We conducted a brief functional analysis to identify maintaining variable for aggressive behavior and an alternative replacement response during a 90-min outpatient evaluation of 3 individuals with severe handicaps. During the initial analogue assessment, which focused on identifying maintaining contingencies for aggressive behavior, each participant displayed a substantially greater frequency of aggressive behavior during one condition than during any other. The contingency that produced the highest percentage of aggressive behavior was then presented for the occurrence of a specific alternative behavior (a mand). During this contingency reversal phase, each participant displayed a substantial reduction in aggressive behavior and a substantial increase in alternative behavior, thus providing a direct analysis of the equivalency of the contingency for maintaining either behavior.

During puberty, plasma insulin levels increase, and insulin sensitivity decreases along with multiple other physical and hormonal changes. To determine 1) the time course of the decrease in insulin sensitivity in relationship to Tanner stage of genital development, and 2) how this change relates to changes in GH secretion, insulin-like growth factor-I (IGF-I), IGF-binding protein-3, and gonadal steroid secretion, we studied 58 healthy children and adolescents (34 males and 24 females; age 7-15 yr) using overnight GH sampling and frequently sampled iv glucose tolerance tests. The insulin sensitivity index (ISI) was calculated using the program MINMOD. ISI differed significantly by Tanner stage (P < 0.05, by analysis of variance) with a decrease from Tanner stage 1 to 2 (P < 0.05). IGF-I and IGF-binding protein-3 followed opposite patterns to ISI, with lower levels in Tanner stage 1 than in stages 2-5 (P < 0.05). Mean GH levels did not increase until Tanner stage 4 (P < 0.05) and then fell during Tanner stage 5. Multiple linear regression analysis revealed negative relationships among ISI, IGF-I, and body mass index. No relationship was found with GH. We conclude that the pubertal change in ISI is not necessarily associated with increased GH secretion, but is associated with increased GH peripheral effect, as indicated by the relationship between ISI and IGF-I.

The complement 3a receptor (C3aR1) participates in microglial signaling under pathological conditions and was recently shown to be activated by the neuropeptide TLQP-21. We previously demonstrated that TLQP-21 elicits hyperalgesia and contributes to nerve injury-induced hypersensitivity through an unknown mechanism in the spinal cord. Here we determined that this mechanism requires C3aR1 and that microglia are the cellular target for TLQP-21. We propose a novel neuroimmune signaling pathway involving TLQP-21-induced activation of microglial C3aR1 that then contributes to spinal neuroplasticity and neuropathic pain. This unique dual-ligand activation of C3aR1 by a neuropeptide (TLQP-21) and an immune mediator (C3a) represents a potential broad-spectrum mechanism throughout the CNS for integration of neuroimmune crosstalk at the molecular level.

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