The Effect of Catecholamines on Learning in Rats

Merlo, Alicia; Izquierdo, Iván

doi:10.1159/000137009

Cited by 10 publications

(6 citation statements)

References 2 publications

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“…This is unlikely, however, given that NE enhances, rather than impedes, memory formation and extinction through β-AR activation (McGaugh, 2000; Mueller and Cahill, 2010). Furthermore, research has demonstrated that β-AR blockade impairs extinction (for review, see Mueller and Cahill, 2010) across multiple memory paradigms (Merlo and Izquierdo, 1967; LaLumiere and Kalivas, 2008; Mueller et al, 2008; Do-Monte et al, 2010). …”

Section: Discussionmentioning

confidence: 99%

Neurobiological Dissociation of Retrieval and Reconsolidation of Cocaine-Associated Memory

2013

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Drug use is provoked by the presentation of drug-associated cues, even following long periods of abstinence. Disruption of these learned associations would therefore limit relapse susceptibility. Drug-associated memories are susceptible to long-term disruption during retrieval and shortly after, during memory reconsolidation. Recent evidence reveals that retrieval and reconsolidation are dependent on β-adrenergic receptor (β-AR) activation. Despite this, whether retrieval and reconsolidation are dependent on identical or distinct neural mechanisms is unknown. The prelimbic medial prefrontal cortex (PL-mPFC) and basolateral amygdala (BLA) have been implicated in the expression and reconsolidation of associative memories. Therefore, we investigated the necessity of β-AR activation within the PL-mPFC and BLA for cocaine-associated memory retrieval and reconsolidation in rats. Before or immediately after a cocaine-induced conditioned place preference (CPP) retrieval trial, β-AR antagonists were infused into the PL-mPFC or BLA, followed by daily testing. PL-mPFC infusions before, but not after, a CPP trial disrupted CPP memory retrieval and induced a persistent deficit in retrieval during subsequent trials. In contrast, BLA β-AR blockade had no effect on initial CPP memory retrieval, but prevented CPP expression during subsequent trials indicative of reconsolidation disruption. Our results reveal a distinct dissociation between the neural mechanisms required for cocaine-associated memory retrieval and reconsolidation. Using patch-clamp electrophysiology, we also show that application of a β-AR antagonist prevents NE-induced potentiation of PL-mPFC pyramidal and GABAergic neuronal excitability. Thus, targeted β-AR blockade could induce long-term deficits in drug-associated memory retrieval by reducing neuronal excitability, providing a novel method of preventing cue-elicited drug seeking and relapse.

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Section: Discussionmentioning

confidence: 99%

Neurobiological Dissociation of Retrieval and Reconsolidation of Cocaine-Associated Memory

2013

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“…However, this interpretation is unlikely given that b-AR activation enhances, rather than impedes, memory formation (McGaugh, 2000). Accordingly, b-AR blockade impairs, rather than facilitates, extinction of several appetitive and aversive behaviors (Merlo and Izquierdo, 1967;Mueller et al, 2008;LaLumiere et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Hippocampal β-Adrenergic Receptors Impairs Retrieval But Not Reconsolidation of Cocaine-Associated Memory and Prevents Subsequent Reinstatement

Otis

Fitzgerald

Mueller

2013

Neuropsychopharmacol

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Retrieval of drug-associated memories is critical for maintaining addictive behaviors, as presentation of drug-associated cues can elicit drug seeking and relapse. Recently, we and others have demonstrated that b-adrenergic receptor (b-AR) activation is necessary for retrieval using both rat and human memory models. Importantly, blocking retrieval with b-AR antagonists persistently impairs retrieval and provides protection against subsequent reinstatement. However, the neural locus at which b-ARs are required for maintaining retrieval and subsequent reinstatement is unclear. Here, we investigated the necessity of dorsal hippocampus (dHipp) b-ARs for drugassociated memory retrieval. Using a cocaine conditioned place preference (CPP) model, we demonstrate that local dHipp b-AR blockade before a CPP test prevents CPP expression shortly and long after treatment, indicating that dHipp b-AR blockade induces a memory retrieval disruption. Furthermore, this retrieval disruption provides long-lasting protection against cocaine-induced reinstatement. The effects of b-AR blockade were dependent on memory reactivation and were not attributable to reconsolidation disruption as blockade of b-ARs immediately after a CPP test had little effect on subsequent CPP expression. Thus, cocaine-associated memory retrieval is mediated by b-AR activity within the dHipp, and disruption of this activity could prevent cue-induced drug seeking and relapse long after treatment.

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“…These theories seem quite reasonable, as NE tone seems inextricably linked to behavior precisely when task contingencies are changing and the production of exploratory behavior would be advantageous: changes in LC activity are correlated with environmental uncertainty (Payzan-LeNestour et al, 2013), are correlated with changes in learning rate (Nassar et al, 2012), and precede changes in behavior (Bouret and Sara, 2004). Further, NE seems to have causal role in changing behavior and associative representations, as increases in global NE tone facilitate reversal (Seu et al, 2009) and extinction learning (Merlo and Izquierdo, 1967, Janak and Corbit, 2011), while decreases in NE tone in cortex impair extinction (Mason and Fibiger, 1979, McCormick and Thompson, 1982), a topic recently reviewed in detail (Mueller and Cahill, 2010) . Recently, modulation of NE release specifically in the ACC has been shown to have direct control of LC-NE over the stochastic versus strategic choice behavior (Tervo et al, 2014).…”

Section: A Role For Tonic Norepinephrine In State Creationmentioning

confidence: 99%

Toward a theoretical role for tonic norepinephrine in the orbitofrontal cortex in facilitating flexible learning

2017

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To adaptively respond in a complex, changing world, animals need to flexibily update their understanding of the world when their expectations are violated. Though several brain regions in rodents and primates have been implicated in aspects of this updating, current models of orbitofrontal cortex (OFC) and norepinephrine neurons of the locus coeruleus (LC-NE) suggest that each plays a role in responding to environmental change, where the OFC allows updating of prior learning to occur without overwriting or unlearning one’s previous understanding of the world that changed, while elevated tonic NE allows for increased flexibility in behavior that tracks an animal’s uncertainty. In light of recent studies highlighting a specific LC-NE projection to the OFC, in this review we discuss current models of OFC and NE function, and their potential synergy in the updating of associations following environmental change.

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The Effect of Catecholamines on Learning in Rats

Cited by 10 publications

References 2 publications

Neurobiological Dissociation of Retrieval and Reconsolidation of Cocaine-Associated Memory

Neurobiological Dissociation of Retrieval and Reconsolidation of Cocaine-Associated Memory

Inhibition of Hippocampal β-Adrenergic Receptors Impairs Retrieval But Not Reconsolidation of Cocaine-Associated Memory and Prevents Subsequent Reinstatement

Toward a theoretical role for tonic norepinephrine in the orbitofrontal cortex in facilitating flexible learning

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