Activation in extended amygdala corresponds to altered hedonic processing during protracted morphine withdrawal

Harris, Glenda C.; Aston‐Jones, Gary

doi:10.1016/j.bbr.2006.10.012

Cited by 70 publications

(59 citation statements)

References 54 publications

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“…How this might have translated into enhanced avoidance of the center region is unclear. Clues to a mechanism, however, derive from studies investigating the neural basis of increased negative affect associated with opiate withdrawal (Delfs et al, 2000;Harris and Aston-Jones, 2007). These studies have indicated a critical role of the BST, and in particular, its catecholaminergic inputs from the caudal brainstem.…”

Section: Patterns Of Neuronal Activation Following the Open Field/holmentioning

confidence: 99%

“…These studies have indicated a critical role of the BST, and in particular, its catecholaminergic inputs from the caudal brainstem. Blockade of adrenergic receptors in the BST prevented development of place aversions in rats undergoing morphine withdrawal (Harris and Aston-Jones, 2007). Like morphine withdrawal, immune challenge with lipopolysaccharide (a component of gramnegative bacterial cell walls) activates caudal brainstem projection neurons (A1/C1 cell group in the VLM and the A2/C2 cell group in the NTS) that target the BST directly (Gaykema et al, 2007).…”

Section: Patterns Of Neuronal Activation Following the Open Field/holmentioning

confidence: 99%

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Campylobacter jejuni infection increases anxiety-like behavior in the holeboard: Possible anatomical substrates for viscerosensory modulation of exploratory behavior

Goehler¹,

Park²,

Opitz³

et al. 2008

Brain, Behavior, and Immunity

248

124

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The presence of certain bacteria in the gastrointestinal tract influences behavior and brain function. For example, challenge with live Campylobacter jejuni (C. jejuni), a common food-born pathogen, reduces exploration of open arms of the plus maze, consistent with anxiety-like behavior, and activates brain regions associated with autonomic function, likely via a vagal pathway. As yet, however, little is known regarding the interface of immune sensory signals with brain substrates that mediate changes in behavioral states. To address this issue, we challenged mice with either C. jejuni or saline, and 7-8h later assessed anxiety-like behavior using the open holeboard, and used immunohistochemical detection of the protein c-Fos as an activation marker in the brain. C. jejuni treatment was associated with increased avoidance of the center regions of the holeboard, compared to saline-treated controls. Exposure to the holeboard induced activation in multiple brain regions previously implicated in anxiety-like behavior, including the lateral septum (LS), paraventricular (PVN) and dorsomedial hypothalamic nuclei (DMH), basolateral and central nuclei of the amygdala (BLA, CEA), bed nucleus of the stria terminalis (BST) and periaquiductal grey (PAG), compared to homecage controls. In C. jejuni-treated animals c-Fos induction also occurred in autonomic regions, as previously reported. The PVN, BLA, parts of the BST, medial prefrontal (mPFC) and anterior cingulate responded to both C. jejuni treatment and the holeboard, suggesting a role for these regions in the enhanced anxiety-like behavior observed. In saline-treated animals, anxiety-like behavior was predicted by activation in the CEA and BLA, whereas in C. jejuni-treated animals, c-Fos expression in the BST predicted the degree of anxiety-like behavior. These findings implicate the PVN, amygdala and BST as interfaces between gastrointestinal pathogenic challenge and brain regions that mediate behavioral responses to stress, and reinforce these nuclei as anatomical substrates by which viscerosensory stimuli can influence behavior.

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Section: Patterns Of Neuronal Activation Following the Open Field/holmentioning

confidence: 99%

Section: Patterns Of Neuronal Activation Following the Open Field/holmentioning

confidence: 99%

Campylobacter jejuni infection increases anxiety-like behavior in the holeboard: Possible anatomical substrates for viscerosensory modulation of exploratory behavior

Goehler¹,

Park²,

Opitz³

et al. 2008

Brain, Behavior, and Immunity

248

124

View full text Add to dashboard Cite

show abstract

“…1) (Zahm et al 2011). Evidence suggests that activity within the CeA and BNST during protracted withdrawal may produce a "stress-like" state that can precipitate relapse (Nakagawa et al 2005b;Harris and Aston-Jones 2007). Indeed, for cocaine, these regions are only critical for reinstatement triggered by stress (McFarland et al 2004).…”

Section: Amygdala Outputsmentioning

confidence: 99%

Glutamate Mechanisms Underlying Opiate Memories

Peters

Vries

2012

Cold Spring Harbor Perspectives in Medicine

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Correspondence: tj.devries@vumc.nlAs the major excitatory neurotransmitter in the brain, glutamate plays an undisputable integral role in opiate addiction. This relates, in part, to the fact that addiction is a disorder of learning and memory, and glutamate is required for most types of memory formation. As opiate addiction develops, the addict becomes conditioned to engage in addictive behaviors, and these behaviors can be triggered by opiate-associated cues during abstinence, resulting in relapse. Some medications for opiate addiction exert their therapeutic effects at glutamate receptors, especially the NMDA receptor. Understanding the neural circuits controlling opiate addiction, and the locus of glutamate's actions within these circuits, will help guide the development of targeted pharmacotherapeutics for relapse.

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“…Increased morphine preference and decreased food preference in protracted abstinence animals have been associated with increased Fos activation in stress-related brain areas, such as extended amygdala and nucleus tractus solitarius (Harris and AstonJones, 2003a;Harris and Aston-Jones, 2007a). In addition, previous exposure to stress has been shown to increase the subsequent acquisition of morphine place preference, an effect that is attenuated by corticosterone inhibition during CPP acquisition, but not during stress exposure (DerAvakian et al, 2005;Will et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Incentive Learning for Morphine-Associated Stimuli During Protracted Abstinence Increases Conditioned Drug Preference

Smith

Aston‐Jones

2013

Neuropsychopharmacol

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Previous studies from our laboratory found that rats express increased preference for drug-paired stimuli following 2 or 5 weeks of protracted abstinence from chronic drug exposure as compared with naive animals. Here, we show that this increased morphine place preference depends upon experiencing drug-stimulus pairings specifically in the abstinent state, indicating a critical role for incentive learning. Male Sprague Dawley rats were initially conditioned for morphine place preference (8 mg/kg) and then made dependent on morphine (by subcutaneous morphine pellets) and subjected to forced abstinence. Place preference was tested every 1-2 weeks with no additional drug-cue conditioning. In this paradigm, there was no difference between morphine-pelleted (dependent) and placebopelleted (non-dependent) rats in place preference at any time during abstinence (up to 6 weeks). However, these same morphinepelleted rats expressed significantly increased preference when they were subsequently re-conditioned for morphine place preference during protracted abstinence. Placebo-pelleted rats did not show enhanced preference after re-conditioning. These findings reveal that incentive learning has a key role in increased morphine place preference when drug is experienced during protracted abstinence. This indicates that incentive learning is involved not only in instrumental responding (as previously reported), but also in updating Pavlovianconditioned responses to morphine-associated stimuli. Therefore, enhanced morphine preference is not a direct consequence of the negative affective state of abstinence, but instead reflects increased acquisition of morphine-stimulus associations during abstinence. These results indicate that, during the development of addiction in humans, drug-associated stimuli acquire increasingly stronger incentive properties each time they are re-experienced.

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Activation in extended amygdala corresponds to altered hedonic processing during protracted morphine withdrawal

Cited by 70 publications

References 54 publications

Campylobacter jejuni infection increases anxiety-like behavior in the holeboard: Possible anatomical substrates for viscerosensory modulation of exploratory behavior

Campylobacter jejuni infection increases anxiety-like behavior in the holeboard: Possible anatomical substrates for viscerosensory modulation of exploratory behavior

Glutamate Mechanisms Underlying Opiate Memories

Incentive Learning for Morphine-Associated Stimuli During Protracted Abstinence Increases Conditioned Drug Preference

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