Modulation of Hippocampus-Dependent Learning and Synaptic Plasticity by Nicotine

Kenney, Justin W.; Gould, Thomas J.

doi:10.1007/s12035-008-8037-9

Cited by 217 publications

(197 citation statements)

References 212 publications

(274 reference statements)

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“…Because glial activation and neuronal loss were most prominent in the hippocampus, we next asked whether they influence hippocampal function. We therefore tested the performance of Cnr1 +/+ and Cnr1 −/− littermates in the Morris water maze (MWM) test, a behavioral paradigm that is highly dependent on hippocampal function (31). In the acquisition phase, we assessed the spatial learning and memory abilities of the mice, whereas on the reversal phase, we investigated the flexibility of memory (Fig.…”

Section: Age-related Reduction In Hippocampal Neuronal Number Andmentioning

confidence: 99%

Role of CB1 cannabinoid receptors on GABAergic neurons in brain aging

Albayram

Alferink

Pitsch

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

100

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Brain aging is associated with cognitive decline that is accompanied by progressive neuroinflammatory changes. The endocannabinoid system (ECS) is involved in the regulation of glial activity and influences the progression of age-related learning and memory deficits. Mice lacking the Cnr1 gene (Cnr1 −/− ), which encodes the cannabinoid receptor 1 (CB1), showed an accelerated agedependent deficit in spatial learning accompanied by a loss of principal neurons in the hippocampus. The age-dependent decrease in neuronal numbers in Cnr1 −/− mice was not related to decreased neurogenesis or to epileptic seizures. However, enhanced neuroinflammation characterized by an increased density of astrocytes and activated microglia as well as an enhanced expression of the inflammatory cytokine IL-6 during aging was present in the hippocampus of Cnr1 −/− mice. The ongoing process of pyramidal cell degeneration and neuroinflammation can exacerbate each other and both contribute to the cognitive deficits. Deletion of CB1 receptors from the forebrain GABAergic, but not from the glutamatergic neurons, led to a similar neuronal loss and increased neuroinflammation in the hippocampus as observed in animals lacking CB1 receptors in all cells. Our results suggest that CB1 receptor activity on hippocampal GABAergic neurons protects against age-dependent cognitive decline by reducing pyramidal cell degeneration and neuroinflammation.glial regulation | Morris water maze | stereological quantification | CD40 expression | telemetric EEG recording

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Section: Age-related Reduction In Hippocampal Neuronal Number Andmentioning

confidence: 99%

Role of CB1 cannabinoid receptors on GABAergic neurons in brain aging

Albayram

Alferink

Pitsch

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

100

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“…Because nicotinic agonists are known as memory enhancers (Leiser et al, 2009;Levin, 2012), nicotinic acetylcholine receptors (nAChRs) are also potential targets against cognitive decline in Alzheimer's disease (Wallace and Bertrand, 2013). The nAChR agonist nicotine (Nic) is of particular interest, given its pro-cognitive effects on learning, memory, and attention (Kenney and Gould, 2008;Changeux, 2010;Gould and Leach, 2014), as well as its modulatory influence on synaptic plasticity and glutamatergic transmission in cortico-limbic circuits (Lambe et al, 2003;Poorthuis and Mansvelder, 2013). Nic treatments could, therefore, modulate cognitive and neurophysiological variables in animal models of Alzheimer's disease, which requires further investigation.…”

Section: Introductionmentioning

confidence: 99%

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

et al. 2017

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Abstract-Brain glucose metabolism is altered in sporadic Alzheimer's disease (sAD), whose pathologies are reproduced in rodents by intracerebroventricular (icv) infusion of streptozotocin (STZ) in subdiabetogenic doses. The icv-STZ model also culminates in central cholinergic dysfunctions, which in turn are known to underlie both the sAD cognitive decline, and synaptic plasticity impairments. Considering the cognitive-enhancing potential of chronic nicotine (Nic), we investigated whether it attenuates icv-STZ-induced impairments in recognition memory and synaptic plasticity in a cognition-relevant substrate: the hippocampal CA1-medial prefrontal cortex (mPFC) pathway. Rats treated with icv-STZ were submitted to a chronic Nic regime, and were evaluated for recognition memory. We then examined long-term potentiation (LTP), paired-pulse facilitation (PPF) under urethane anesthesia, and brains were also evaluated for hippocampus-mPFC cell density. We found that Nic treatment prevents icv-STZ-induced disruptions in recognition memory and LTP. STZ did not precipitate neuronal death, while Nic alone was associated with higher neuronal density in CA1 when compared to vehicle-injected animals. Through combining behavioral, neurophysiological, and neuropathological observations into the Nic-STZ interplay, our study reinforces that cholinergic treatments are of clinical importance against earlystage Alzheimer's disease and mild cognitive impairments.

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“…The administration of cocaine or nicotine modifies spatial memory and synaptic plasticity in the DG (Scerri et al 2006;Kenney and Gould 2008;Perez et al 2010;Fole et al 2011;Iniguez et al 2012). Lesion of the DG blocks cocaine-induced conditioned place preference (CPP) (Meyers et al 2006;Hernandez-Rabaza et al 2008).…”

mentioning

confidence: 99%

D1/D5 receptors and histone deacetylation mediate the Gateway Effect of LTP in hippocampal dentate gyrus

et al. 2014

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The dentate gyrus (DG) of the hippocampus is critical for spatial memory and is also thought to be involved in the formation of drug-related associative memory. Here, we attempt to test an aspect of the Gateway Hypothesis, by studying the effect of consecutive exposure to nicotine and cocaine on long-term synaptic potentiation (LTP) in the DG. We find that a single injection of cocaine does not alter LTP. However, pretreatment with nicotine followed by a single injection of cocaine causes a substantial enhancement of LTP. This priming effect of nicotine is unidirectional: There is no enhancement of LTP if cocaine is administrated prior to nicotine. The facilitation induced by nicotine and cocaine can be blocked by oral administration of the dopamine D1/D5 receptor antagonist (SKF 83566) and enhanced by the D1/D5 agonist (SKF 38393). Application of the histone deacetylation inhibitor suberoylanilide hydroxamic acid (SAHA) simulates the priming effect of nicotine on cocaine. By contrast, the priming effect of nicotine on cocaine is blocked in genetically modified mice that are haploinsufficient for the CREB-binding protein (CBP) and possess only one functional CBP allele and therefore exhibit a reduction in histone acetylation. These results demonstrate that the DG of the hippocampus is an important brain region contributing to the priming effect of nicotine on cocaine. Moreover, both activation of dopamine-D1 receptor/ PKA signaling pathway and histone deacetylation/CBP mediated transcription are required for the nicotine priming effect in the DG.

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Modulation of Hippocampus-Dependent Learning and Synaptic Plasticity by Nicotine

Cited by 217 publications

References 212 publications

Role of CB1 cannabinoid receptors on GABAergic neurons in brain aging

Role of CB1 cannabinoid receptors on GABAergic neurons in brain aging

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

D1/D5 receptors and histone deacetylation mediate the Gateway Effect of LTP in hippocampal dentate gyrus

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