Localization of a Memory Trace in the Mammalian Brain

Krupa, David J.; Thompson, Judith K.; Thompson, Richard F.

doi:10.1126/science.8493536

Cited by 484 publications

(339 citation statements)

References 31 publications

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“…Consistent with previous studies, this abolished normal conditioned responses to the tone-CS (Fig. 2, top left and bottom, cyan) (n ϭ 6; F (2,10) ϭ 49.7; p Ͻ 0.001) (Krupa et al, 1993;Garcia and Mauk, 1998). Subsequently, we made electrolytic lesions of the cerebellar cortex to unmask SLRs (Fig.…”

Section: Experiments 1: Glutamatergic Transmission In the Ain Is Necessupporting

confidence: 63%

“…The effectiveness of the infusion was assessed by its ability to prevent expression of normal conditioned eyelid responses (Chapman et al, 1990;Krupa et al, 1993). Therefore, animals were included in the analysis only if they expressed Ͻ10% conditioned responses across the five sessions of training (n ϭ 3) (Fig.…”

Section: Experiments 2: the Site Of Plasticity Underlying Slrs Is Upstmentioning

confidence: 99%

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Learning-Induced Plasticity in Deep Cerebellar Nucleus

Ohyama¹,

Nores²,

Medina³

et al. 2006

J. Neurosci.

139

131

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Evidence that cerebellar learning involves more than one site of plasticity comes from, in part, pavlovian eyelid conditioning, where disconnecting the cerebellar cortex abolishes one component of learning, response timing, but spares the expression of abnormally timed short-latency responses (SLRs). Here, we provide evidence that SLRs unmasked by cerebellar cortex lesions are mediated by an associative form of learning-induced plasticity in the anterior interpositus nucleus (AIN) of the cerebellum. We used pharmacological inactivation and/or electrical microstimulation of various sites afferent and efferent to the AIN to systematically eliminate alternative candidate sites of plasticity upstream or downstream from this structure. Collectively, the results suggest that cerebellar learning is mediated in part by plasticity in target nuclei downstream of the cerebellar cortex. These data demonstrate an instance in which an aspect of associative learning, SLRs, can be used as an index of plasticity at a specific site in the brain.

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Section: Experiments 1: Glutamatergic Transmission In the Ain Is Necessupporting

confidence: 63%

Section: Experiments 2: the Site Of Plasticity Underlying Slrs Is Upstmentioning

confidence: 99%

Learning-Induced Plasticity in Deep Cerebellar Nucleus

Ohyama¹,

Nores²,

Medina³

et al. 2006

J. Neurosci.

139

131

View full text Add to dashboard Cite

show abstract

“…However, the mechanisms underlying the improvement of spatial learning and memory involved in sevoflurane postconditioning are not completely understood. Neurons in specific brain areas including cerebral cortex and hippocampus are known to play an important role in learning and memory processes (12,13). Therefore, we further evaluated the expression of hippocampus proteins which could serve as memory enhancement biomarkers including c-jun/AP-1, PSD -95 and GAP-43.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, spatial memory in rats and humans is largely dependent on the hippocampus, and hippocampal neuronal damage induced by ischemia is associated with spatial memory impairment (12)(13)(14). Brain functions, such as memory formation and recovery of function after injury, depend on subtle regulation of hippocampal proteins, including growthassociated protein-43 (GAP-43) (15), postsynaptic density-95 (PSD -95) (16) and the transcription factor c-jun/activator protein-1 (AP-1) (17).…”

mentioning

confidence: 99%

“…The hippocampus and cortex of rats are the most vulnerable brain regions to global ischemia/ reperfusion injury in terms of cognitive dysfunction, particularly memory decline (12,13), which are often accompanied with cardiopulmonary resuscitation after CA. Moreover, spatial memory in rats and humans is largely dependent on the hippocampus, and hippocampal neuronal damage induced by ischemia is associated with spatial memory impairment (12)(13)(14).…”

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confidence: 99%

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Sevoflurane Postconditioning Increases the Activities of Antioxidant Enzymes and Improves Spatial Learning and Memory after Cardiac Arrest in Rats

Ye¹,

Zhou²,

Wang³

et al. 2016

J Anesth Perioper Med

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Background: Sevoflurane, as a novel volatile anesthetic with minimal pungency, low solubility, and less toxicity, is widely used in anesthetic practice. The purpose of this study was to investigate the effect of sevoflurane postconditioning on endogenous antioxidant status and spatial learning and memory ability after cardiac arrest (CA) and the potential underlying mechanisms. Methods: A rat model of CA was established by delivering an alternating current between the esophagus and chest wall to induce ventricular fibrillation. Animals were randomly divided into three groups: sham group (no CA), CA group, and CA + sevoflurane postconditioning (CA + SE) group. Sevoflurane postconditioning was achieved by administration of 2.5% sevoflurane for 60 min after resuscitation. The spatial learning and memory ability of rats was measured by the Morris water maze. The antioxidant enzymes activities were assessed at 4 hours, 1 day and 8 days after resuscitation. Moreover, the expressions of hippocampal proteins which could serve as memory enhancement biomarkers including growth-associated protein-43 (GAP-43), postsynaptic density-95 (PSD -95) and the transcription factor c-jun/activator protein-1 (AP-1), were detected at 8 days after resuscitation. Results: We found that CA significantly decreased the ability of spatial learning and memory in contrast to the sham controls. However, sevoflurane postconditioning significantly increased survival rate and antioxidant enzyme activities as well as ameliorated the spatial learning and memory deficits induced by CA. Furthermore, sevoflurane postconditioning regulated hippocampal memory enhancement proteins. Conclusions: Postconditioning with sevoflurane improved learning and memory deficits in a CA model possibly due to the reduction of oxidative stress and up-regulation of the memory enhancement biomarkers in hippocampus.

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Developmental dyslexia: The role of the cerebellum

Nicolson

Fawcett

1999

Dyslexia

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Children with dyslexia suffer from unexpected problems in reading, writing and spelling. The dominant causal hypothesis has been that the deficits arise from some impairment in phonological processing ability. Initial studies revealed that children with dyslexia suffered severe deficits in skills including not only phonological skill but also picture naming speed, bead threading and balance. Given the growing evidence that the cerebellum is directly involved in acquiring ‘language dexterity’, all the above deficits are directly consistent with cerebellar impairment. Further studies established that the panel of children with dyslexia showed severe deficits on clinical and theoretical tests of cerebellar function, among the largest obtained in our research programme. The cerebellar impairment hypothesis provides a causal explanation for developental dyslexia, subsuming the phonological deficit account within a broader framework. Copyright © 1999 John Wiley & Sons, Ltd.

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Localization of a Memory Trace in the Mammalian Brain

Cited by 484 publications

References 31 publications

Learning-Induced Plasticity in Deep Cerebellar Nucleus

Learning-Induced Plasticity in Deep Cerebellar Nucleus

Sevoflurane Postconditioning Increases the Activities of Antioxidant Enzymes and Improves Spatial Learning and Memory after Cardiac Arrest in Rats

Developmental dyslexia: The role of the cerebellum

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