NMDA depolarizations and long-term potentiation are reduced in the aged rat neocortex
References (26)
- et al.
Altered modulatory actions of serotonin on dentate granule cells of aged rats
Brain Research
(1987) - et al.
Age-related reduction in responses of rat hippocampal neurons to locally applied monoamines
Neurobiol. Aging
(1988) - et al.
Presynaptic and postsynaptic glutamatergic function in Alzheimer's disease
Neurosci. Lett.
(1988) - et al.
Long-term potentiation in the hippocampus involves activation onN-methyl-d-aspartate receptors
Brain Research
(1984) - et al.
Linear relation between the magnitude of long-term potentiation in the dentate gyrus and associative learning in the rat. A demonstration using commissural inhibition and local infusion of anN-methyl-d-aspartte receptor antagonist
Neuroscience
(1989) Sustained enhancement of evoked potentials following brief, high-frequency stimulation of the cerebral cortex in vitro
Brain Research
(1982)- et al.
Conformational changes in muscarinic receptors may produce diminished cholinergic neurotransmission and memory deficits in aged rats
Neurobiol. Aging
(1985) - et al.
Glutamate dysfunction in Alzheimer's disease: an hypothesis
Trends Neurosci.
(1987) - et al.
The effects of serotonin onN-methyl-d-aspartate and synaptically evoked depolarizations in rat neocortical neurons
Brain Research
(1988) - et al.
Long-term potentiation in frontal cortex: role of NMDA-modulated polysynaptic excitatory pathways
Neurosci. Lett.
(1989)
The postnatal development of post-activation potentiation in the rat neocortex
Dev. Brain Res.
Long-term potentiation and NMDA receptors in rat visual cortex
Nature
Memory deficits associated with senescence: a neurophysiological and behavioral study in the rat
J. Comp. Physiol. Psychol.
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Age-related decline of neuroplasticity to intermittent theta burst stimulation of the lateral prefrontal cortex and its relationship with late-life memory performance
2020, Clinical NeurophysiologyCitation Excerpt :There have been numerous studies showing age-related changes in synaptic plasticity in animal models, particularly in the rodent hippocampus (Deupree et al., 1993; Moore et al., 1993; Rosenzweig et al., 1997; Barnes et al., 2000). However, perhaps most relevant to the present findings is the study by Baskys et al. (Baskys et al., 1990), which used neocortical slice preparations from young and aged rats to examine age-related differences in NMDA receptor function and LTP induction in frontoparietal cortex. While frontoparietal neocortical neurons from both groups responded to increasing doses of NMDA with increased membrane depolarisation, a much steeper dose-response relationship was observed in slices from young rats, suggesting reduced NMDA responsiveness in aged frontoparietal cortex.
Age-related deficits in a forebrain-dependent task, trace-eyeblink conditioning
2011, Neurobiology of AgingCitation Excerpt :Trace conditioning is also impaired with age (Graves and Solomon, 1985; Finkbiner and Woodruff-Pak, 1991; Kishimoto et al., 2001; Knuttinen et al., 2001a,b; Villarreal et al., 2004; Woodruff-Pak et al., 2007) and is initially dependent upon hippocampal processing (Solomon et al., 1986; Moyer et al., 1990; Kim et al., 1995; McGlinchey-Berroth et al., 1997; Clark and Squire, 1998; Weiss et al., 1999; Takehara et al., 2002; Tseng et al., 2004), a structure shown to exhibit age-related functional alterations (Landfield and Pitler, 1984; Moyer et al., 1992, 2000; Oh et al., 1999). The neocortex, the most likely site of permanent storage for trace associations (Eichenbaum et al., 1992; Christian and Thompson, 2003; Squire et al., 2004; Smith and Squire, 2009), also exhibits age-related functional alterations including a reduction in NMDAR-independent (Ohmura et al., 2003) and -dependent long-term-potentiation (LTP) (Baskys et al., 1990; Mullany and Lynch, 1997; Yoshimura et al., 2003); reduced LTP-induced protein expression (Mullany and Lynch, 1997); and an absence of layer IV metabolic barrel deprivation-induced reorganization (Skibinska et al., 2000). These studies suggest a loss in neocortical plasticity with age, indicating that neocortical memory consolidation may also be impaired with aging.
Expression of groups I and II metabotropic glutamate receptors in the rat brain during aging
2005, Brain ResearchCitation Excerpt :Activation of mGlu5 receptors positively modulates NMDA receptors (see Ref. [9] and references therein) and appears to be required for the induction of NMDA-dependent long-term potentiation (LTP) and spatial learning [17,20]. Thus, a reduced expression of mGlu5 receptors might contribute to the attenuation of NMDA-mediated responses observed in different brain regions of aged animals [4,7,16], and is in line with the evidence that potentiation of NMDA responses by DHPG is attenuated in the aged striatum [39]. Group II mGlu receptors (i.e., mGlu2 and -3 receptors) are negatively coupled to adenylyl cyclase activity, although they also regulate other signaling pathways, as well as a variety of membrane ion channels (reviewed by Refs. [11,44]).
Brain, aging and neurodegeneration: Role of zinc ion availability
2005, Progress in Neurobiology
This work was supported by the Ontario Mental Health Foundation and Medical Research Council of Canada. Authors wish to thank Dr. Martin Wojtowicz for his valuable suggestions and criticisms.
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Present address: Faculty of Medicine, Memorial University of Newfoundland, St. John's Newfoundland A1B 3V6, Canada.