Metaplastic contribution of neuropeptide Y receptors to spatial memory acquisition

Méndez-Couz, Marta; Manahan‐Vaughan, Denise; Silva, Ana P.; González-Pardo, Héctor; Árias, Jorge L.; Conejo, Nélida M.

doi:10.1016/j.bbr.2020.112864

Cited by 11 publications

(19 citation statements)

References 106 publications

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“…In this regard, stress and locomotor activity could have affected the performance in the MWM test. In previous studies with this model (Méndez-Couz et al, 2021), we found, however, no anxiogenic or anxiolytic behavioural effects, ruling out the exclusively stress-related treatment influence on the subsequent MWM task. Additionally, previous studies in knockout Y 2 R (-/-) mice failed to show alterations in locomotor activity (Redrobe et al, 2004;Tschenett et al, 2003) or anxiety-related behaviour (Zambello et al, 2011).…”

Section: Intrahippocampal Administration Of An Npy Y 2 R Antagonist Rapidly Improves the Early Recall Of Spatial Reference Memorycontrasting

confidence: 46%

“…In a previous NPY receptor expression study, we showed changes in spatial memory task performed under serial Y 2 R blockade (Méndez-Couz et al, 2021), associated with NPY Y 1 R and Y 2 R brain expression changes in the dorsal hippocampus and the prefrontal cortex, suggesting a rapid metaplastic regulation of NPY receptors contributing to spatial memory.…”

Section: Introductionmentioning

confidence: 63%

“…Regarding the specific effects of the NPYergic system on learning and memory, a growing body of literature suggests its involvement in the encoding and recall learning phases (Bertocchi et al, 2021;dos Santos et al, 2013;Hörmer et al, 2018;Méndez-Couz et al, 2021). Interestingly, NPY showed a neuroprotective role against methamphetamine-induced excitotoxicity in the hippocampus (Gonçalves et al, 2012) or against oxidative stress, via Y 2 R, preventing depressive behaviour and spatial memory deficits in mice (dos Santos et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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Hippocampal Neuropeptide Y₂receptor blockade improves spatial memory retrieval and modulates limbic brain metabolism

Méndez-Couz

González-Pardo

Árias

et al. 2021

Preprint

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IntroductionThe neuropeptide Y (NPY) is broadly distributed in the central nervous system (CNS), and it has been related to neuroprotective functions. NPY seems to be an important component to counteract brain damage and cognitive impairment mediated by drugs of abuse and neurodegenerative diseases, and both NPY and its Y2 receptor (Y2R) are highly expressed in the hippocampus, critical for learning and memory. We have recently demonstrated its influence on cognitive functions; however, the specific mechanism and involved brain regions where NPY modulates spatial memory by acting on Y2R remain unclear.MethodsHere, we examined the involvement of the hippocampal NPY Y2R in spatial memory and associated changes in brain metabolism by bilateral administration of the selective antagonist BIIE0246 into the rat dorsal hippocampus. To further evaluate the relationship between memory functions and neuronal activity, we analysed the regional expression of the mitochondrial enzyme cytochrome c oxidase (CCO) as an index of oxidative metabolic capacity in limbic and non-limbic brain regions.ResultsThe acute blockade of NPY Y2R significantly improved spatial memory recall in rats trained in the Morris water maze that matched metabolic activity changes in spatial memory processing regions. Specifically, CCO activity changes were found in the dentate gyrus of the dorsal hippocampus and CA1 subfield of the ventral hippocampus, the infralimbic region of the PFC and the mammillary bodies.ConclusionsThese findings suggest that the NPY hippocampal system, through its Y2R receptor, influences spatial memory recall (retrieval) and exerts control over patterns of brain activation that are relevant for associative learning, probably mediated by Y2R modulation of long-term potentiation and long-term depression.HighlightsUnder hippocampal Y2R antagonism, place preference memory retrieval is enhancedSpatial retrieval enhancement under Y2R blockade is correlated with changes in regional brain energy metabolismEnhanced retrieval associated CCO activity increases in the dorsal DG, while decreasing in the ventral CA1, IL cortex and mammillary bodiesY2R exert control over patterns of brain activation that are relevant for spatial memory expression

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Section: Intrahippocampal Administration Of An Npy Y 2 R Antagonist Rapidly Improves the Early Recall Of Spatial Reference Memorycontrasting

confidence: 46%

Section: Introductionmentioning

confidence: 63%

Section: Introductionmentioning

confidence: 99%

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Hippocampal Neuropeptide Y₂receptor blockade improves spatial memory retrieval and modulates limbic brain metabolism

Méndez-Couz

González-Pardo

Árias

et al. 2021

Preprint

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“…The hippocampus is very sensitive to insults and is commonly involved in cognitive impairment ( Fang et al, 2016 ). NPY and its receptors are highly expressed in the hippocampus and NPY is released as a co-transmitter with neurotransmitters such as GABA ( Méndez-Couz et al, 2021 ). Moreover, NPY exerts anti-inflammatory effects via Y1/Y2 receptors ( Wheway et al, 2007 ; Wang W. et al, 2019 ).…”

Section: Advances In Treatmentmentioning

confidence: 99%

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

Wang

Chen

Zhang

et al. 2021

Front. Aging Neurosci.

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Sevoflurane is one of the most widely used anesthetics for the induction and maintenance of general anesthesia in surgical patients. Sevoflurane treatment may increase the incidence of postoperative cognitive dysfunction (POCD), and patients with POCD exhibit lower cognitive abilities than before the operation. POCD affects the lives of patients and places an additional burden on patients and their families. Understanding the mechanism of sevoflurane-induced POCD may improve prevention and treatment of POCD. In this paper, we review the diagnosis of POCD, introduce animal models of POCD in clinical research, analyze the possible mechanisms of sevoflurane-induced POCD, and summarize advances in treatment for this condition.

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“…Several hypothalamic neuropeptidergic systems play a pivotal role in synchronizing the stress responses of animals with their feeding behavior [26]. Of these, neuropeptide Y (NPY) is associated with fear extinction, spatial memory, and stress-related behaviors such as anxiety [27,28]. Within the framework of the hypothalamus, it has been strongly linked to food intake [29][30][31].…”

Section: Introductionmentioning

confidence: 99%

Role for Histone Deacetylation in Traumatic Brain Injury-Induced Deficits in Neuropeptide Y in Arcuate Nucleus: Possible Implications in Feeding Behavior

et al. 2020

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Introduction: Repeated traumatic events result in long-lasting neuropsychiatric ailments, including neuroendocrine imbalances. Neuropeptide Y (NPY) in the arcuate nucleus (Arc) is an important orexigenic peptide. However, the molecular underpinnings of its dysregulation owing to traumatic brain injury remain unknown. Methods: Rats were subjected to repeated mild traumatic brain injury (rMTBI) using the closed-head weight drop model. Feeding behaviour and the regulatory epigenetic parameters of NPY expression were measured at 48 hrs and 30 days post rMTBI. Further, sodium butyrate, a pan-HDAC inhibitor, was administered to examine whether histone deacetylation is involved in NPY expression post rMTBI. Results: The rMTBI attenuated food intake, which was coincident with a decrease in NPY mRNA and protein levels in the Arc post rMTBI. Further, rMTBI also reduced the mRNA levels of the cAMP response element-binding protein (CREB) and CREB-binding protein (CBP) and altered the mRNA levels of the various isoforms of the histone deacetylases (HDACs). Concurrently, the acetylated H3-K9 levels and the binding of CBP at the NPY promoter in the Arc of the rMTBI-exposed rats were reduced. However, the treatment with sodium butyrate corrected the rMTBI-induced deficits in the H3-K9 acetylation levels and CBP occupancy at the NPY promoter, restoring both the NPY expression and the food intake. Conclusions: These findings suggest that histone deacetylation at the NPY promoter persistently controls NPY function in the Arc after rMTBI. This study also demonstrates the efficacy of HDAC inhibitors in mitigating trauma-induced neuroendocrine maladaptations in the hypothalamus.

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Metaplastic contribution of neuropeptide Y receptors to spatial memory acquisition

Cited by 11 publications

References 106 publications

Hippocampal Neuropeptide Y₂receptor blockade improves spatial memory retrieval and modulates limbic brain metabolism

Hippocampal Neuropeptide Y₂receptor blockade improves spatial memory retrieval and modulates limbic brain metabolism

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

Role for Histone Deacetylation in Traumatic Brain Injury-Induced Deficits in Neuropeptide Y in Arcuate Nucleus: Possible Implications in Feeding Behavior

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Metaplastic contribution of neuropeptide Y receptors to spatial memory acquisition

Cited by 11 publications

References 106 publications

Hippocampal Neuropeptide Y2receptor blockade improves spatial memory retrieval and modulates limbic brain metabolism

Hippocampal Neuropeptide Y2receptor blockade improves spatial memory retrieval and modulates limbic brain metabolism

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

Role for Histone Deacetylation in Traumatic Brain Injury-Induced Deficits in Neuropeptide Y in Arcuate Nucleus: Possible Implications in Feeding Behavior

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Hippocampal Neuropeptide Y₂receptor blockade improves spatial memory retrieval and modulates limbic brain metabolism

Hippocampal Neuropeptide Y₂receptor blockade improves spatial memory retrieval and modulates limbic brain metabolism