Activation of mesolimbic reward circuitry is postulated to preferentially suppress affective reactions to noxious stimuli (affective analgesia). The ventral tegmental area (VTA) is the origin of mesolimbic projections that control the brain reward circuitry. VTA dopamine neurons are activated via cholinergic inputs, and we observed that microinjections of the acetylcholine agonist carbachol suppressed vocalizations of rats that occur following administration of brief (1 sec) tail-shocks (vocalization afterdischarges = VAD). VADs are a validated rodent model of pain affect. Ikemoto & Wise (2002) reported regional differences within the VTA in the capacity of carbachol to support reinforcement. Carbachol was self-administered in the posterior VTA, but not anterior VTA. The present study evaluated regional (anterior vs. posterior) differences in the VTA in the capacity of carbachol to suppress rats' affective response to pain. Pain behaviors organized at spinal (spinal motor reflexes = SMR), medullary (vocalizations during shock = VDS), and forebrain (VAD) levels of the neuraxis were elicited by tailshock. The threshold current intensity to elicit each behavior was determined following unilateral microinjections of carbachol (1µg or 4µg in 0.25µl/side), or vehicle into posterior VTA and anterior VTA. In both VTA regions, carbachol increased the threshold current intensity for eliciting VADs, whereas VDS and SMR thresholds were unaffected. These findings suggest that affective analgesia elicited by carbachol injected into the VTA: 1) does not rely on the rewarding effects elicited by VTA injected carbachol, and/or 2) different neurobiological mechanism underlie the antinociceptive action elicited from the aVTA and pVTA. Further studies are warranted to elucidate the mechanism through which anterior and posterior VTA are involved in affective analgesia. Grant R01 NS045720 from the National Institute of Neurological Disorders and Stroke supported this research.