The evidence for hippocampal long-term potentiation as a basis of memory for simple tasks

Izquierdo, Iván; Cammarota, Martı́n; Silva, Weber C. Da; Bevilaqua, Lia R.; Rossato, Janine I.; Bonini, Juliana Sartori; Mello, Pâmela Billig; Benetti, Fernando; Costa, Jaderson Costa da; Medina, Jorge H.

doi:10.1590/s0001-37652008000100007

Cited by 39 publications

(29 citation statements)

References 128 publications

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“…LTP-like synaptic enhancement occurs at thalamo-cortical synapses during perceptual learning on a visual task (Cooke and Bear 2012) and in the hippocampal CA1 region during inhibitory avoidance learning (Whitlock et al 2006). The molecular requirement for experimental models of neuronal plasticity, experience-dependent forms of plasticity, and memory overlap significantly (Izquierdo et al 2008;Smith et al 2009;Ye and Carew 2010;Johansen et al 2011;Korb and Finkbeiner 2011), and altering this requirement by molecular manipulations frequently alters all three processes (Nedivi 1999). Accordingly, CaN inhibition enhances memory, whether achieved pharmacologically (Christie-Fougere et al 2009), by expression of a CaN inhibitor in forebrain excitatory neurons (Malleret et al 2001;Baumgartel et al 2008), or through antisense oligonucleotide-mediated knockdown, applied pre-training (Ikegami and Inokuchi 2000) or post-training (Gerdjikov and Beninger 2005).…”

Section: Basic Properties Of Canmentioning

confidence: 99%

Neural functions of calcineurin in synaptic plasticity and memory: Figure 1.

2012

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Major brain functions depend on neuronal processes that favor the plasticity of neuronal circuits while at the same time maintaining their stability. The mechanisms that regulate brain plasticity are complex and engage multiple cascades of molecular components that modulate synaptic efficacy. Protein kinases (PKs) and phosphatases (PPs) are among the most important of these components that act as positive and negative regulators of neuronal signaling and plasticity, respectively. In these cascades, the PP protein phosphatase 2B or calcineurin (CaN) is of particular interest because it is the only Ca 2+ -activated PP in the brain and a major regulator of key proteins essential for synaptic transmission and neuronal excitability. This review describes the primary properties of CaN and illustrates its functions and modes of action by focusing on several representative targets, in particular glutamate receptors, striatal enriched protein phosphatase (STEP), and neuromodulin (GAP43), and their functional significance for synaptic plasticity and memory.

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Section: Basic Properties Of Canmentioning

confidence: 99%

Neural functions of calcineurin in synaptic plasticity and memory: Figure 1.

2012

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“…Apparently, SC animals did not demand the fear-conditioning circuits to avoid the shock, since their areas related to attention and memory consolidation (cortex and hippocampus) were intact [28]. There is evidence that LTP occurs in Py and DG [39,40] and also that 7 receptors are involved with this process [1,3,5].…”

Section: Relationship Between Increases In 7 Density and Memory Maintmentioning

confidence: 99%

Chronic Infusion of Amyloid-β Peptide and Sustained Attention Altered α7 Nicotinic Receptor Density in the Rat Brain

Viel

Caetano²,

Albuquerque³

et al. 2012

CAR

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2012Chronic infusion of amyloid-peptide and sustained attention altered 7 nicotinic receptor density in the rat brain Current Alzheimer Research, Sharjah, v. 9, n. 10, supl., Part 2, pp. 1210-1220, dec, 2012 Abstract: It is already known that progressive degeneration of cholinergic neurons in brain areas such as the hippocampus and the cortex leads to memory deficits, as observed in Alzheimer's disease. This work verified the effects of the infusion of amyloid-(A ) peptide associated to an attentional rehearsal on the density of 7 nicotinic cholinergic receptor (nAChR) in the brain of male Wistar rats. Animals received intracerebroventricular infusion of A or vehicle (control -C) and their attention was stimulated weekly (Stimulated A group: S-A and Stimulated Control group: SC) or not (NonStimulated A group: N-SA and Non-Stimulated Control group: N-SC), using an active avoidance apparatus. Conditioned avoidance responses (CAR) were registered. Chronic infusion of A caused a 37% reduction in CAR for N-SA . In S-A , this reduction was not observed. At the end, brains were extracted and autoradiography for 7 nAChR was conducted using [125 I]--bungarotoxin. There was an increase in 7 density in hippocampus, cortex and amygdala of SA animals, together with the memory preservation. In recent findings from our lab using mice infused with A and the 7 antagonist methyllycaconitine, and stimulated weekly in the same apparatus, it was observed that memory maintenance was abolished. So, the increase in 7 density in brain areas related to memory might be related to a participation of this receptor in the long-lasting change in synaptic plasticity, which is important to improve and maintain memory consolidation.

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“…The hippocampal formation (HF) is critical to memory and cognition (Blozovski, 1983; Izquierdo et al, 2008), and mediates the influences of nicotine on memory (Blozovski, 1985; Davis et al, 2007). The HF includes four main subregions (Amaral and Witter, 1995); the dentate gyrus, the hippocampal proper (including CA1, CA2 and CA3 regions), the subicular complex (including subiculum (Sb)), and the entorhinal cortex (EC; including layers I through VI).…”

Section: Introductionmentioning

confidence: 99%

“…Each subregion plays distinct roles in memory and cognition (Hunsaker et al, 2008; Li and Chao, 2008). Thus far, investigations regarding the influence of nicotine on hippocampal neurons have been focused on the hippocampal proper and dentate regions (Alkondon and Albuquerque, 2001; Fayuk and Yakel, 2004, 2005; Frazier et al, 1998a, 1998b; Jones and Yakel, 1997; Khiroug et al, 2003; Klein and Yakel, 2005; McQuiston and Madison, 1999; Sudweeks and Yakel, 2000; Welsby et al, 2007); this is likely due to the well-studied role of this region in learning and memory (Chen et al, 2006; Hasselmo, 2005; Hunsaker et al, 2008; Izquierdo et al, 2008; Lee et al, 2005; Li and Chao, 2008) and the ability of nicotine to induce synaptic potentiation (Fujii et al, 1999, 2000; Gray et al, 1996; He et al, 2003; Hunter et al, 1994; Matsuyama et al, 2000; Sawada et al, 1994). However, whether nicotine influences neurons in either the subicular complex or EC is still unknown.…”

Section: Introductionmentioning

confidence: 99%

Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex

Tu¹,

Gu²,

Shen³

et al. 2009

J. Neurosci.

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The entorhinal cortex (EC) is a part of the hippocampal complex that is essential to learning and memory, and nicotine affects memory by activating nicotinic acetylcholine receptors (nAChRs) in the hippocampal complex. However, it is not clear what types of neurons in the EC are sensitive to nicotine and whether they play a role in nicotine-induced memory functions. Here, we have used voltage-sensitive dye imaging methods to locate the neuronal populations responsive to nicotine in entorhino-hippocampal slices and to clarify which nAChR subtypes are involved. In combination with patch-clamp methods, we found that a concentration of nicotine comparable to exposure during smoking depolarized neurons in layer VI of the EC (ECVI) by acting through the non-␣7 subtype of nAChRs. Neurons in the subiculum (Sb; close to the deep EC layers) also contain nicotine-sensitive neurons, and it is known that Sb neurons project to the ECVI. When we recorded evoked EPSCs (eEPSCs) from ECVI neurons while stimulating the Sb near the CA1 region, a low dose of nicotine not only enhanced synaptic transmission (by increasing eEPSC amplitude) but also enhanced plasticity by converting tetanus stimulationinduced short-term potentiation to long-term potentiation; nicotine enhanced synaptic transmission and plasticity of ECVI synapses by acting on both the ␣7 and non-␣7 subtypes of nAChRs. Our data suggest that ECVI neurons are important regulators of hippocampal function and plasticity during smoking.

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The evidence for hippocampal long-term potentiation as a basis of memory for simple tasks

Cited by 39 publications

References 128 publications

Neural functions of calcineurin in synaptic plasticity and memory: Figure 1.

Neural functions of calcineurin in synaptic plasticity and memory: Figure 1.

Chronic Infusion of Amyloid-β Peptide and Sustained Attention Altered α7 Nicotinic Receptor Density in the Rat Brain

Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex

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The evidence for hippocampal long-term potentiation as a basis of memory for simple tasks

Cited by 39 publications

References 128 publications

Neural functions of calcineurin in synaptic plasticity and memory: Figure 1.

Neural functions of calcineurin in synaptic plasticity and memory: Figure 1.

Chronic Infusion of Amyloid-&beta; Peptide and Sustained Attention Altered &alpha;7 Nicotinic Receptor Density in the Rat Brain

Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex

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Chronic Infusion of Amyloid-β Peptide and Sustained Attention Altered α7 Nicotinic Receptor Density in the Rat Brain