Reduced density of NMDA receptors and increased sensitivity to dizocilpine-induced learning impairment in aged rats
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Cited by (66)
Contribution of N-methyl-D-aspartate receptors to attention and episodic spatial memory during senescence
2015, Neurobiology of Learning and MemoryCitation Excerpt :In the same way, a decline in NMDAR activity could underlie the decreased expression of synaptic and neuroprotective genes in aged-memory impaired animals (Aenlle & Foster, 2010; Blalock et al., 2003). Indeed, due to a decline NMDAR function with advancing age, it might be expected that older subjects are more susceptible to impairments following NMDAR blockade (Ingram et al., 1992). Interestingly, some studies have reported that activity-dependent NMDAR channel antagonists at low doses have little effect or impair memory and yet improve attention and executive function in humans (Ferris, Schneider, Farmer, Kay, & Crook, 2007; Nakamura, Kitamura, Homma, Shiosakai, & Matsui, 2014; Rammsayer, 2001; Riepe et al., 2007; Wroolie et al., 2009) and in animals (Benn & Robinson, 2014; Higgins, Ballard, Enderlin, Haman, & Kemp, 2005; Pehrson, Bondi, Totah, & Moghaddam, 2013; Smith et al., 2011).
Age-associated learning and memory deficits in two mouse versions of the stone T-maze
2012, Neurobiology of AgingCitation Excerpt :Other classes of drugs have also shown efficacy in enhancing learning performance of old rats in the STM including the nitric oxide donor, molsidomine (Meyer et al., 1998a), while the nootropic drug, codergocrine (Walovitch et al., 1987), and the mitochondrial energy enhancer, acetyl-L-carnitine, were not effective (Barnes et al., 1990). Many other studies have been conducted in young rats to demonstrate that STM learning is impaired by inhibition of signaling in muscarinic cholinergic (Spangler et al., 1986), NMDA glutamatergic (Ingram et al., 1992), D2 dopaminergic (Umegaki et al., 2001), and nitric oxidergic (Meyer et al., 1998a; Meyer et al., 1998b) systems. Impaired learning in the STM is also observed in rats with lesions to the septohippocampal system (Kametani et al., 1989; Kametani et al., 1993), hippocampus (Duffy et al., 2008), striatum (Pistell et al., 2009), and temporal-parietal, but not to striate cortex (Jucker et al., 1990; Spangler et al., 1994) nor the (Spangler et al., 1990).
Changes in expression of splice cassettes of NMDA receptor GluN1 subunits within the frontal lobe and memory in mice during aging
2011, Behavioural Brain ResearchCitation Excerpt :Within the group of aged C57BL/6 mice, higher expression of the GluN1 subunit within the synaptic membrane of the hippocampus was found in the mice with the worst spatial reference memory [70]. High densities of NMDA receptor binding within old rats in regions of the hippocampus have also been shown to be associated with poor long-term memory retention in the water maze [67] and a non-spatial complex maze task [29] and in the striatum are related to poor set shifting [56] and poor spatial learning [57]. Aged rats that were unimpaired in a spatial memory task showed greater age-related declines in MK801 binding in the cortex and hippocampus than those that were impaired [35].
The N-methyl-d-aspartate receptor modulator GLYX-13 enhances learning and memory, in young adult and learning impaired aging rats
2011, Neurobiology of AgingCitation Excerpt :Protein levels of NR1 (Adams et al., 2001) and NMDAR binding (Davis et al., 1993) in rats both correlate positively with learning acquisition rates in the MWM. Moreover, old rats are more sensitive than young adult rats to the memory impairing effect of the NMDA open channel blocker MK-801 (Ingram et al., 1992). GLYX-13 is a recently developed tetrapeptide (Thr-Pro-Pro-Thr) that acts as a NMDAR receptor partial agonist at the glycine site with therapeutic potential as a cognitive enhancer (Moskal et al., 2005).
Effect of chronic MK-801 and/or phenytoin on the acquisition of complex behaviors in rats
2007, Neurotoxicology and TeratologyCitation Excerpt :If this were true, then it may help to explain why the rodent subjects examined in the present experiment, who were post-pubescent over the course of most of the experiment, appear to be more sensitive to the effects of NMDA receptor antagonism than the juvenile primate subjects used in previous studies [26,27]. This suggestion is also supported by a previous report of an increased sensitivity with age to the learning impairment associated with NMDA receptor antagonism in rats [19]. Fig. 10 is our attempt at approximating the different developmental periods for rats, monkeys and humans and how we predict (based on the literature) they would respond to neurotoxic insults from NMDA receptor antagonists.
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Present address: Department of Radiology, Nigata University School of Medicine, Ashachimachi 1, Nigata City, Japan 951.