Hypothalamic control of pain vocalization and affective dimension of pain signaling

Borszcz, George S.; Spuz, Catherine A.

doi:10.1016/b978-0-12-374593-4.00027-9

Cited by 3 publications

(5 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Stimulating this structure in rats elicits pain‐like emotional behaviors, and manipulating inhibitory neurotransmitters within this structure alters rats' emotional response to a painful shock (Borszcz, 2006). Furthermore, partial kindling of the basolateral amygdala in rats generates long‐term sensitization of neurons in this structure, which correlates with increases in their affective response to painful shocks (Borszcz & Spuz, 2009). This form of central sensitization may contribute to the persistent pain of fibromyalgia, for example, because people with this condition have augmented defensive reactions to threatening stimuli (Bartley, Rhudy, & Williams, 2009).…”

Section: Neurobiology Emotions and Painmentioning

confidence: 99%

Pain and emotion: a biopsychosocial review of recent research

et al. 2011

Self Cite

View full text Add to dashboard Cite

Objective and Method Research on emotion and pain has burgeoned. We review the last decade’s literature, focusing on links between emotional processes and persistent pain. Results Neurobiological research documents the neural processes that distinguish affective from sensory pain dimensions, link emotion and pain, and generate central nervous system pain sensitization. Psychological research demonstrates that greater pain is related to emotional stress and limited emotional awareness, expression, and processing. Social research shows the potential importance of emotional communication, empathy, attachment, and rejection. Conclusions Emotions are integral to the conceptualization, assessment, and treatment of persistent pain. Research should clarify when to eliminate or attenuate negative emotions, and when to access, experience, and express them. Theory and practice should integrate emotion into cognitive-behavioral models of persistent pain.

show abstract

Section: Neurobiology Emotions and Painmentioning

confidence: 99%

Pain and emotion: a biopsychosocial review of recent research

et al. 2011

Self Cite

View full text Add to dashboard Cite

show abstract

“…VADs occur immediately following application of noxious tail shock and are a validated rodent model of pain affect (Caroll and Lim, 1960; Borszcz, 1993, 1995, 2006; Borszcz and Spuz, 2009). However, regional differences within VTA were reported in the capacity of carbachol to activate the brain reward circuit.…”

Section: Introductionmentioning

confidence: 99%

Separating analgesia from reward within the ventral tegmental area

2014

View full text Add to dashboard Cite

Activation of the dopaminergic mesolimbic reward circuit that originates in the ventral tegmental area (VTA) is postulated to preferentially suppress emotional responses to noxious stimuli, and presumably contributes to the addictive liability of strong analgesics. VTA dopamine neurons are activated via cholinergic afferents and microinjection of carbachol (cholinergic agonist) into VTA is rewarding. Here, we evaluated regional differences within VTA in the capacity of carbachol to suppress rats' affective response to pain (vocalization afterdischarges, VADs) and to support conditioned place preference (CPP) learning. As carbachol is a non-specific agonist, muscarinic and nicotinic receptor involvement was assessed by administering atropine (muscarinic antagonist) and mecamylamine (nicotinic antagonist) into VTA prior to carbachol treatment. Unilateral injections of carbachol (4 μg) into anterior VTA (aVTA) and posterior VTA (pVTA) suppressed VADs and supported CPP; whereas, injections into midVTA failed to effect either VADs or CPP. These findings corroborate the hypothesis that the neural substrates underlying affective analgesia and reward overlap. However, the extent of the overlap was only partial. Whereas both nicotinic and muscarinic receptors contributed to carbachol-induced affective analgesia in aVTA, only muscarinic receptors mediated the analgesic action of carbachol in pVTA. The rewarding effects of carbachol are mediated by the activation of both nicotinic and muscarinic receptors in both aVTA and pVTA. The results indicate that analgesia and reward are mediated by separate cholinergic mechanisms within pVTA. Nicotinic receptor antagonism within pVTA failed to attenuate carbachol-induced analgesia, but prevented carbachol-induced reward. As addictive liability of analgesics stem from their rewarding properties, the present findings suggest that these processes can be neuropharmacologically separated within pVTA.

show abstract

“…2,46 This glutamatergic input to CeLC activates projections neurons of CeLC that target limbic-forebrain sites that integrate execution of affective pain behaviors. 9,12,55 Increases in vocalization thresholds following AP5 injection into CeA are presumably mediated by suppression of noxious evoked neural activity in CeLC.…”

Section: Discussionmentioning

confidence: 99%

“…38 The hypothalamus contributes to innate defensive responses 67 and to generation of pain-induced VADs. 9,12 Processing of noxious input by CeLC that is sufficient to activate the hypothalamus may also engage the CeM projections to the vlPAG that moderate further nociceptive processing. A similar compensatory mechanism was proposed for the NMDA receptor activation in the rostral versus caudal anterior cingulate cortex that contributed to antinociception and nociception, respectively.…”

Section: Discussionmentioning

confidence: 99%

“…The amygdaloid central nucleus (CeA) contributes to the execution of affective behaviors to environmental threats. 44 The prototypical threat to an individual is exposure to a noxious stimulus, 9,12,22 and the CeA receives direct nociceptive inputs from the spinal cord dorsal horn 18,56 and indirect nociceptive inputs relayed via the parabrachial nucleus (PB) 2,41 and intralaminar thalamic nuclei. 58,74 …”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

N-Methyl-d-Aspartate Receptor Agonism and Antagonism Within the Amygdaloid Central Nucleus Suppresses Pain Affect: Differential Contribution of the Ventrolateral Periaqueductal Gray

Spuz

Tomaszycki

Borszcz

2014

The Journal of Pain

Self Cite

View full text Add to dashboard Cite

The amygdala contributes to the generation of pain affect and the amygdaloid central nucleus (CeA) receives nociceptive input that is mediated by glutamatergic neurotransmission. The present study compared the contribution of N-methyl-D-aspartate (NMDA) receptor agonism and antagonism in CeA to generation of the affective response of rats to an acute noxious stimulus. Vocalizations that occur following a brief tail shock (vocalization afterdischarges) are a validated rodent model of pain affect, and were preferentially suppressed, in a dose dependent manner, by bilateral injection into CeA of NMDA (.1 µg, .25 µg, .5 µg, or 1 µg/side), or the NMDA receptor antagonist D-2-amino-5-phosphonovalerate (AP5, 1 µg, 2 µg, or 4 µg/side). Vocalizations that occur during tail shock were suppressed to a lesser degree, whereas, spinal motor reflexes (tail flick and hind limb movements) were unaffected by injection of NMDA or AP5 into CeA. Injection of NMDA, but not AP5, into CeA increased c-Fos immunoreactivity in the ventrolateral periaqueductal gray (vlPAG), and unilateral injection of the µ-opiate receptor antagonist H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP, 0.25 µg) into vlPAG prevented the antinociception generated by injection of NMDA into CeA. These findings demonstrate that although NMDA receptor agonism and antagonism in CeA produce similar suppression of pain behaviors they do so via different neurobiological mechanisms. Perspective The amygdala contributes to production of the emotional dimension of pain. NMDA receptor agonism and antagonism within the central nucleus of the amygdala suppressed rats’ emotional response to acute painful stimulation. Understanding the neurobiology underlying emotional responses to pain will provide insights into new treatments for pain and its associated affective disorders.

show abstract

Hypothalamic control of pain vocalization and affective dimension of pain signaling

Cited by 3 publications

References 61 publications

Pain and emotion: a biopsychosocial review of recent research

Pain and emotion: a biopsychosocial review of recent research

Separating analgesia from reward within the ventral tegmental area

N-Methyl-d-Aspartate Receptor Agonism and Antagonism Within the Amygdaloid Central Nucleus Suppresses Pain Affect: Differential Contribution of the Ventrolateral Periaqueductal Gray

Contact Info

Product

Resources

About