and Pribram, 1956;Simon et al, 1980). Starting from day 4 after the last self-administration session, rats were food-deprived to 85% body weight and habituated to the T-maze until they readily ate a sucrose pellet placed at the end of each arm.…”

Section: Behavioral Tasksmentioning

confidence: 99%

“…To test these hypotheses, the integrity of working memory under high and low cognitive demands and high-and low-incentive conditions was assessed in rats with a history of extended or limited access to cocaine 3-17 days after the last self-administration session. Working memory under high incentive and cognitive demands was measured in food-restricted rats using a delayed nonmatching-to-sample procedure, a task sensitive to prefrontal cortical dysfunction (Divac, 1971;Brozoski et al, 1979;Jacobsen, 1936;Mishkin and Pribram, 1956;Simon et al, 1980;Aggleton et al, 1995;Walton et al, 2003). Specifically, the percentage of correct responses in this task is decreased after dmPFC lesion, particularly when a delay is used to increase the working memory load.…”

Section: Introductionmentioning

confidence: 99%

Extended Access to Cocaine Self-Administration Produces Long-Lasting Prefrontal Cortex-Dependent Working Memory Impairments

George

Mandyam

Wee

et al. 2007

Neuropsychopharmacol

153

127

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Humans with drug addiction exhibit compulsive drug-seeking associated with impairment of prefrontal cortex cognitive function. Whether prefrontal cortex dysfunction is a consequence of chronic drug exposure, or mediates the transition from drug use to drug dependence, is unknown. The current study investigates whether a history of escalated vs controlled cocaine intake is associated with specific working memory impairments, and long-lasting alterations of the dorsomedial prefrontal cortex and orbitofrontal cortex in rats. Working memory was assessed in rats with a history of extended (6 h per session) or limited (1 h per session) access to cocaine (0.5 mg/kg per injection), 3-17 days after the last self-administration session, using a delayed nonmatching-to-sample task. The density of neurons, oligodendrocytes, and astrocytes was quantified in the dorsomedial prefrontal cortex and orbitofrontal prefrontal cortex 2 months after the last self-administration session. Working memory impairments were observed after a history of chronic and escalated cocaine intake, but not after repeated limited access to cocaine. Moreover, working memory impairments were correlated with a decreased density of neurons and oligodendrocytes but not astrocytes in the dorsomedial prefrontal cortex, and with a decreased density of oligodendrocytes in the orbitofrontal cortex. Considering the role of the prefrontal cortex in goal-directed behavior, the prefrontal cortex dysfunctions observed here may exacerbate the loss of control associated with increased drug use and facilitate the progression to drug addiction.

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“…Similarly, macaques with temporary dorsolateral "lesions" brought about by cortical cooling or electrical current show significant delay-task impairments (see, e.g., Bauer & Fuster, 1976;Fuster & Bauer, 1974;Quintana & Fuster, 1993;Shindy, Posley, & Fuster, 1994;Stamm, 1961;Stamm & Rosen, 1973). However, lesions to many other brain areas, even in more ventral or superior PFC, often do not produce such deficits (see, e.g., Goldman et al, 1971;Mishkin & Pribram, 1955, 1956Oscar-Berman, 1975;Pohl, 1973;but see, e.g., Battig et al, 1960;Rosvold & Delgado, 1956;Zola-Morgan & Squire, 1985).…”

Section: Nonhuman Primate Researchmentioning

confidence: 99%

“…Accuracy drops to near-chance levels in monkeys with lesions to Walker's areas 9, 10, and 46, even with delays of mere seconds (see, e.g., Battig, Rosvold, & Mishkin, 1960;Funahashi, Bruce, & Goldman-Rakic, 1993;Goldman & Rosvold, 1970;Goldman, Rosvold, Vest, & Galkin, 1971;Mishkin & Pribram, 1955, 1956Oscar-Berman, 1975;W. A. Wilson, 1962; but see Petrides, 1995).…”

Section: Nonhuman Primate Researchmentioning

confidence: 99%