Interaction between M1-muscarinic and glutamatergic NMDA receptors on an inhibitory avoidance task

Moreira, Karin M.; Ferreira, Tatiana Lima; Fornari, Raquel Vecchio; Zeggio, Larissa; Oliveira, Maria Gabriela Menezes

doi:10.1016/j.brainresbull.2005.07.019

Cited by 17 publications

(5 citation statements)

References 37 publications

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“…In turn, attenuated M 1 mAChR functioning has been linked to disrupted memory processing. Administration of selective M 1 mAChR antagonists impaired the consolidation of long-term memory in rats (Moreira, Ferreira, Fornari, Figueredo, & Oliveira, 2005;Roldan, BolanosBadillo, Gonzales-Sanchez, Quirarte, & Prado-Alcala, 1997). And M 1 À/À knockout mice demonstrated selective long-term memory deficits (Anagnostaras et al, 2003).…”

Section: Discussionmentioning

confidence: 96%

M1 Muscarinic Acetylcholine Receptor Agonism Alters Sleep without Affecting Memory Consolidation

Nissen

Power

Nofzinger

et al. 2006

Journal of Cognitive Neuroscience

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Preclinical studies have implicated cholinergic neurotransmission, specifically M1 muscarinic acetylcholine receptor (mAChR) activation, in sleep-associated memory consolidation. In the present study, we investigated the effects of administering the direct M1 mAChR agonist RS-86 on pre-post sleep memory consolidation. Twenty healthy human participants were tested in a declarative word-list task and a procedural mirror-tracing task. RS-86 significantly reduced rapid eye movement (REM) sleep latency and slow wave sleep (SWS) duration in comparison with placebo. Presleep acquisition and postsleep recall rates were within the expected ranges. However, recall rates in both tasks were almost identical for the RS-86 and placebo conditions. These results indicate that selective M1 mAChR activation in healthy humans has no clinically relevant effect on pre-post sleep consolidation of declarative or procedural memories at a dose that reduces REM sleep latency and SWS duration.

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Section: Discussionmentioning

confidence: 96%

M1 Muscarinic Acetylcholine Receptor Agonism Alters Sleep without Affecting Memory Consolidation

Nissen

Power

Nofzinger

et al. 2006

Journal of Cognitive Neuroscience

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“…Several studies have established through pharmacological manipulations that interactive modulation between the cholinergic and glutamatergic neurotransmitters systems represents a critical mechanism in different cognitive functions [61], [62], [63], [64], [65], [66], [67]. Furthermore, interaction of these neurotransmitter systems in the hippocampus has also been reported to regulate cognitive tasks [68], [69], [70], [71].…”

Section: Discussionmentioning

confidence: 99%

Selective Cholinergic Depletion in Medial Septum Leads to Impaired Long Term Potentiation and Glutamatergic Synaptic Currents in the Hippocampus

et al. 2012

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Cholinergic depletion in the medial septum (MS) is associated with impaired hippocampal-dependent learning and memory. Here we investigated whether long term potentiation (LTP) and synaptic currents, mediated by alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate (AMPA) and N-methyl-D-aspartate (NMDA) receptors in the CA1 hippocampal region, are affected following cholinergic lesions of the MS. Stereotaxic intra-medioseptal infusions of a selective immunotoxin, 192-saporin, against cholinergic neurons or sterile saline were made in adult rats. Four days after infusions, hippocampal slices were made and LTP, whole cell, and single channel (AMPA or NMDA receptor) currents were recorded. Results demonstrated impairment in the induction and expression of LTP in lesioned rats. Lesioned rats also showed decreases in synaptic currents from CA1 pyramidal cells and synaptosomal single channels of AMPA and NMDA receptors. Our results suggest that MS cholinergic afferents modulate LTP and glutamatergic currents in the CA1 region of the hippocampus, providing a potential synaptic mechanism for the learning and memory deficits observed in the rodent model of selective MS cholinergic lesioning.

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“…Furthermore, although the glutamatergic and cholinergic systems can promote plasticity by independent mechanisms (Rosenblum et al, 2000;Hu et al, 2002;Lynch, 2004), it is worth noting that the interaction between these two systems was observed in hippocampus-dependent memory tasks (Moreira et al, 2005;Figueredo et al, 2008) and in in vitro studies of hippocampal slices (Isaac et al, 2009;Buchanan et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Hippocampal NMDA receptor blockade impairs CREB phosphorylation in amygdala after contextual fear conditioning

et al. 2013

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In contextual fear conditioning (CFC), hippocampus is thought to process environmental stimuli into a configural representation of the context and send it to amygdala nuclei, which current evidences point to be the site of CS-US association and fear memory storage. If it is true, hippocampus should influence learning-induced plasticity in the amygdala nuclei after CFC acquisition. To test this, we infused wistar rats with saline or AP5, a NMDA receptor antagonist, in the dorsal hippocampus just before a CFC session, in which they were conditioned to a single shock, exposed to the context with no shocks or received an immediate shock. The rats were perfused, their brains harvested and immunohistochemically stained for cAMP element binding protein (CREB) phosphorylation ratio (pCREB/CREB) in lateral (LA), basal (B) and central (CeA) amygdala nuclei. CFC showed a learning-specific increase in pCREB ratio in B and CeA, in conditioned-saline rats compared to context and immediate shocked ones. Further, conditioned rats that received AP5 showed a decrease in pCREB ratio in LA, B and CeA. Our results support the current ideas that the role of hippocampus in contextual fear conditioning occurs by sending contextual information to amygdala to serve as conditioned stimulus.

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Interaction between M1-muscarinic and glutamatergic NMDA receptors on an inhibitory avoidance task

Cited by 17 publications

References 37 publications

M1 Muscarinic Acetylcholine Receptor Agonism Alters Sleep without Affecting Memory Consolidation

M1 Muscarinic Acetylcholine Receptor Agonism Alters Sleep without Affecting Memory Consolidation

Selective Cholinergic Depletion in Medial Septum Leads to Impaired Long Term Potentiation and Glutamatergic Synaptic Currents in the Hippocampus

Hippocampal NMDA receptor blockade impairs CREB phosphorylation in amygdala after contextual fear conditioning

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