This paper offers a model for integrating a nurturance framework into family therapy approaches with adolescents. This approach is seen as adding an important but neglected dimension to commonly used approaches, thus increasing both flexibility in treatment and the likelihood of a positive outcome. Steps to an effective treatment approach are outlined and guidelines offered for both in-session work and out-of-session tasks.Family therapy has become increasingly accepted as an important modality of treatment for adolescents. Family theory and research suggest that parental connection and its overt expression in the form of parental nurturance are positively correlated with health in both the adolescent and the family. However, the literature that addresses family therapy applications to adolescent treatment tends to neglect this dimension in favor of focus on issues of power/control and separatiodautonomy.This article will first. briefly review research supporting the importance of parental connection and nurturance in effective parenting of adolescents. Second, a review of the applications of family therapy to the treatment of adolescents will be organized into three prevalent frameworks: (a) the family life cycle/developmental task of individuatiodseparation; (b) the use of organizational concepts; and (c) behavioral focuses on conflict, power, and control issues. A discussion follows that suggests how parental connectiodnurturance can be incorporated into these frameworks. The article then addresses specifically how therapists can help parents develop greater connectedness with their adolescents within the context of therapy. Finally, the article offers guidelines for out-of-session tasks designed to increase parental nurturance. Therapists incorporating this framework and corresponding in-session and out-of-session tasks will enhance their flexibility in therapy with adolescents and their families and increase the overall effectiveness of treatment.I define nurturance as a subset of behavior within the more general category of interconnectedness or attachment behavior. Nurturant acts are behaviors directed toward another individual with the intent of providing physical or psychological nourishment. Like Wood (1989, I believe that an important dimension of a successful nurturant act is that the nurturer accurately assesses and responds to the emotions and needs of the other individual.This idea is also supported by attachment therapy, which suggests that secure attachment is characterized not only by the amount of contact between parent and child but also by how well the contact fits both the personal rhythms of the child and the child's developmental stage (Bowlby, 1982). This means that the parent needs to discriminate between the parent's own needs and emotions and those of the adolescent. Thus, an example of a successful nurturant act with an adolescent might be a parent who pats hisher adolescent on the arm instead of hugging himher in front of the adolescent's peers.

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Chronic constriction injury (CCI) of the rodent sciatic nerve causes light touch mechanical sensitivity (allodynia) and leads to activation of spinal astrocytes and microglia. The endocannabinoid system includes the cannabinoid receptor 1 (CB1R) present on neurons and the cannabinoid receptor 2 (CB2R) present mostly on immune cells. CB2R agonists, like AM1710, believed to exert analgesic effects through CB2R actions, are effective in controlling pathological pain states in animal models. However, activation of CB1R could be partly responsible for the analgesic effects of AM1710 through non-specific binding. We sought to determine whether AM1710 could lead to anti-allodynia and produce changes in spinal pro-and anti-inflammatory protein IR in mice lacking functional CB1R (CB1R-/-). We first characterized the allodynia profile of CB1R+/+, CB1R+/-and CB1R-/-mice. Following CCI, CB1R-/-mice displayed allodynia similar to wild-type and heterozygous littermates, with reliable 27-day chronic allodynia. Following baseline threshold assessment, mice underwent sham or CCI surgery, and thresholds were reassessed 5 and 12 days later. Mice were given an intraperitoneal (i.p.) injection of either AM1710 (25 mg/kg/ml) or equivolume vehicle. Following behavioral reassessment at 25 min after injection, spinal tissues were harvested. AM1710, given i.p. reversed CCI-induced allodynia in CB1R-KO mice to control levels. Next, we sought to determine an effective timecourse for AM1710 (5 mg) delivered intrathecally (i.t.) to reverse allodynia in wild type mice. Allodynia reversal occurred 2 hours after administration. Finally, we sought to determine if spinal CB1R were responsible for intrathecal AM170 effects. We found AM1710 robustly reversed chronic allodynia in CB1R-/-mice. Ongoing studies using spectral analysis of IR will examine glial activation, and pro-and anti-inflammatory cytokine changes in these tissues.