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Hemispheric lateralization of pain processing by amygdala neurons.

ABSTRACT: Recent biochemical and behavioral data suggest right-hemispheric lateralization of amygdala functions in pain. Our previous electrophysiological studies showed pain-related neuroplasticity in the latero-capsular division of the central nucleus of the amygdala (CeLC) in the right brain hemisphere. Here we determined differences in the processing of pain-related signals in right versus left CeLC neurons. Individual CeLC neurons were recorded extracellularly before and after induction of an arthritis pain state in anesthetized rats. Brief innocuous and noxious test stimuli were applied to peripheral tissues ipsi- and contralateral to the recording site. A monoarthritis was induced in the ipsi- or contralateral knee by intraarticular injections of kaolin and carrageenan. Under normal conditions, CeLC neurons in the left amygdala had smaller receptive fields than those in the right, but the magnitude of background and evoked activity was not significantly different. After arthritis induction, neurons in the right, but not left, CeLC developed increased background activity and evoked responses, irrespective of the location of the arthritis (ipsi- or contralateral to the recording site). A protein kinase A (PKA) inhibitor decreased the activity of right CeLC neurons after arthritis induction but had no effect in the left amygdala. Forskolin, however, increased the activity of left and right CeLC neurons under normal conditions. The results show for the first time laterality of pain-related electrophysiological activity changes in individual amygdala neurons. Whereas both left and right amygdala neurons receive nociceptive inputs and can become sensitized in principle, a yet unknown mechanism prevents PKA activation and pain-related changes in the left amygdala.

SUBMITTER: Ji G

PROVIDER: S-EPMC2776996 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The amygdala is an important neural substrate for the emotional-affective dimension of pain and modulation of pain. The central nucleus (CeA) serves major amygdala output functions and receives nociceptive and affected-related information from the spino-parabrachial and lateral-basolateral amygdala (LA-BLA) networks. The CeA is a major site of extra-hypothalamic expression of corticotropin releasing factor (CRF, also known as corticotropin releasing hormone, CRH), and amygdala CRF neurons form widespread projections to target regions involved in behavioral and descending pain modulation. Here we explored the effects of modulating amygdala neurons on nociceptive processing in the spinal cord and on pain-like behaviors, using optogenetic activation or silencing of BLA to CeA projections and CeA-CRF neurons under normal conditions and in an acute pain model. Extracellular single unit recordings were made from spinal dorsal horn wide dynamic range (WDR) neurons, which respond more strongly to noxious than innocuous mechanical stimuli, in normal and arthritic adult rats (5-6 h postinduction of a kaolin/carrageenan-monoarthritis in the left knee). For optogenetic activation or silencing of CRF neurons, a Cre-inducible viral vector (DIO-AAV) encoding channelrhodopsin 2 (ChR2) or enhanced Natronomonas pharaonis halorhodopsin (eNpHR3.0) was injected stereotaxically into the right CeA of transgenic Crh-Cre rats. For optogenetic activation or silencing of BLA axon terminals in the CeA, a viral vector (AAV) encoding ChR2 or eNpHR3.0 under the control of the CaMKII promoter was injected stereotaxically into the right BLA of Sprague-Dawley rats. For wireless optical stimulation of ChR2 or eNpHR3.0 expressing CeA-CRF neurons or BLA-CeA axon terminals, an LED optic fiber was stereotaxically implanted into the right CeA. Optical activation of CeA-CRF neurons or of BLA axon terminals in the CeA increased the evoked responses of spinal WDR neurons and induced pain-like behaviors (hypersensitivity and vocalizations) under normal condition. Conversely, optical silencing of CeA-CRF neurons or of BLA axon terminals in the CeA decreased the evoked responses of spinal WDR neurons and vocalizations, but not hypersensitivity, in the arthritis pain model. These findings suggest that the amygdala can drive the activity of spinal cord neurons and pain-like behaviors under normal conditions and in a pain model.

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Hemispheric lateralization of pain processing by amygdala neurons.

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