Sulindac improves memory and increases NMDA receptor subunits in aged Fischer 344 rats

Mesches, Michael H.; Gemma, Carmelina; Veng, Lone; Allgeier, Chrissy; Young, David A.; Browning, Michael; Bickford, Paula C.

doi:10.1016/s0197-4580(03)00116-7

Cited by 78 publications

(67 citation statements)

References 64 publications

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“…Down-regulation of NR1 and NR2B expression has been found in the brains of APP transgenic mice (Dewachter et al 2009), aged rats (Mesches et al 2004), and AD patients (Amada et al 2005;Hynd et al 2004). As mentioned above, significant memory decline was associated with a decrease in NR1 and NR2B expression after 30 days of chronic excess formaldehyde treatment (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…NR2B, one of the subunits of N-methyl-D-aspartate (NMDA) receptor, is critical in regulating the agedependent synaptic plasticity and memory formation (Tang et al 1999). In addition, expression of NR1 and NR2B markedly decreases in the hippocampus of APP transgenic mice, aged rats (Mesches et al 2004), and AD patients (Amada et al 2005;Hynd et al 2004). However, which endogenous factors associated with the decline in NR1/NR2B expression contribute to memory impairment has not been ascertained.…”

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confidence: 99%

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Accumulated hippocampal formaldehyde induces age-dependent memory decline

Tong

Han

Luo

et al. 2012

AGE

187

151

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Aging is an important factor in memory decline in aged animals and humans and in Alzheimer's disease and is associated with the impairment of hippocampal long-term potentiation (LTP) and downregulation of NR1/NR2B expression. Gaseous formaldehyde exposure is known to induce animal memory loss and human cognitive decline; however, it is unclear whether the concentrations of endogenous formaldehyde are elevated in the hippocampus and how excess formaldehyde affects LTP and memory formation during the aging process. In the present study, we report that hippocampal formaldehyde accumulated in memorydeteriorating diseases such as age-related dementia. Spatial memory performance was gradually impaired in normal Sprague-Dawley rats by persistent intraperitoneal injection with formaldehyde. Furthermore, excess formaldehyde treatment suppressed the hippocampal LTP formation by blocking N-methyl-D-aspartate (NMDA) receptor. Chronic excess formaldehyde treatment over a period of 30 days markedly decreased the viability of the hippocampus and down-regulated the expression of the NR1 and NR2B subunits of the NMDA receptor. Our results indicate that excess endogenous formaldehyde is a critical factor in memory loss in age-related memory-deteriorating diseases.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Accumulated hippocampal formaldehyde induces age-dependent memory decline

Tong

Han

Luo

et al. 2012

AGE

187

151

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“…Classically, COX-2 is considered the inducible form of COX and IL-1β strongly upregulates COX-2 mRNA within brain glial cells (O'Banion et al, 1996). Furthermore, selective COX-2 inhibitors prevent impairments from LPS, immobilization stress, traumatic brain injury, and aging, although to our knowledge selective COX-1 inhibitors have never been examined (Jain et al, 2002;Mesches et al, 2004;Gopez et al, 2005;Bishnoi et al, 2005;Dhir et al, 2006). Therefore, COX-2 seems critically involved in memory impairments from elevated PG levels, however a role for COX-1 cannot be ruled out.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, a number of studies have shown that COX inhibitors can reverse memory impairments produced by LPS injection, immobilization stress, traumatic brain injury, and aging (Mesches et al, 2004;Shaw et al, 2005;Gopez et al, 2005;Bishnoi et al, 2005;Dhir et al, 2006), all of which increase brain levels of IL-1β. However, many pro-inflammatory processes other than elevated IL-1β levels are also engaged by the above manipulations.…”

Section: Nih Public Accessmentioning

confidence: 99%

Prostaglandins are necessary and sufficient to induce contextual fear learning impairments after interleukin-1 beta injections into the dorsal hippocampus

et al. 2007

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The intra-hippocampal administration of interleukin-1β (IL-1β) as well as the induction of elevated but physiological levels of IL-1β within the hippocampus interferes with the formation of long-term memory. There is evidence suggesting that the induction of prostaglandin (PG) formation by IL-1β is involved in impairments in working and spatial memory following IL-1β. The present experiments extend these findings by showing that PGs are responsible for memory deficits in contextual fear conditioning that occur following IL-1β injection into the dorsal hippocampus. Cyclooxygenase (COX) inhibition blocked the disruption in contextual fear conditioning produced by IL-1β and COX inhibition alone also disrupted contextual memory, suggesting an inverted Ushaped relationship between PG levels and memory. In addition to demonstrating the necessity of PGs in IL-1β mediated memory deficits, we also show that PGs injected directly into the dorsal hippocampus are sufficient to impair context memory and significantly reduce post-conditioning levels of BDNF within the hippocampus, suggesting a possible mechanism for the memory-impairing effects of PGs. Keywords memory; brain derived neurotrophic factor; cyclooxygenase; EP receptorThe pro-inflammatory cytokine interleukin-1β (IL-1β) exerts powerful central and peripheral actions. Recently, there has been considerable interest in its influence within the brain on learning and memory. This interest initially derived in part from findings that Alzheimer's disease and AIDS-related dementia are associated with elevated brain levels of IL-1β (Griffen et al., 1989;Lombardi et al., 1999). More direct evidence implicating IL-1β in learning and memory has come from animal studies. Manipulations that increase levels of IL-1β within the hippocampus have been shown to impair memory formation. These manipulations include the injection of the gram-negative bacterial component lipopolysaccharide (LPS;Pugh et al. 1998), social isolation stress (Pugh et al., 1999), and aging (Gemma et al., 2005). The blockade of IL-1 receptors and/or the inhibition of IL-1 synthesis prevents these memory impairments, supporting the conclusion that they are mediated by IL-1β (Pugh et al. 1998;Pugh et al., 1999;Gemma et al., 2005). Moreover, direct injection of IL-1β into the dorsal hippocampus Tel.: +1 303 492 9616; fax: +1 303 492 2967., E-mail address: amy.hein@colorado.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. (Barrientos et al., 2002). Consistent with these data, IL-1β potently inhibits long-term potentiation (LTP), a form of synaptic strengthenin...

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“…For example, the cingulate cortex participates in the regulation of contextual fear conditioning (Frankland et al, 2004) and in the affective response to pain (Johansen et al, 2001). Aging leads to deficits in contextual fear conditioning Mesches et al, 2004;Gemma et al, 2006), as does mutation of the 5-HT 7 receptor (Roberts et al, 2004). If the age-related decrease in 5-HT 7 receptor mRNA expression in the cingulate cortex is also associated with a decrease in 5-HT 7 receptors, it would likely contribute to aging deficits in contextual fear conditioning.…”

Section: Discussionmentioning

confidence: 99%

Expression of 5-HT7 receptor mRNA in the hamster brain: Effect of aging and association with calbindin-D28K expression

Duncan

Franklin

2007

Brain Research

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Aging affects several processes modulated by the 5-HT 7 receptor subtype, including circadian rhythms, learning and memory, and depression. Previously, we showed that aging induces a decrease in the hamster dorsal raphe (DRN) in both 5-HT 7 receptor binding and circadian phase resetting responses to 8-OH-DPAT microinjection. To elucidate the mechanisms underlying the aging decrease in 5-HT 7 receptors, we investigated aging modulation of 5-HT 7 receptor mRNA expression in the DRN, brain regions afferent to the DRN, and brain regions regulating circadian rhythms or memory. In situ hybridization for 5-HT 7 receptor mRNA was performed on coronal sections prepared from the brains of young, middle-aged, and old male Syrian hamsters. 5-HT 7 receptor mRNA expression was quantified by densitometry of X-ray film autoradiograms. The results showed that aging did not significantly affect 5-HT 7 receptor mRNA expression in the DRN or most other brain regions examined, with the exception of the cingulate cortex and paraventricular thalamic nucleus. Within the suprachiasmatic nucleus, the site of the master circadian pacemaker in mammals, 5-HT 7 receptor mRNA expression was localized in a discrete subregion resembling the calbindin subnucleus previously described. A second experiment using adjacent tissue sections showed that 5-HT 7 receptor mRNA and calbindin mRNAs were concentrated in the same region of the SCN, and as well as in the same region of several other brain structures. The localization of 5-HT 7 receptors and calbindin mRNAs within the same regions suggests that proteins they encode may interact to modulate processes such as circadian timekeeping.

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Sulindac improves memory and increases NMDA receptor subunits in aged Fischer 344 rats

Cited by 78 publications

References 64 publications

Accumulated hippocampal formaldehyde induces age-dependent memory decline

Accumulated hippocampal formaldehyde induces age-dependent memory decline

Prostaglandins are necessary and sufficient to induce contextual fear learning impairments after interleukin-1 beta injections into the dorsal hippocampus

Expression of 5-HT7 receptor mRNA in the hamster brain: Effect of aging and association with calbindin-D28K expression

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