The lexical boost effect is not diagnostic of lexically-specific syntactic representations
Publication date: August 2017 Source:Journal of Memory and Language, Volume 95 Author(s): Christoph Scheepers, Claudine N. Raffray, Andriy Myachykov Structural priming implies that speakers/listeners unknowingly re-use syntactic structure over subsequent utterances. Previous research found that structural priming is reliably enhanced when lexical content is repeated (lexical boost effect). A widely held assumption is that structure-licensing heads enjoy a privileged role in lexically boosting structural priming. The present comprehension-to-production priming experiments investigated whether head-constituents (verbs) versus non-head constituents (argument nouns) contribute differently to boosting ditransitive structure priming in English. Experiment 1 showed that lexical boosts from repeated agent or recipient nouns (and to a lesser extent, repeated theme nouns) were comparable to those from repeated verbs. Experiments 2 and 3 found that increasing numbers of content words shared between primes and targets led to increasing magnitudes of structural priming (again, with no ‘special’ contribution of verb-repetition). We conclude that lexical boost effects are not diagnostic of lexically-specific syntactic representations, even though such representations are supported by other types of evidence.
Altered levels and function of gamma-aminobutyric acidergic interneurons that coexpress the neuropeptide somatostatin (SST) are consistently found in major depressive disorder (MDD). In this review, Fee et al. (pages 549--559) highlight evidence linking SST cell deficits to cortical inhibitory deficits underlying emotion and cognitive disruptions in MDD, f ocusing on recent insights into SST cell roles in cortical microcircuits. They then discuss the putative origins of SST cell deficits and implications for targeting this cellular pathology in the development of antidepressant therapies.
Pain insists upon being attended to. God whispers to us in our pleasures, speaks in our consciences, but shouts in our pains. It is his megaphone to rouse a deaf world.
Allostasis (1), a stress-related dysfunction of the brain –body connection that is closely related to interoception (i.e., processing and integrating body-relevant signals together with external stimuli to affect motivated behavior) (2,3), plays a major role in the pathophysiology of mood and anxiety disorders (4,5). However, our understanding of the com putational processes associated with the disruption of the brain–body connection is still developing (6). Thus, examining how stress affects the computational processes underlying functional and dysfunctional adaptation is important for bringing allostasis into...
Trauma- and stressor-related disorders, such as posttraumatic stress disorder (PTSD), cost billions of dollars in health care every year. Symptoms of these disorders vary dramatically among individuals, and many individuals that experience a traumatic event never develop PTSD (1). This suggests that individuals vary in their fear responses and propensity to develop PTSD. Despite this evidence, most research into the neurobiology of fear and the underlying mechanisms of PTSD combines individuals into group averages to improve analytical power.
Major depressive disorder involves aberrant affective processing, the normalization of which has been associated with treatment in both pharmacological and cognitive behavioral interventions (1,2). In this issue of Biological Psychiatry, Young et al. (3) present data suggesting that the normalization of affective processing via a real-time functional magnetic resonance imaging (fMRI) neurofeedback intervention may be the mechanism underlying treatment response. A randomized trial of neurofeedback training patients with major depressive disorder to upregulate their amygdala activity during positive autobiographical memory r...
Slightly more than 10% of pregnant women experience a major depressive episode (MDE) in pregnancy and slightly less than 10% of women have a MDE in the year postdelivery (1,2). Many women do not receive treatment because of concerns about the safety of antidepressant medication in pregnancy or while breastfeeding. Others find behavioral approaches too costly or time-consuming and do not access these treatments. Thus, understanding the biology and factors that can trigger an MDE or sustain it among vulnerable women may help women avoid or manage the condition.
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