Intellectual Disability
Intellectual disability (ID) is defined as the presence of incomplete mental development (Katz & Lazcano-Ponce, 2008). An intelligence quotient (IQ) score below 70-75 is commonly used to diagnose ID, and in affected children, observable deficits in linguistic, social, and cognitive skills reveal underlying delays in their development. ID may result from various developmental disorders such as Down and Fragile-X syndromes. Symptoms of ID in children include poorer long-term memory (LTM) than peers of the same age (Conners, Moore, Loveall, & Merrill, 2011). Since long-term potentiation (LTP) is widely believed to be the cellular basis of LTM (Lynch, 2004), pathological effects on LTP may underlie these overt memory deficits. For example, dendritic
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Spines play an essential role in long term-potentiation, the process by which activity between synapsing neurons strengthens their connection. LTP occurs when glutamate released by a pre-synaptic neuron binds to an NMDA receptor on the post-synaptic cell (Lynch, 2004). If the post-synaptic cell is sufficiently depolarized at this time, a magnesium ion will be expelled from the channel, allowing for an influx of calcium ions. In this way, NMDA activation functions as a coincidence detector, indicating simultaneous activity by the pre- and post-synaptic cell. The calcium flow caused by this process triggers cellular processes that enhance the signaling strength between the two cells: added receptors, larger synaptic surface area, and so forth. Matsuzaki and colleagues (2004) investigated the process of LTP on dendritic spines in the hippocampus, a brain structure particularly involved in memory. When NMDA receptors on a spine are activated, the spine grows in size. This enlargement may be permanent and is subsequently associated with greater signal strength from the pre-synaptic cell. Spine pathology, then, may disrupt LTP responses in individuals with intellectual
Spines play an essential role in long term-potentiation, the process by which activity between synapsing neurons strengthens their connection. LTP occurs when glutamate released by a pre-synaptic neuron binds to an NMDA receptor on the post-synaptic cell (Lynch, 2004). If the post-synaptic cell is sufficiently depolarized at this time, a magnesium ion will be expelled from the channel, allowing for an influx of calcium ions. In this way, NMDA activation functions as a coincidence detector, indicating simultaneous activity by the pre- and post-synaptic cell. The calcium flow caused by this process triggers cellular processes that enhance the signaling strength between the two cells: added receptors, larger synaptic surface area, and so forth. Matsuzaki and colleagues (2004) investigated the process of LTP on dendritic spines in the hippocampus, a brain structure particularly involved in memory. When NMDA receptors on a spine are activated, the spine grows in size. This enlargement may be permanent and is subsequently associated with greater signal strength from the pre-synaptic cell. Spine pathology, then, may disrupt LTP responses in individuals with intellectual