α2-Adrenoceptor modulation of long-term potentiation elicited in vivo in rat occipital cortex

Mondaca, Mauricio; Hernández, Alejandro; Pérez, Hernán; Valladares, Luis; Sierralta, Walter; Fernández, Vı́ctor; Soto-Moyano, Rubén

doi:10.1016/j.brainres.2004.07.020

Cited by 22 publications

(20 citation statements)

References 24 publications

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“…As opposed to yohimbine, administering the a2-adrenergic receptor agonist clonidine, which attenuates locus coeruleus discharge, noradrenergic activity, and LTP induction/maintenance (Abercrombie et al 1988;Mondaca et al 2004), disrupted both consolidation and reconsolidation of a contextual fear memory in a dose-dependent manner. Importantly, these effects are not attributable to a possible anxiolytic-like effect of this drug (Table 5).…”

Section: Discussionmentioning

confidence: 97%

“…Systemically administering adrenaline also increases noradrenaline release in the brain and facilitates the consolidation of emotion-driven memories (Gold and Van Buskirk 1975). Both yohimbine and adrenaline have been shown to strengthen the induction and maintenance of hippocampal LTP (Mondaca et al 2004;Korol and Gold 2008). As this type of neuronal plasticity is believed to sustain memories and depend on noradrenergic activity (Harley 1991), it is suggested that the effects produced by yohimbine and adrenaline may rely at least in part on this mechanism.…”

Section: Discussionmentioning

confidence: 99%

“…The yohimbine dose selection was based both on a pilot experiment, in which doses ranging from 0.5 to 2.5 mg/kg were tested, and on previously published studies showing its facilitating role in memory extinction and LTP induction (Mondaca et al 2004;and Bouton 2007). The choice of propranolol, nadolol, and prazosin doses was based on pilot experiments or studies where these drugs prevented the behavioral effects of selective agonists for a1-and b-adrenergic receptors (Do-Monte et al 2010a,b).…”

Section: Drugsmentioning

confidence: 99%

“…The choice of propranolol, nadolol, and prazosin doses was based on pilot experiments or studies where these drugs prevented the behavioral effects of selective agonists for a1-and b-adrenergic receptors (Do-Monte et al 2010a,b). The clonidine range was selected based on studies showing its ability to reduce both the brain's noradrenaline efflux and the LTP in vivo (Abercrombie et al 1988;Mondaca et al 2004). All solutions were prepared immediately before use and injected intraperitoneally in a volume of 1.0 mL/kg.…”

Section: Drugsmentioning

confidence: 99%

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Enhanced noradrenergic activity potentiates fear memory consolidation and reconsolidation by differentially recruiting α1- and β-adrenergic receptors

et al. 2013

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Consolidation and reconsolidation are phases of memory stabilization that diverge slightly. Noradrenaline is known to influence both processes, but the relative contribution of a1-and b-adrenoceptors is unclear. The present study sought to investigate this matter by comparing their recruitment to consolidate and/or reconsolidate a contextual fear memory trace under enhanced noradrenergic activity induced by yohimbine. We report that this a2-adrenoceptor antagonist was able to potentiate fear memory trace consolidation or reconsolidation when administered immediately after acquisition or retrieval, respectively, resulting in increased freezing expression. In either case, generalization of this response to an unpaired context was also seen when it achieved a ceiling level in the paired context. These effects endured for over 7 d and relied on action at central rather than peripheral sites, but were prevented when a memory trace was not acquired, when memory reactivation was omitted, or when administration of yohimbine was delayed until 6 h after acquiring or retrieving the memory trace. The b-adrenoceptor antagonist propranolol was able to prevent the above-mentioned effects of yohimbine, while pretreatment with the a1-adrenoceptor antagonist prazosin blocked only its facilitating effects on memory reconsolidation. These results highlight a differential participation of a1-and b-adrenoceptors in fear memory processing. Moreover, it was shown that the a2-adrenoceptor agonist clonidine, as opposed to yohimbine, mitigates fear expression by weakening memory consolidation or reconsolidation.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Section: Drugsmentioning

confidence: 99%

Section: Drugsmentioning

confidence: 99%

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Enhanced noradrenergic activity potentiates fear memory consolidation and reconsolidation by differentially recruiting α1- and β-adrenergic receptors

et al. 2013

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“…This results in NA release in the projection areas of the LC, for example, the basolateral amygdala, the hippocampus, and also the parahippocampus (Joyce et al, 1992;Berridge and Waterhouse, 2003). NA modulates activity in the basolateral amygdala and also mediates an increase in cortical neuronal responsiveness as well as in cortical synaptic plasticity (Mondaca et al, 2004;Flores et al, 2010;Tully and Bolshakov, 2010). Thus, the activation of the central noradrenergic system could affect processing in the parahippocampal cortex directly via afferents from the LC and/or indirectly via the basolateral amygdala (Suzuki, 1996).…”

Section: Functional Mri Datamentioning

confidence: 99%

Event-Related Nociceptive Arousal Enhances Memory Consolidation for Neutral Scenes

Schwarze

Bingel²,

Sommer³

2012

J. Neurosci.

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The superior memory for emotional events has been attributed to the beneficial effects of noradrenaline released into the amygdala attributable to arousal. Noradrenaline mediates the effects of different hormones and neurotransmitters, including adrenal stress hormones on consolidation ( Recently, it was highlighted that emotional stimuli elicit not only arousal but also intensify cognitive processes that contribute to the enhanced memory. In particular, the enhanced use of selective attention as well as the greater distinctiveness and semantic relatedness of emotional stimuli influence memory formation (Talmi et al., 2007a). The present study aimed to explore the effects of arousal on memory formation independent of these cognitive factors in an event-related manner. Arousal was induced by the application of a nociceptive stimulus briefly after the presentation of neutral scenes. The results show a purely arousal-driven memory enhancement for the neutral scenes that differs in critical aspects from the superior memory for emotional stimuli. In particular, the enhancement was only evident after consolidation and exclusively based on an increase in item familiarity but not recollection. Moreover, successful memory formation for stimuli followed by arousal was correlated with activity in the parahippocampal cortex but not the amygdala, as is the case for emotional stimuli.

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EGCG Ameliorates the Suppression of Long-Term Potentiation Induced by Ischemia at the Schaffer Collateral-CA1 Synapse in the Rat

Ding

Zhao

et al. 2011

Cell Mol Neurobiol

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The function of Epigallocatechin gallate (EGCG), a main component of green tea, has been widely investigated, amelioration of synaptic transmission and neuroprotective effects against ischemia-induced brain damage among others. However, the mechanism underlying is still unveiled. We investigated the effects of EGCG on high frequency stimulation-induced long-term potentiation (LTP) in the Schaffer collateral-CA1 synapse with or without cerebral ischemia injury induced by middle cerebral artery occlusion (MCAO) in vivo to examine the possible relations between EGCG and synaptic transmission. Application of EGCG modulated synaptic transmission and produced a dose-dependent improvement of the induction of LTP. However, relative high-dose EGCG can block the induction of LTP at the Schaffer collateral-CA1 synapse in normal rat in vivo. In addition, the effects of EGCG were observed on the infarct volume and neurological deficit in rats subjected to MCAO; furthermore, the cell viability of primary cultured rat hippocampal and cortical neurons suffered from oxygen-glucose deprivation were evaluated with MTT and LDH assay, which showed significant neuroprotective properties in vitro. Surprisingly, the contents of the glutamate (Glu), glycine (Gly), and gamma-aminobutyric acid amino acids were totally disequilibrated before and after cerebral ischemia injury and could be rebalanced to original level by application of EGCG. Our results suggest that EGCG is able to improve the efficiency of synaptic transmission in cerebral ischemia injury with attenuated effect related to the neuroprotection of EGCG through regulating excitatory and inhibitory amino acid balance.

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α2-Adrenoceptor modulation of long-term potentiation elicited in vivo in rat occipital cortex

Cited by 22 publications

References 24 publications

Enhanced noradrenergic activity potentiates fear memory consolidation and reconsolidation by differentially recruiting α1- and β-adrenergic receptors

Enhanced noradrenergic activity potentiates fear memory consolidation and reconsolidation by differentially recruiting α1- and β-adrenergic receptors

Event-Related Nociceptive Arousal Enhances Memory Consolidation for Neutral Scenes

EGCG Ameliorates the Suppression of Long-Term Potentiation Induced by Ischemia at the Schaffer Collateral-CA1 Synapse in the Rat

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