The left central nucleus of the amygdala contributes to mechanical allodynia and hyperalgesia following right-sided peripheral nerve injury.

The left and right central nucleus of the amygdala (CeA) exert asymmetric pronociceptive functions. In the setting of a transient noxious stimulus or persistent inflammatory pain, neuronal activity increases in the right but not left CeA, regardless of side of injury. Much less is known regarding this lateralization with respect to the behavioral manifestations of persistent neuropathic pain. To address this question, we conducted spared nerve injury (SNI) to the left or right hindlimb and then inactivated the left and/or right CeA with local microinjection of lidocaine. We evaluated injury-induced hypersensitivity with von Frey hairs (mechanical allodynia), a blunt pin (mechanical hyperalgesia), and acetone application (cold allodynia). Following left-sided SNI, inactivation of the right or bilateral CeA attenuated mechanical allodynia and hyperalgesia as well as cold hypersensitivity, while inactivation of the left CeA had no effect. Following right-sided SNI, we observed a modality-dependent effect: mechanical allodynia was attenuated by inactivation of the left but neither the right nor bilateral CeA, mechanical hyperalgesia was attenuated by left, right and bilateral intra-CeA lidocaine, and cold allodynia was unaffected. These data suggest that CeA-mediated control of neuropathic pain is not strictly limited to the right CeA as previously assumed. We conclude that functional lateralization depends on the type of pain, side of injury and the sensory modality, and that the left CeA contributes to mechanical allodynia and hyperalgesia after peripheral nerve injury to the right side of the body.