Effect of noxious somesthetic stimulation on the activity of neurons of the nucleus centralis of the amygdala

Bernard, Jean‐François; Huang, Guo-Fen; Besson, J. M.

doi:10.1016/0006-8993(90)91512-f

Cited by 55 publications

(13 citation statements)

References 13 publications

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“…In accordance with neuroadaptations described in the previous section, converging lines of evidence suggest that pain-induced levels of CRF modify the electrophysiological properties of nociceptive CeA neurons (Bernard, Huang, & Besson, 1990) to promote pain sensitization (Neugebauer, Li, Bird, & Han, 2004). Rats placed in a state of arthritic inflammatory pain exhibit increased CeA excitability that is alleviated by CRF1R antagonism (Ji & Neugebauer, 2007).…”

Section: Sensitization Of Pain-related Negative Affect In Addictionsupporting

confidence: 80%

The affective dimension of pain as a risk factor for drug and alcohol addiction

LeBlanc

McGinn

Itoga

et al. 2015

Alcohol

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Addiction, or substance use disorder (SUD), is a devastating psychiatric disease composed of multiple elemental features. As a biobehavioral disorder, escalation of drug and/or alcohol intake is both a cause and consequence of molecular neuroadaptations in central brain reinforcement circuitry. Multiple mesolimbic areas mediate a host of negative affective and motivational symptoms that appear to be central to the addiction process. Brain stress- and reinforcement-related regions such as the central amygdala (CeA), prefrontal cortex (PFC), and nucleus accumbens (NAc) also serve as central processors of ascending nociceptive input. We hypothesize that a sensitization of brain mechanisms underlying the processing of persistent and maladaptive pain contributes to a composite negative affective state to drive the enduring, relapsing nature of addiction, particularly in the case of alcohol and opioid use disorder. At the neurochemical level, pain activates central stress-related neuropeptide signaling, including the dynorphin and corticotropin-releasing factor (CRF) systems, and by this process may facilitate negative affect and escalated drug and alcohol use over time. Importantly, the widespread prevalence of unresolved pain and associated affective dysregulation in clinical populations highlights the need for more effective analgesic medications with reduced potential for tolerance and dependence. The burgeoning epidemic of prescription opioid abuse also demands a closer investigation into the neurobiological mechanisms of how pain treatment could potentially represent a significant risk factor for addiction in vulnerable populations. Finally, the continuing convergence of sensory and affective neuroscience fields is expected to generate insight into the critical balance between pain relief and addiction liability, as well as provide more effective therapeutic strategies for chronic pain and addiction.

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Section: Sensitization Of Pain-related Negative Affect In Addictionsupporting

confidence: 80%

The affective dimension of pain as a risk factor for drug and alcohol addiction

LeBlanc

McGinn

Itoga

et al. 2015

Alcohol

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“…The CeA is an autonomic-projecting region, which has been suggested to constitute a “visceromotor striatum” (Swanson and Petrovich 1998). Since both the jcBNST (Dong et al, 2000) and the CeA receive nociceptive information (Bernard and Besson 1990; Bernard et al 1990), changes in the excitability of the jcBNST in rats with history of morphine dependence are likely to contribute to the hyperalgesia observed in these rats. Allostatic adaptation of circuits involving the BNST and the CeA are expected to affect descending regulation of the periaqueductal gray matter (PAG) in the brainstem and its role in integrating nociceptive inputs arriving from the ascending pain pathways (Elman et al 2013; Hayes and Northoff 2012)…”

Section: Discussionmentioning

confidence: 99%

Opiate dependence induces cell type-specific plasticity of intrinsic membrane properties in the rat juxtacapsular bed nucleus of stria terminalis (jcBNST)

et al. 2017

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RATIONALE Drugs of abuse can alter circuit dynamics by modifying synaptic efficacy and/or the intrinsic membrane properties of neurons. The juxtacapsular subdivision of the bed nucleus of stria terminalis (jcBNST) has unique connectivity that positions it to integrate cortical and amygdala inputs and provide feed-forward inhibition to the central nucleus of the amygdala (CeA), among other regions. In this study, we investigated changes in the synaptic and intrinsic properties of neurons in the rat jcBNST during protracted withdrawal from morphine dependence using a combination of conventional electrophysiological methods and the dynamic clamp technique. RESULTS A history of opiate dependence induced a form of cell-type specific plasticity characterized by reduced inward rectification associated with more depolarized resting membrane potentials and increased membrane resistance. This cell type also showed a lower rheobase when stimulated with direct current (DC) pulses as well as a decreased firing threshold under simulated synaptic bombardment with the dynamic clamp. Morphine dependence also decreased excitatory postsynaptic potential amplification, suggesting the downregulation of the persistent Na+-current (INaP). CONCLUSION These findings show that a history of morphine dependence leads to persistent cell type-specific plasticity of the passive membrane properties of a jcBNST neuronal population, leading to an overall increased excitability of such neurons. By altering the activity of extended amygdala circuits where they are embedded, changes in the integration properties of jcBNST neurons may contribute to emotional dysregulation associated with drug dependence and withdrawal.

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“…Strong evidence suggests that the neural substrates associated with addiction may also overlap with substrates of emotional aspects of nociceptive processing in areas such as the central amygdala (Neugebauer et al, 2004), cingulate cortex (Vogt, 2005), and nucleus accumbens (Gear and Levine, 1995; Barrot et al, 2002), where ascending pain pathways connect for processing the emotional components of pain perception. Specifically, pain-responsive neurons are abundant in the lateral part of the central amygdala (also known as the “nociceptive amygdala”; Bernard and Besson, 1990). As a potentially powerful negative motivational symptom, pain represents a subjective experience that can have a substantial influence on drug reinforcement, possibly facilitating the transition to drug addiction (Miller and Gold, 2007).…”

Section: Discussionmentioning

confidence: 99%

Development of mechanical hypersensitivity in rats during heroin and ethanol dependence: Alleviation by CRF1 receptor antagonism

et al. 2012

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Animal models of drug dependence have described both reductions in brain reward processes and potentiation of stress-like (or anti-reward) mechanisms, including a recruitment of corticotropin-releasing factor (CRF) signaling. Accordingly, chronic exposure to opiates often leads to the development of mechanical hypersensitivity. We measured paw withdrawal thresholds (PWTs) in male Wistar rats allowed limited (short access group: ShA) or extended (long access group: LgA) access to heroin or cocaine self-administration, or in rats made dependent on ethanol via ethanol vapor exposure (ethanol-dependent group). In heroin self-administering animals, after transition to LgA conditions, thresholds were reduced to around 50% of levels observed at baseline, and were also significantly lower than thresholds measured in animals remaining on the ShA schedule. In contrast, thresholds in animals self-administering cocaine under either ShA (1 h) or LgA (6 h) conditions were unaltered. Similar to heroin LgA rats, ethanol-dependent rats also developed mechanical hypersensitivity after eight weeks of ethanol vapor exposure compared to non-dependent animals. Systemic administration of the CRF1R antagonist MPZP significantly alleviated the hypersensitivity observed in rats dependent on heroin or ethanol. The emergence of mechanical hypersensitivity with heroin and ethanol dependence may thus represent one critical drug-associated negative emotional state driving dependence on these substances. These results also suggest a recruitment of CRF-regulated nociceptive pathways associated with escalation of intake and dependence. A greater understanding of relationships between chronic drug exposure and pain-related states may provide insight into mechanisms underlying the transition to drug addiction, as well as reveal new treatment opportunities.

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Effect of noxious somesthetic stimulation on the activity of neurons of the nucleus centralis of the amygdala

Cited by 55 publications

References 13 publications

The affective dimension of pain as a risk factor for drug and alcohol addiction

The affective dimension of pain as a risk factor for drug and alcohol addiction

Opiate dependence induces cell type-specific plasticity of intrinsic membrane properties in the rat juxtacapsular bed nucleus of stria terminalis (jcBNST)

Development of mechanical hypersensitivity in rats during heroin and ethanol dependence: Alleviation by CRF1 receptor antagonism

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