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Learned control over distraction is disrupted in amnesia.

ABSTRACT: Recent studies have demonstrated that brief periods of training facilitate the ability to overcome distraction during future performance of a given task, and researchers have proposed that these effects rely on relational memory systems that enable individuals to link specific attentional states to their learned context. In the current work, we examined whether medial temporal lobe (MTL) structures critical for relational and contextual learning contribute to these effects. A group of amnesic patients with bilateral MTL damage and a group of matched comparison subjects both completed an attentional-capture task in which a brief training session typically leads to decreased distraction in a subsequent testing session. Whereas the comparison subjects showed normal training-related decreases in distractibility, the amnesic patients did not. Thus, our results indicate that MTL-mediated learning plays a critical role in the ability to use past experience to overcome distraction. This suggests a tight linkage between MTL-dependent relational-learning mechanisms and cognitive control.

SUBMITTER: Cosman JD

PROVIDER: S-EPMC3970839 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature

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Learned control over distraction is disrupted in amnesia.

Cosman Joshua D JD Vecera Shaun P SP

Psychological science 20130612 8

Recent studies have demonstrated that brief periods of training facilitate the ability to overcome distraction during future performance of a given task, and researchers have proposed that these effects rely on relational memory systems that enable individuals to link specific attentional states to their learned context. In the current work, we examined whether medial temporal lobe (MTL) structures critical for relational and contextual learning contribute to these effects. A group of amnesic pa ...[more]

PMID: 23761926

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Project description:BackgroundIn dystrophic skeletal muscle, osmotic stimuli somehow relieve inhibitory control of dihydropyridine receptors (DHPR) on spontaneous sarcoplasmic reticulum elementary Ca(2+) release events (ECRE) in high Ca(2+) external environments. Such 'uncontrolled' Ca(2+) sparks were suggested to act as dystrophic signals. They may be related to mechanosensitive pathways but the mechanisms are elusive. Also, it is not known whether truncated dystrophins can correct the dystrophic disinhibition.Methodology/principal findingsWe recorded ECRE activity in single intact fibers from adult wt, mdx and mini-dystrophin expressing mice (MinD) under resting isotonic conditions and following hyper-/hypo-osmolar external shock using confocal microscopy and imaging techniques. Isotonic ECRE frequencies were small in wt and MinD fibers, but were markedly increased in mdx fibers. Osmotic challenge dramatically increased ECRE activity in mdx fibers. Sustained osmotic challenge induced marked exponential ECRE activity adaptation that was three times faster in mdx compared to wt and MinD fibers. Rising external Ca(2+) concentrations amplified osmotic ECRE responses. The eliminated ECRE suppression in intact osmotically stressed mdx fibers was completely and reversibly resuscitated by streptomycine (200 microM), spider peptide GsMTx-4 (5 microM) and Gd(3+) (20 microM) that block unspecific, specific cationic and Ca(2+) selective mechanosensitive channels (MsC), respectively. ECRE morphology was not substantially altered by membrane stress. During hyperosmotic challenge, membrane potentials were polarised and a putative depolarisation through aberrant MsC negligible excluding direct activation of ECRE through tubular depolarisation.Conclusions/significanceDystrophin suppresses spontaneous ECRE activity by control of mechanosensitive pathways which are suggested to interact with the inhibitory DHPR loop to the ryanodine receptor. MsC-related disinhibition prevails in dystrophic muscle and can be resuscitated by transgenic mini-dystrophin expression. Our results have important implications for the pathophysiology of DMD where abnormal MsC in dystrophic muscle confer disruption of microdomain Ca(2+) homeostasis. MsC blockers should have considerable therapeutic potential if more muscle specific compounds can be found.

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Learned control over distraction is disrupted in amnesia.

Publications

Learned control over distraction is disrupted in amnesia.

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