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Circuitry-based models of cognition
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people tend to consider only one model of the premises – a point made by other researchers2,3. Moreover, the new model shows that prior knowledge affects the process of model construction and not a search for alternative models. Thus, human reasoning cannot be studied independently of world knowledge. 1 Klauer, K.C. et al. (2000) On belief bias in syllogistic reasoning. Psychol. Rev. 107, 852–884
TRENDS in Cognitive Sciences Vol.5 No.5 May 2001
2 Evans, J.St.B.T. et al. (1999) Reasoning about necessity and possibility: a test of the mental model theory of deduction. J. Exp. Psychol. Learn. Mem. Cognit. 25, 1495–1513 3 Newstead, S.E. et al. (1999) Falsifying mental models: testing the predictions of theories of syllogistic reasoning. Mem. Cognit. 27, 344–354
Mike Oaksford [email protected]
False beliefs and the frontal lobe The role of the frontal lobes in social cognition has been a subject of interest since 1848 when Phineas Gage (that friend of the first year Psychology student) was struck in the head by a tamping iron. Some researchers think that the marked behavioural changes seen as a result of frontal lobe damage – insensitivity to social cues, indifference to the opinion of others and rampant egocentrism – are indicative of a specific impairment in the domain of social interaction. Work on childhood autism has reached a similar conclusion, suggesting that a specific deficit in an innate ‘Theory-of-Mind’ (ToM) function – the ability to ascribe mental states to others – underlies the social aspects of this disorder. However, others argue that the behavioural deficits seen in these conditions are the result of impairments in domain-general executive functions1. A new study by Andrea Rowe and colleagues attempts to shed some light on this controversy by comparing ToM abilities with executive function performance in patients with frontal lobe damage2. A group of adult neurosurgical patients who had undergone surgery on either the left frontal (LF) or right frontal (RF) lobes were compared with a group of matched healthy control subjects. The ToM tests were of the classic ‘false belief’ story format, where individuals are required to account for a character’s behaviour in terms of their mistaken belief about a given situation1. Subjects were tested on both first-order false belief tasks (‘A thinks that X…’) and more demanding second-order false belief tasks (‘A thinks that B thinks that X…’). A battery of executive-function tests were also administered to assess cognitive initation and selection, response inhibition, mental flexibility, and monitoring and organization.
The results showed that LF and RF patients were impaired compared with controls on both first- and second-order ToM tasks, with a much greater reduction in performance on the second-order tests. As predicted, frontal patients also showed significantly impaired executive function compared with controls. ‘deficits in Theory of Mind [tasks] and executive function were found to be independent of each other’ However, the size and locus of lesions did not correlate with performance on either set of tasks. More significantly, the deficits in ToM and executive function were found to be independent of each other; controlling for deficits in executive functioning had no effect on the robustness of the ToM findings. Overall, Rowe et al.’s results suggest that the ToM impairment seen in frontal lobe patients is an independent phenomenon and not the consequence of a loss of executive function, although it is difficult to localize these ToM abilities to a specific brain area. Rowe et al. therefore conclude that, although ToM abilities might be too complex to pin down to a single region, their findings are consistent with the view that ToM is a specialized modular ability instantiated in the frontal lobe. 1 Perner, J. and Lang, B. (1999) Development of theory of mind and executive control. Trends Cognit. Sci. 3, 337–344 2 Rowe, A.D. et al. (2001) ‘Theory-of-mind’ impairments and their relationship to executive functioning following frontal lobe excision. Brain 124, 600–616
Louise Barrett [email protected]
187
Circuitry-based models of cognition A primary mission of cognitive neuroscience is to identify how specific neural circuits enable complex behavior, and why these functional neural systems occasionally go awry. A complex cognitive disorder such as schizophrenia, for example, is associated with circuitry anomalies in several corticolimbic brain areas. One that has received considerable attention is the hippocampus, a structure critical for binding disparate memory traces into holistic representations of memory episodes. The capacity of the hippocampus to achieve such cognitive feats is mirrored in its high degree of neuronal connectivity. The hippocampus receives many neuronal projections from cortical (e.g. prefrontal cortex) and limbic regions (e.g. amygdala) that are processed within its individual sectors. Critical to regulating hippocampal activity are inhibitory interneurons that depend on the neurotransmitter GABA, and, indeed, this inhibitory GABA system is thought to be relevant to the pathophysiology of schizophrenia. For example, GABA system abnormalities in both post-mortem tissue, and basal hippocampal hyperactivity have been observed1,2. An important question with regard to circuitry-based models of schizophrenia is whether structural or functional changes in the hippocampus can be induced by abnormal activity arising from other corticolimbic areas. Berretta et al. elegantly address the structural part of this question using a ‘partial rodent model’ of the GABA-system’s response to amygdala hyperactivity in freely behaving rats3. The amygdala was selected as a candidate region because it sends many excitatory projections to the hippocampus and its activity has been found to co-vary with that of the hippocampus. In the experimental animals Berretta et al. infused the basolateral nucleus of the amygdala with picrotoxin, a substance that blocks inhibitory inputs, thus increasing amygdala output to the hippocampus (control animals did not receive infusions of picrotoxin). Two hours following infusion, the experimenters painstakingly identified cellular markers of altered GABA activity in the hippocampus. The results for the picrotoxin-infused animals showed clear alterations in the GABA system of hippocampal sectors known to be
http://tics.trends.com 1364-6613/01/$ – see front matter © 2001 Elsevier Science Ltd. All rights reserved.
188
News & Comment
structurally anomalous in schizophrenia. By contrast, no significant alterations were found in the GABA system of one sector (CA1), previously found to be intact in schizophrenia. These results offer a circuitry-based mechanism through which amygdala dysfunction, plus other potentially dysfunctional components of corticolimbic circuitry, could contribute to hippocampal pathology in schizophrenia. In addition to the importance of this finding for understanding schizophrenia, an even more important contribution is the development of a method allowing for selective, in vivo, pharmacological dissections of neuronal interaction. Although Berreta et al. emphasized the structural consequences of amygdala hyperactivity on the hippocampus,
TRENDS in Cognitive Sciences Vol.5 No.5 May 2001
their future work could address the physiological or behavioral consequences as well. The ability to manipulate one small part of a complex functional neural system in behaving animals has far-reaching applicability to many important questions in cognitive neuroscience.
In Brief
Where the brain gets jokes
1 Benes, F. (1999) Evidence for altered trisynaptic circuitry in schizophrenic hippocampus. Biol. Psychiatry 46, 589–599 2 Heckers, S. et al. (1998) Impaired recruitment of the hippocampus in during conscious recollection in schizophrenia. Nat. Neurosci. 1, 318–323 3 Berretta, S. et al. (2001) Amygdalar activation alters the hippocampal GABA system: ‘partial’ modelling for postmortem changes in schizophrenia. J. Comp. Neurol. 431, 129–138
Debra Titone [email protected]
Universal dyslexia? Estimates of the prevalence of dyslexia in different countries seem to reflect differences in orthographic complexity; dyslexia is more common in countries where the orthography (spelling) is complex (e.g. USA and Britain), compared with those where orthography is transparent (e.g. Italy). A recent study by Paulesu et al. has shown that, although the manifestation of dyslexia might differ depending on the precise orthography used, the core cognitive deficit and brain basis is universal1. The study compared dyslexic and normal readers from countries with transparent (Italian) and complex (English and French) orthographies. Behaviourally, the dyslexics from each of the three countries showed a similar pattern of results, all performing poorly on subtests that required phonological short-term memory. Italian dyslexics did perform better than either the English or French dyslexics on reading tasks, but comparisons between dyslexic and normal readers from the same country revealed similarly marked differences irrespective of language. At a neurophysiological level, the story was the same. PET scanning during implicit and explicit reading tasks revealed very similar patterns of brain activity in Italian, French and English dyslexic subjects: reduced activation in left inferior and superior temporal cortex and mid-occipital cortex. This pattern is consistent with previous findings from PET, MRI and magnetoencephalography studies of
dyslexia. The marked similarity of brain activity across all three dyslexic groups contrasts with the situation in normal readers. A previous study by the same authors2 found that Italian readers showed greater activation of left superior temporal regions but English readers showed greater activations of left posterior inferior temporal gyrus and anterior inferior frontal gyrus, differences which are consistent with the idea that Italians might be decoding words phoneme by phoneme whereas English readers require access to whole word information. These findings suggest that there is a core impairment in phonological processing in dyslexia, regardless of orthography. The degree of orthographic complexity does, however, affect the manifestation of the impairment. In a transparent orthography such as Italian, reading problems will be less severe whereas complex orthographies are likely to magnify the problem. But the similarity in brain activation between the Italian and English dyslexics might also suggest that the dyslexic brain is less able to adapt to the subtle requirements of an orthographic system. 1 Paulesu, E. et al. (2001) Dyslexia: cultural diversity and biological unity. Science 291, 2165–2167 2 Paulesu, E. et al. (2000) A cultural effect on brain function. Nat. Neurosci. 3, 91–96
Lauren Stewart [email protected]
“Why don’t sharks bite lawyers? Professional courtesy” and “Why did the golfer wear two pairs of pants? He had a hole in one” are both jokes and make people laugh (well, some people, at least), but the type of humor is quite different in each case. Is there nevertheless a central brain mechanism responsible for finding something funny? It appears so, according to a recent study by Vinod Goel and Ray Dolan [Nature Neurosci.(2001) 4, 237–238]. Using singleevent fMRI, these authors studied the brain activation of subjects who listened to jokes (but not extremely funny ones, to keep them from moving their heads). Semantic jokes (such as the one about lawyers) and puns (the golfer joke) activate different networks in the brain, but when subjects find either kind of joke genuinely funny, another brain area is activated – the orbital prefrontal cortex, which has been associated with reward – and the funnier the joke (as rated by the subject), the stronger the activation. MW
Premotor cortex called to attention We know that the premotor cortex (PMC) is involved in movement planning. However, a new single-cell recording study suggests that PMC also contains cells with a purely attentional function [Lebedev, M.A. and Wise, S.P. (2001) Eur. J. Neurosci. 13, 1002–1008]. In this ingenious experiment, a sophisticated eye-movement tracking system and food-delivering robots were used to allow the researchers to separate out effects of eye
http://tics.trends.com 1364-6613/01/$ – see front matter © 2001 Elsevier Science Ltd. All rights reserved.
people tend to consider only one model of the premises – a point made by other researchers2,3. Moreover, the new model shows that prior knowledge affects the process of model construction and not a search for alternative models. Thus, human reasoning cannot be studied independently of world knowledge. 1 Klauer, K.C. et al. (2000) On belief bias in syllogistic reasoning. Psychol. Rev. 107, 852–884
TRENDS in Cognitive Sciences Vol.5 No.5 May 2001
2 Evans, J.St.B.T. et al. (1999) Reasoning about necessity and possibility: a test of the mental model theory of deduction. J. Exp. Psychol. Learn. Mem. Cognit. 25, 1495–1513 3 Newstead, S.E. et al. (1999) Falsifying mental models: testing the predictions of theories of syllogistic reasoning. Mem. Cognit. 27, 344–354
Mike Oaksford [email protected]
False beliefs and the frontal lobe The role of the frontal lobes in social cognition has been a subject of interest since 1848 when Phineas Gage (that friend of the first year Psychology student) was struck in the head by a tamping iron. Some researchers think that the marked behavioural changes seen as a result of frontal lobe damage – insensitivity to social cues, indifference to the opinion of others and rampant egocentrism – are indicative of a specific impairment in the domain of social interaction. Work on childhood autism has reached a similar conclusion, suggesting that a specific deficit in an innate ‘Theory-of-Mind’ (ToM) function – the ability to ascribe mental states to others – underlies the social aspects of this disorder. However, others argue that the behavioural deficits seen in these conditions are the result of impairments in domain-general executive functions1. A new study by Andrea Rowe and colleagues attempts to shed some light on this controversy by comparing ToM abilities with executive function performance in patients with frontal lobe damage2. A group of adult neurosurgical patients who had undergone surgery on either the left frontal (LF) or right frontal (RF) lobes were compared with a group of matched healthy control subjects. The ToM tests were of the classic ‘false belief’ story format, where individuals are required to account for a character’s behaviour in terms of their mistaken belief about a given situation1. Subjects were tested on both first-order false belief tasks (‘A thinks that X…’) and more demanding second-order false belief tasks (‘A thinks that B thinks that X…’). A battery of executive-function tests were also administered to assess cognitive initation and selection, response inhibition, mental flexibility, and monitoring and organization.
The results showed that LF and RF patients were impaired compared with controls on both first- and second-order ToM tasks, with a much greater reduction in performance on the second-order tests. As predicted, frontal patients also showed significantly impaired executive function compared with controls. ‘deficits in Theory of Mind [tasks] and executive function were found to be independent of each other’ However, the size and locus of lesions did not correlate with performance on either set of tasks. More significantly, the deficits in ToM and executive function were found to be independent of each other; controlling for deficits in executive functioning had no effect on the robustness of the ToM findings. Overall, Rowe et al.’s results suggest that the ToM impairment seen in frontal lobe patients is an independent phenomenon and not the consequence of a loss of executive function, although it is difficult to localize these ToM abilities to a specific brain area. Rowe et al. therefore conclude that, although ToM abilities might be too complex to pin down to a single region, their findings are consistent with the view that ToM is a specialized modular ability instantiated in the frontal lobe. 1 Perner, J. and Lang, B. (1999) Development of theory of mind and executive control. Trends Cognit. Sci. 3, 337–344 2 Rowe, A.D. et al. (2001) ‘Theory-of-mind’ impairments and their relationship to executive functioning following frontal lobe excision. Brain 124, 600–616
Louise Barrett [email protected]
187
Circuitry-based models of cognition A primary mission of cognitive neuroscience is to identify how specific neural circuits enable complex behavior, and why these functional neural systems occasionally go awry. A complex cognitive disorder such as schizophrenia, for example, is associated with circuitry anomalies in several corticolimbic brain areas. One that has received considerable attention is the hippocampus, a structure critical for binding disparate memory traces into holistic representations of memory episodes. The capacity of the hippocampus to achieve such cognitive feats is mirrored in its high degree of neuronal connectivity. The hippocampus receives many neuronal projections from cortical (e.g. prefrontal cortex) and limbic regions (e.g. amygdala) that are processed within its individual sectors. Critical to regulating hippocampal activity are inhibitory interneurons that depend on the neurotransmitter GABA, and, indeed, this inhibitory GABA system is thought to be relevant to the pathophysiology of schizophrenia. For example, GABA system abnormalities in both post-mortem tissue, and basal hippocampal hyperactivity have been observed1,2. An important question with regard to circuitry-based models of schizophrenia is whether structural or functional changes in the hippocampus can be induced by abnormal activity arising from other corticolimbic areas. Berretta et al. elegantly address the structural part of this question using a ‘partial rodent model’ of the GABA-system’s response to amygdala hyperactivity in freely behaving rats3. The amygdala was selected as a candidate region because it sends many excitatory projections to the hippocampus and its activity has been found to co-vary with that of the hippocampus. In the experimental animals Berretta et al. infused the basolateral nucleus of the amygdala with picrotoxin, a substance that blocks inhibitory inputs, thus increasing amygdala output to the hippocampus (control animals did not receive infusions of picrotoxin). Two hours following infusion, the experimenters painstakingly identified cellular markers of altered GABA activity in the hippocampus. The results for the picrotoxin-infused animals showed clear alterations in the GABA system of hippocampal sectors known to be
http://tics.trends.com 1364-6613/01/$ – see front matter © 2001 Elsevier Science Ltd. All rights reserved.
188
News & Comment
structurally anomalous in schizophrenia. By contrast, no significant alterations were found in the GABA system of one sector (CA1), previously found to be intact in schizophrenia. These results offer a circuitry-based mechanism through which amygdala dysfunction, plus other potentially dysfunctional components of corticolimbic circuitry, could contribute to hippocampal pathology in schizophrenia. In addition to the importance of this finding for understanding schizophrenia, an even more important contribution is the development of a method allowing for selective, in vivo, pharmacological dissections of neuronal interaction. Although Berreta et al. emphasized the structural consequences of amygdala hyperactivity on the hippocampus,
TRENDS in Cognitive Sciences Vol.5 No.5 May 2001
their future work could address the physiological or behavioral consequences as well. The ability to manipulate one small part of a complex functional neural system in behaving animals has far-reaching applicability to many important questions in cognitive neuroscience.
In Brief
Where the brain gets jokes
1 Benes, F. (1999) Evidence for altered trisynaptic circuitry in schizophrenic hippocampus. Biol. Psychiatry 46, 589–599 2 Heckers, S. et al. (1998) Impaired recruitment of the hippocampus in during conscious recollection in schizophrenia. Nat. Neurosci. 1, 318–323 3 Berretta, S. et al. (2001) Amygdalar activation alters the hippocampal GABA system: ‘partial’ modelling for postmortem changes in schizophrenia. J. Comp. Neurol. 431, 129–138
Debra Titone [email protected]
Universal dyslexia? Estimates of the prevalence of dyslexia in different countries seem to reflect differences in orthographic complexity; dyslexia is more common in countries where the orthography (spelling) is complex (e.g. USA and Britain), compared with those where orthography is transparent (e.g. Italy). A recent study by Paulesu et al. has shown that, although the manifestation of dyslexia might differ depending on the precise orthography used, the core cognitive deficit and brain basis is universal1. The study compared dyslexic and normal readers from countries with transparent (Italian) and complex (English and French) orthographies. Behaviourally, the dyslexics from each of the three countries showed a similar pattern of results, all performing poorly on subtests that required phonological short-term memory. Italian dyslexics did perform better than either the English or French dyslexics on reading tasks, but comparisons between dyslexic and normal readers from the same country revealed similarly marked differences irrespective of language. At a neurophysiological level, the story was the same. PET scanning during implicit and explicit reading tasks revealed very similar patterns of brain activity in Italian, French and English dyslexic subjects: reduced activation in left inferior and superior temporal cortex and mid-occipital cortex. This pattern is consistent with previous findings from PET, MRI and magnetoencephalography studies of
dyslexia. The marked similarity of brain activity across all three dyslexic groups contrasts with the situation in normal readers. A previous study by the same authors2 found that Italian readers showed greater activation of left superior temporal regions but English readers showed greater activations of left posterior inferior temporal gyrus and anterior inferior frontal gyrus, differences which are consistent with the idea that Italians might be decoding words phoneme by phoneme whereas English readers require access to whole word information. These findings suggest that there is a core impairment in phonological processing in dyslexia, regardless of orthography. The degree of orthographic complexity does, however, affect the manifestation of the impairment. In a transparent orthography such as Italian, reading problems will be less severe whereas complex orthographies are likely to magnify the problem. But the similarity in brain activation between the Italian and English dyslexics might also suggest that the dyslexic brain is less able to adapt to the subtle requirements of an orthographic system. 1 Paulesu, E. et al. (2001) Dyslexia: cultural diversity and biological unity. Science 291, 2165–2167 2 Paulesu, E. et al. (2000) A cultural effect on brain function. Nat. Neurosci. 3, 91–96
Lauren Stewart [email protected]
“Why don’t sharks bite lawyers? Professional courtesy” and “Why did the golfer wear two pairs of pants? He had a hole in one” are both jokes and make people laugh (well, some people, at least), but the type of humor is quite different in each case. Is there nevertheless a central brain mechanism responsible for finding something funny? It appears so, according to a recent study by Vinod Goel and Ray Dolan [Nature Neurosci.(2001) 4, 237–238]. Using singleevent fMRI, these authors studied the brain activation of subjects who listened to jokes (but not extremely funny ones, to keep them from moving their heads). Semantic jokes (such as the one about lawyers) and puns (the golfer joke) activate different networks in the brain, but when subjects find either kind of joke genuinely funny, another brain area is activated – the orbital prefrontal cortex, which has been associated with reward – and the funnier the joke (as rated by the subject), the stronger the activation. MW
Premotor cortex called to attention We know that the premotor cortex (PMC) is involved in movement planning. However, a new single-cell recording study suggests that PMC also contains cells with a purely attentional function [Lebedev, M.A. and Wise, S.P. (2001) Eur. J. Neurosci. 13, 1002–1008]. In this ingenious experiment, a sophisticated eye-movement tracking system and food-delivering robots were used to allow the researchers to separate out effects of eye
http://tics.trends.com 1364-6613/01/$ – see front matter © 2001 Elsevier Science Ltd. All rights reserved.