So-called "place cells" located in this region become active only when the rat is in a particular location — called a "place field" — in the environment. Since these place fields are distributed throughout the environment, one interpretation is that groups of place cells form maps in the hippocampus. The accuracy of these maps determines how well a rat learns about its environment and thus how well it can navigate it. Tonegawa found that by impairing the NMDA receptor, specifically by genetically removing the NR1 subunit in the CA1 region, the place fields generated were substantially less specific than those of controls. That is, mice produced faulty spatial maps when their NMDA receptors were impaired. As expected, these mice performed very poorly on spatial tasks compared to controls, further supporting the role of LTP in spatial learning. In 2006, Jonathan Whitlock and colleagues reported on a series of experiments that provided perhaps the strongest evidence of LTP's role in behavioral memory, arguing that to conclude that LTP underlies behavioral learning, the two processes must both mimic and occlude one another. Employing an inhibitory avoidance learning paradigm, researchers trained rats in a two-chambered apparatus with light and dark chambers, the latter being fitted with a device that delivered a foot shock to the rat upon entry. An analysis of CA1 hippocampal synapses revealed that inhibitory avoidance training induced "in vivo" AMPA receptor phosphorylation of the same type as that seen in LTP "in vitro"; that is, inhibitory avoidance training mimicked LTP. In addition, synapses potentiated during training could not be further potentiated by experimental manipulations that would have otherwise induced LTP; that is, inhibitory avoidance training occluded LTP. In a response to the article, Timothy Bliss and colleagues remarked that these and related experiments "substantially advance the case for LTP as a neural mechanism for memory." The role of LTP in disease is less clear than its role in basic mechanisms of synaptic plasticity. However, alterations in LTP may contribute to a number of neurological diseases, including depression, Parkinson's disease, epilepsy, and neuropathic pain. Impaired LTP may also have a role in Alzheimer's disease and drug addiction. LTP has received much attention among those who study Alzheimer's disease (AD), a neurodegenerative disease that causes marked cognitive decline and dementia. Much of this deterioration occurs in association with degenerative changes in the hippocampus and other medial temporal lobe structures. Because of the hippocampus' well established role in LTP, some have suggested that the cognitive decline seen in individuals with AD may result from impaired LTP.