SENSITIZATION--BEHAVIORAL PROPERTIES & NEURAL MECHANISMS

厌恶刺激引起反应的程度，以及

The degree to which an aversive stimulus elicits responding, and engenders learning, varies tremendously. Under some conditions, a noxious stimulus may be hardly noticed. At other times, even mild stimulation can produce incapacitating pain. The aim of our reach is to explain this variability; how physiological and psychological systems modulate the processing of nociceptive information. Past research has focused on the mechanisms that decrease the flow of nociceptive information, effectively undermining its psychological impact. These "analgesic" systems are commonly studied by exposing rats to an aversive event (e.g., shock). Changes in nociceptive processing are then assessed by measuring the latency to exhibit a tail-movement in response to a thermal stimulus (the tail-flick test) or the amount of paw-directed behavior elicited by a chemical irritant (the formalin test). Using these tests, researchers have found reduced nociceptive reactivity. But recent work, using other behavioral measures, indicates that pain is actually enhanced (hyperalgesia), for exposure to shock lowers vocalization thresholds to a variety of stimuli and increases the affective impact of thermal and shock stimuli in both a Pavlovian and operant conditioning paradigm. The experiments we propose focus on the sensitization of pain; when is it observed, how it affects nociceptive processing, and the underlying neural systems. To bolster our inference of hyperalgesia, and to clarify its relationship to other behavioral phenomena, multiple behavioral endpoints will be monitored. Our behavioral studies will clarify the circumstances that induce hyperalgesia, whether it is tied to the induction of fear, its effect on other behavioral processes (e.g., startle), and how it enhances learning in a Pavlovian paradigm. Subsequent experiments will explore the neuroanatomical systems involved. Neurochemical lesions will be used to examine the role of the dorsal and lateral regions of the periaqueductal gray and the central nucleus and basolateral complex of the amygdala. This lesion approach will be complimented by experiments testing the impact of chemically activating neural systems within the periaqueductal gray and our inferences will be strengthened by obtaining multiple measures of pain reactivity.