scholarly journals Increasing CREB in the dorsal hippocampus is sufficient to induce spatial memory

2009 ◽  
Vol 3 ◽  
Author(s):  
Josselyn Sheena
Keyword(s):  
Spatial Memory ◽  
Dorsal Hippocampus

scholarly journals Pharmacological Blockade of PPARα Exacerbates Inflammatory Pain-Related Impairment of Spatial Memory in Rats

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 610
Author(s):  
Jessica C. Gaspar ◽  
Catherine Healy ◽  
Mehnaz I. Ferdousi ◽  
Michelle Roche ◽  
David P. Finn
Keyword(s):  
Spatial Memory ◽  
Cognitive Processing ◽  
Inflammatory Pain ◽  
Dorsal Hippocampus ◽  
Memory Function ◽  
Intraperitoneal Administration ◽  
Compensatory Mechanism ◽  
Chronic Inflammatory Pain ◽  
Pharmacological Blockade ◽  
Innate Anxiety

Peroxisome proliferator-activated receptors (PPARs) are ligand-dependent transcription factors that exist in three isoforms: PPARα, PPARβ/δ and PPARγ. Studies suggest that the PPAR signalling system may modulate pain, anxiety and cognition. The aim of the present study was to investigate whether endogenous signalling via PPARs differentially modulates innate anxiety responses and mnemonic function in the presence and absence of inflammatory pain. We examined the effects of intraperitoneal administration of GW6471 (PPARα antagonist), GSK0660 (PPARβ/δ antagonist), GW9662 (PPARγ antagonist), and N-palmitoylethanolamide (PEA) on rat behaviour in the elevated plus maze (EPM), open field (OF), light-dark box (LDB), and novel object recognition (NOR) tests in the presence or absence of chronic inflammatory pain. Complete Freund’s Adjuvant (CFA)-injected rats exhibited impaired recognition and spatial mnemonic performance in the NOR test and pharmacological blockade of PPARα further impaired spatial memory in CFA-treated rats. N-oleoylethanolamide (OEA) levels were higher in the dorsal hippocampus in CFA-injected animals compared to their counterparts. The results suggest a modulatory effect of CFA-induced chronic inflammatory pain on cognitive processing, but not on innate anxiety-related responses. Increased OEA-PPARα signalling may act as a compensatory mechanism to preserve spatial memory function following CFA injection.

Partial unilateral inactivation of the dorsal hippocampus impairs spatial memory in the MWM

2005 ◽  
Vol 25 (3) ◽  
pp. 741-746 ◽  
Author(s):  
José M. Cimadevilla ◽  
Ruben Miranda ◽  
Laudino López ◽  
Jorge L. Arias
Keyword(s):  
Spatial Memory ◽  
Dorsal Hippocampus

scholarly journals Hippocampal Infusion of Zeta Inhibitory Peptide Impairs Recent, but Not Remote, Recognition Memory in Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Jena B. Hales ◽  
Amber C. Ocampo ◽  
Nicola J. Broadbent ◽  
Robert E. Clark
Keyword(s):  
Object Recognition ◽  
Recognition Memory ◽  
Spatial Memory ◽  
Dorsal Hippocampus ◽  
Late Phase ◽  
Recognition Task ◽  
Long Term Potentiation ◽  
Inhibitory Peptide ◽  
Term Potentiation ◽  
Novel Object Recognition Task

Spatial memory in rodents can be erased following the infusion of zeta inhibitory peptide (ZIP) into the dorsal hippocampus via indwelling guide cannulas. It is believed that ZIP impairs spatial memory by reversing established late-phase long-term potentiation (LTP). However, it is unclear whether other forms of hippocampus-dependent memory, such as recognition memory, are also supported by hippocampal LTP. In the current study, we tested recognition memory in rats following hippocampal ZIP infusion. In order to combat the limited targeting of infusions via cannula, we implemented a stereotaxic approach for infusing ZIP throughout the dorsal, intermediate, and ventral hippocampus. Rats infused with ZIP 3–7 days after training on the novel object recognition task exhibited impaired object recognition memory compared to control rats (those infused with aCSF). In contrast, rats infused with ZIP 1 month after training performed similar to control rats. The ability to form new memories after ZIP infusions remained intact. We suggest that enhanced recognition memory for recent events is supported by hippocampal LTP, which can be reversed by hippocampal ZIP infusion.

scholarly journals Hydrophilic Glycoproteins of an Edible Green Alga Capsosiphon fulvescens Prevent Aging-Induced Spatial Memory Impairment by Suppressing GSK-3β-Mediated ER Stress in Dorsal Hippocampus

Marine Drugs ◽  
2019 ◽  
Vol 17 (3) ◽  
pp. 168 ◽  
Author(s):  
Jeong Oh ◽  
Taek-Jeong Nam
Keyword(s):  
Oral Administration ◽  
Spatial Memory ◽  
Er Stress ◽  
Cognitive Dysfunction ◽  
Memory Impairment ◽  
Glycogen Synthase ◽  
Dorsal Hippocampus ◽  
Extracellular Signal ◽  
Capsosiphon Fulvescens ◽  
Gsk 3Β

Endoplasmic reticulum (ER) stress is involved in various neurodegenerative disorders. We previously found that Capsosiphon fulvescens (C. fulvescens) crude proteins enhance spatial memory by increasing the expression of brain-derived neurotrophic factor (BDNF) in rat dorsal hippocampus. The present study investigated whether the chronic oral administration of hydrophilic C. fulvescens glycoproteins (Cf-hGP) reduces aging-induced cognitive dysfunction by regulating ER stress in the dorsal hippocampus. The oral administration of Cf-hGP (15 mg/kg/day) for four weeks attenuated the aging-induced increase in ER stress response protein glucose-regulated protein 78 (GRP78) in the synaptosome of the dorsal hippocampus; this was attenuated by the function-blocking anti-BDNF antibody (1 μg/μL) and a matrix metallopeptidase 9 inhibitor 1 (5 μM). Aging-induced GRP78 expression was associated with glycogen synthase kinase-3 beta (GSK-3β) (Tyr216)-mediated c-Jun N-terminal kinase phosphorylation, which was downregulated upon Cf-hGP administration. The Cf-hGP-induced increase in GSK-3β (Ser9) phosphorylation was downregulated by inhibiting tyrosine receptor kinase B and extracellular signal-regulated kinase (ERK)1/2 with cyclotraxin-B (200 nM) and SL327 (10 μM), respectively. Cf-hGP administration or the inhibition of ER stress with salubrinal (1 mg/kg, i.p.) significantly decreased aging-induced spatial memory impairment. These findings suggest that the activation of the synaptosomal BDNF-ERK1/2 signaling in the dorsal hippocampus by Cf-hGP attenuates age-dependent ER stress-induced cognitive dysfunction.

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