Hoi-Ki Ding

University of Toronto, Toronto, Ontario, Canada

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Publications (4)17.67 Total impact

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    ABSTRACT: Following initial encoding, memories undergo a prolonged period of reorganization. While such reorganization may occur in many different memory systems, its purpose is not clear. Previously, we have shown that recall of recent contextual fear memories engages the dorsal hippocampus (dHPC). In contrast, recall of remote contextual fear memories engages a number of different cortical regions, including the anterior cingulate cortex (ACC). To examine whether this reorganization leads to greater memory stability, we examined reconsolidation of 1 d-old (recent) and 36 d-old (remote) contextual fear memory in mice. We infused the protein synthesis inhibitor, anisomycin (ANI), into either the dHPC or ACC immediately following retrieval of either a recent or remote contextual fear memory. In the dHPC, ANI infusions disrupted subsequent expression of recent, but not remote, contextual fear memory. Similar infusions into the ACC had no effect on either recent or remote contextual fear memories, whereas systemically applied ANI blocked subsequent remote memory expression when long re-exposure durations were used. Together, these data suggest that as memories mature they become increasingly stable. Furthermore, the dissociation between the effects of systemically and centrally administered ANI on remote memory suggests that stability is due, in part, to the distributed nature of remote contextual fear memories.
    Full-text · Article · Jul 2006 · Learning & Memory
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    ABSTRACT: Trace fear memory requires the activity of the anterior cingulate cortex (ACC) and is sensitive to attention-distracting stimuli. Fragile X syndrome is the most common form of mental retardation with many patients exhibiting attention deficits. Previous studies in fragile X mental retardation 1 (FMR1) knock-out (KO) mice, a mouse model for fragile X, focused mainly on hippocampal-dependent plasticity and spatial memory. We demonstrate that FMR1 knock-out mice show a defect in trace fear memory without changes in locomotion, anxiety, and pain sensitivity. Whole-cell path-clamp recordings in the ACC show that long-term potentiation (LTP) was completely abolished. A similar decrease in LTP was found in the lateral amygdala, another structure implicated in fear memory. No significant changes were found in basal synaptic transmission. This suggests that synaptic plasticity in the ACC and amygdala of FMR1 KO mice plays an important role in the expression of behavioral phenotypes similar to the symptoms of fragile X syndrome.
    Full-text · Article · Sep 2005 · The Journal of Neuroscience : The Official Journal of the Society for Neuroscience
  • Hoi-Ki Ding · Fanny W F Shum · Shanelle W Ko · Min Zhuo
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    ABSTRACT: The hot plate test is a standard way to measure nociceptive response latencies to a noxious thermal stimulus. Here we have modified the classic hot plate by allowing animals to escape to an adjacent chamber after exposure to the heated surface. In this test, the animals escape to the adjacent chamber after exposure to the hot plate set at 50 degrees C. Repeated exposure to the hot plate resulted in a facilitation of escape responses, as measured by a reduced latency to escape from the noxious thermal stimulus. Signs of nociceptive behavior, such as licking or jumping, were not affected in animals that received hot plate training. The reduction of escape latencies after repeated hot plate exposure might be a useful measure for studying the facilitation of escape responses. In addition, the modified hot plate described here might be useful in studying performance and memory deficits related to noxious thermal stimuli. PERSPECTIVE: We modified a hot plate to measure facilitation of escape responses to a noxious thermal stimulus. The measure of escape responses might be useful in the assessment of memory defects, evaluation of drug therapies, and the behavioral characterization of transgenic mice.
    No preview · Article · Aug 2005 · Journal of Pain
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    ABSTRACT: Identifying higher brain central region(s) that are responsible for the unpleasantness of pain is the focus of many recent studies. Here we show that direct stimulation of the anterior cingulate cortex (ACC) in mice produced fear-like freezing responses and induced long-term fear memory, including contextual and auditory fear memory. Auditory fear memory required the activation of N-methyl-D-aspartate (NMDA) receptors in the amygdala. To test the hypothesis that neuronal activity in the ACC contributes to unpleasantness, we injected a GABAA receptor agonist, muscimol bilaterally into the ACC. Both contextual and auditory memories induced by foot shock were blocked. Furthermore, activation of metabotropic glutamate receptors in the ACC enhanced behavioral escape responses in a noxious hot-plate as well as spinal nociceptive tail-flick reflex. Our results provide strong evidence that the excitatory activity in the ACC contribute to pain-related fear memory as well as descending facilitatory modulation of spinal nociception.
    Full-text · Article · Feb 2005 · Molecular Pain