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Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1
TLDR
The results indicate that the learning deficits associated with NF1 may be caused by excessive Ras activity, which leads to impairments in long-term potentiation caused by increased GABA-mediated inhibition.
Selective cognitive dysfunction in acetylcholine M1 muscarinic receptor mutant mice
TLDR
Memory in mice with a null mutation of the gene coding the M1 receptor, the most densely distributed muscarinic receptor in the hippocampus and forebrain is examined, suggesting that the M 1 receptor is specifically involved in memory processes for which the cortex and hippocampus interact.
Mediation of classical conditioning in Aplysia californica by long-term potentiation of sensorimotor synapses.
TLDR
A cellular analog of classical conditioning in Aplysia was used to determine whether this form of invertebrate learning involves N-methyl-D-aspartate (NMDA)-type LTP, and NMDA receptor-antagonist dl-2-amino-5-phosphonovalerate significantly disrupted synaptic enhancement after associative training but did not disrupt synaptic Enhancement after nonassociative training.
Modulation of Presynaptic Plasticity and Learning by the H-ras/Extracellular Signal-Regulated Kinase/Synapsin I Signaling Pathway
TLDR
It is demonstrated that presynaptic plasticity represents an important evolutionarily conserved mechanism for modulating learning and memory in mice and is compatible with previous invertebrate studies.
L-type voltage-gated calcium channels in conditioned fear: a genetic and pharmacological analysis.
TLDR
Data is presented demonstrating that the L-VGCC antagonist nifedipine, which has been used in previous conditioned fear extinction studies, impairs locomotion, and induces an aversive state, which can enter into associations with conditioned stimuli that are present at the time that it is experienced, suggesting that previous studies were likely confounded by drug toxicity.
Compensatory network changes in the dentate gyrus restore long-term potentiation following ablation of neurogenesis in young-adult mice
TLDR
It is found that ablation of neurogenesis resulted in significant deficits in dentate gyrus long-term potentiation (LTP) when examined at a time proximal to the ablation, but the observed deficits in LTP were not permanent.
The L-Type voltage-gated calcium channel Cav1.3 mediates consolidation, but not extinction, of contextually conditioned fear in mice.
TLDR
This study uses mice in which the gene for the pore-forming subunit (alpha1D) Cav1.3 was deleted to elucidate its contribution to consolidation and extinction of conditioned fear, and finds that Cav 1.3 knockout mice exhibit significant impairments in consolidation of contextual fear conditioning.
Deletion of the L‐type calcium channel CaV1.3 but not CaV1.2 results in a diminished sAHP in mouse CA1 pyramidal neurons
TLDR
The results of the study demonstrate that deletion of CaV1.3, but not CaV 1.2, significantly impacts the generation of the sAHP, and reduces in both the area and 1 s amplitude suggest the involvement of calcium influx via CaV2.3 in the slow AHP (sAHP).
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