Rosiglitazone enhances learning, place cell activity, and synaptic plasticity in middle-aged rats

Wang, Boon Wan; Hok, Vincent; Della-Chiesa, Andrea; Callaghan, Charlotte K.; Barlow, Sally; Tsanov, Marian; Bechara, Ranya; Irving, Elaine; Virley, David; Upton, Neil; O’Mara, Shane M.

doi:10.1016/j.neurobiolaging.2011.08.013

Cited by 26 publications

(17 citation statements)

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“…Consistent with the results from HPWM test, significant LTP deficits were noticeable in 24 month-old mice and this decline was further exacerbated in 30 month-old mice. In rats, impairments in temporal/spatial learning memory (Morris, et al, 2013, Morris, et al, 1982, Morris, et al, 1986b, Moser, et al, 1998, Thibault and Landfield, 1996) and LTP (Rex, et al, 2005, Rex, et al, 2006, Wang, et al, 2012) begin as early as 18 months of age. The differences observed between rats and mice may be explained by species variance and/or methods used for experimentation or analysis.…”

Section: Discussionmentioning

confidence: 99%

Subacute ibuprofen treatment rescues the synaptic and cognitive deficits in advanced-aged mice

Rogers

Liu

Zhao

et al. 2017

Neurobiology of Aging

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Aging is accompanied by increased neuroinflammation, synaptic dysfunction and cognitive deficits both in rodents and humans, yet the onset and progression of these deficits throughout the life span remain unknown. These aging-related deficits affect the quality of life and present challenges to our aging society. Here, we defined age-dependent and progressive impairments of synaptic and cognitive functions and showed that reducing astrocyte-related neuroinflammation through anti-inflammatory drug treatment in aged mice reverses these events. By comparing young (3 months), middle-aged (18 months), aged (24 months) and advanced-aged wild-type mice (30 months), we found that the levels of an astrocytic marker, GFAP, progressively increased after 18 months of age, which preceded the decreases of the synaptic marker PSD-95. Hippocampal long-term potentiation (LTP) was also suppressed in an age-dependent manner, where significant deficits were observed after 24 months of age. Fear conditioning tests demonstrated that associative memory in the context and cued conditions was decreased starting at the ages of 18 and 30 months, respectively. When the mice were tested on hidden platform water maze, spatial learning memory was significantly impaired after 24 months of age. Importantly, subacute treatment with the anti-inflammatory drug ibuprofen suppressed astrocyte activation, and restored synaptic plasticity and memory function in advanced-aged mice. These results support the critical contribution of aging-related inflammatory responses to hippocampal-dependent cognitive function and synaptic plasticity, in particular during advanced aging. Our findings provide strong evidence that suppression of neuroinflammation could be a promising treatment strategy to preserve cognition during aging.

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Section: Discussionmentioning

confidence: 99%

Subacute ibuprofen treatment rescues the synaptic and cognitive deficits in advanced-aged mice

Rogers

Liu

Zhao

et al. 2017

Neurobiology of Aging

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“…Single hippocampal pyramidal cells and interneurons were identified using spike shape and firing frequency characteristics (Wilson & McNaughton, 1993;Csicsvari et al, 1999). Place fields were identified as described before (Wang et al, 2012). The firing map reflected the frequency of firing calculated from the top firing bins down to the bins with lowest firing rate by scaling them in decreasing intervals of 20% of the peak firing (Hollup et al, 2001;Brun et al, 2002).…”

Section: Criteria For Data Inclusionmentioning

confidence: 99%

Respiratory cycle entrainment of septal neurons mediates the fast coupling of sniffing rate and hippocampal theta rhythm

Tsanov

Chah

Reilly

et al. 2013

Eur J of Neuroscience

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Memory for odour information may result from temporal coupling between the olfactory and hippocampal systems. Respiration defines the frequency of olfactory perception, but how the respiratory rate affects hippocampal oscillations remains poorly understood. The afferent connectivity of the medial septum/diagonal band of Broca complex (MS/DB) proposes this region as a crossroads between respiratory and limbic pathways. Here we investigate if the firing rates of septal neurons integrate respiratory rate signals. We demonstrate that approximately 50% of MS/DB neurons are temporally correlated with sniffing frequency. Moreover, a group of slow-spiking septal neurons are phase-locked to the sniffing cycle. We show that inter-burst intervals of MS/DB theta cells relate to the sniff rate. Intranasal odour infusion evokes sniff phase preference for the activity of fast-spiking MS/DB neurons. Concurrently, the infusion augments the correlation between sniffing and limbic theta oscillations. During periods of sniffing–theta correlation, CA1 place cells fired preferentially during the inhalation phase, suggesting the theta cycle as a coherent time frame for central olfactory processing. Furthermore, injection of the GABAergic agonist muscimol into medial septum induces a parallel decrease of sniffing and theta frequencies. Our findings provide experimental evidence that MS/DB does not merely generate theta rhythm, but actively integrates sensorimotor stimuli that reflect sniffing rate. Such integration may provide temporal oscillatory synchronisation of MS/DB-innervated limbic structures with the sniffing cycle.

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“…In addition, increasing amounts of evidence demonstrate an association between dementia and T2DM (Janson et al 2004, Zhao & Townsend 2009, Kim et al 2010. In this context, anti-diabetic agents such as rosiglitazone and glucagon-like peptide (GLP-1) have been reported to negate cognitive decline (During et al 2003, Escribano et al 2009, Wang et al 2011. Recently developed oral anti-diabetic drugs, DDP-4 inhibitors including sitagliptin and vildagliptin, have been used to treat T2DM patients.…”

Section: Introductionmentioning

confidence: 99%

DPP-4 inhibitors improve cognition and brain mitochondrial function of insulin-resistant rats

Pintana

Apaijai²,

Chattipakorn³

2013

Journal of Endocrinology

172

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Recent evidence has demonstrated that insulin resistance is related to the development of type 2 diabetes mellitus. Our previous study found that high-fat diet (HFD) consumption caused not only peripheral and brain insulin resistance but also brain mitochondrial dysfunction and cognitive impairment. Vildagliptin and sitagliptin, dipeptidyl-peptidase-4 inhibitors, are recently developed anti-diabetic drugs. However, the effects of both drugs on cognitive behaviors and brain mitochondrial function in HFD-induced insulin-resistant rats have not yet been investigated. Sixty male Wistar rats were divided into two groups to receive either normal diet or HFD for 12 weeks. Rats in each group were then further divided into three treatment groups to receive either vehicle, vildagliptin (3 mg/kg per day), or sitagliptin (30 mg/kg per day) for 21 days. The cognitive behaviors of the rats were tested using the Morris Water Maze test. Blood samples were collected to determine metabolic parameters and plasma oxidative stress levels. Upon completion of the study, the animals were killed and the brains were removed to investigate brain and hippocampal mitochondrial function as well as to determine oxidative stress levels. We demonstrated that both drugs significantly improved the metabolic parameters and decreased circulating and brain oxidative stress levels in HFD-induced insulin-resistant rats. In addition, both drugs completely prevented brain and hippocampal mitochondrial dysfunction and equally improved the learning behaviors impaired by the HFD. Our findings suggest that the inhibition of dipeptidyl-peptidase-4 enzymes with vildagliptin or sitagliptin in insulinresistant rats not only increases peripheral insulin sensitivity but also decreases brain dysfunction. Key Words" insulin resistance " high-fat diet " DDP-4 inhibitors " memory decline " brain mitochondrial dysfunction

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Rosiglitazone enhances learning, place cell activity, and synaptic plasticity in middle-aged rats

Cited by 26 publications

References 100 publications

Subacute ibuprofen treatment rescues the synaptic and cognitive deficits in advanced-aged mice

Subacute ibuprofen treatment rescues the synaptic and cognitive deficits in advanced-aged mice

Respiratory cycle entrainment of septal neurons mediates the fast coupling of sniffing rate and hippocampal theta rhythm

DPP-4 inhibitors improve cognition and brain mitochondrial function of insulin-resistant rats

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