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cortex CRH receptors (Nemeroff, Owens, changes mood from one state to another based Bissette, Andorn, ing was interpreted to reflect increased CRH thew, Ubriani, Tayfor, release in the frontal cortex resulting in a recent data indicate that the increase in avail-down-regulation of CRH receptors. Finally, able NE that results from antidepressant use Brady, Whitfield, Fox, Gold, and Herkenham gradually results a decrease in the firing (1991) found evidence that antidepressants rate of the LC, which then reduces anxiety produce a down-regulation of the CRH sys-and arousal (Wong et al., 2000). tem. Specifically, they showed that chronic, but not short-term, administration of an anti-depressant (imipramine) Developmental Sequelae to rats caused a sig-nificant decrease in PVN CRH of Major Depression mRNA levels association with a significant increase in At any age, the onset of depression appears Type I glucocorticoid receptor mRNA levels to result in longlasting functional impairment, the hippocampus, which are thought to play even beyond that associated with chronic ill-an important role in restraining the HPA axis. ness (Judd, Akiskal, Zeller, Paulus, Leon, Norepinephrine is perhaps the more widely Maser, Endicott, Coryell, Kunovac, Mueller, studied neurotransmitter biological studies Rice, & Keller, 2000; Wells, Stewart, Hays, of major depression. The first significant bio-Burnam, Rogers, Daniels, Berry, Green-logical hypothesis regarding major depres-field, sion, the catecholamine hypothesis, stated that ler, Endicott, Maser and Klerman (1993) re-major depression resulted from reduced levels ported that adults with unipolar depression of available NE (Schildkraut, 1965). This the-were less likely get married, and those who ory was based on clinical observations that did get married were twice likely to get drugs, such tricyclic antidepressants and separated or divorced. Furthermore, the au-monoamine oxidase inhibitors, which appar-thors found that psychosocial impairments ently increased NE the synapse, had antide-that were associated with depression persisted pressant effects. More recently, many con-even after a significant period of remission. flicting studies have appeared in the literature Adolescents who suffer from depression are regarding noradrenergic function in depres-more likely quit school (Kandel & Davies, sion. This most likely reflects diagnostic het-1986) and to have difficulty adjusting to adult erogeneity and the fact that studies have mea-roles. Specifically, Kandel and Davies (1986) sured CSF NE at a single time point. On the found that women who had suffered from ad-other hand, we recently measured CSF NE ev-olescent depression were more likely to di-ery hour for 24 hr in patients with melan-vorce than were their never-depressed peers, cholic depression. Results indicated that these and men who were depressed in adolescence patients exhibit chronic elevations in NE, experienced more periods of unemployment even during sleep (Wong, Kling, Munson, than did their never-depressed counterparts. In Listwak, Licinio, Prolo, Karp, McCutcheon, terms of direction of causality, Cole and Geracioti, De Bellis, Rice, Goldstein, Veld-Milstead (1989) showed that, in children, de-huis, Chrousos, Oldfield, McCann, & Gold, pression preceded social skill deficits, as well 2000). The elevated NE levels in melancholic a decline in self-perceived competence. patients are compatible with their pathological Granger, Weisz, McCracken, Ikeda, and hyperarousal, anxiety, and physiological hy-Douglas (1996) found evidence that the stress perreactivity. As noted, NE serves as an alarm system may play a role in this association. system in the brain and inhibits neurovegeta-Specifically, they showed that, among chil-tive functions such as sleep, feeding, and sex-dren who had been referred for treatment, ual behavior. NE also activates the amygdala continuity of internalizing problems predicted fear system Doux, 1992) and inhibits the subsequent HPA axis reactivity to psychoso-medial prefrontal cortex, which ordinarily cial challenge, which turn predicted a sig-
DOI link for cortex CRH receptors (Nemeroff, Owens, changes mood from one state to another based Bissette, Andorn, ing was interpreted to reflect increased CRH thew, Ubriani, Tayfor, release in the frontal cortex resulting in a recent data indicate that the increase in avail-down-regulation of CRH receptors. Finally, able NE that results from antidepressant use Brady, Whitfield, Fox, Gold, and Herkenham gradually results a decrease in the firing (1991) found evidence that antidepressants rate of the LC, which then reduces anxiety produce a down-regulation of the CRH sys-and arousal (Wong et al., 2000). tem. Specifically, they showed that chronic, but not short-term, administration of an anti-depressant (imipramine) Developmental Sequelae to rats caused a sig-nificant decrease in PVN CRH of Major Depression mRNA levels association with a significant increase in At any age, the onset of depression appears Type I glucocorticoid receptor mRNA levels to result in longlasting functional impairment, the hippocampus, which are thought to play even beyond that associated with chronic ill-an important role in restraining the HPA axis. ness (Judd, Akiskal, Zeller, Paulus, Leon, Norepinephrine is perhaps the more widely Maser, Endicott, Coryell, Kunovac, Mueller, studied neurotransmitter biological studies Rice, & Keller, 2000; Wells, Stewart, Hays, of major depression. The first significant bio-Burnam, Rogers, Daniels, Berry, Green-logical hypothesis regarding major depres-field, sion, the catecholamine hypothesis, stated that ler, Endicott, Maser and Klerman (1993) re-major depression resulted from reduced levels ported that adults with unipolar depression of available NE (Schildkraut, 1965). This the-were less likely get married, and those who ory was based on clinical observations that did get married were twice likely to get drugs, such tricyclic antidepressants and separated or divorced. Furthermore, the au-monoamine oxidase inhibitors, which appar-thors found that psychosocial impairments ently increased NE the synapse, had antide-that were associated with depression persisted pressant effects. More recently, many con-even after a significant period of remission. flicting studies have appeared in the literature Adolescents who suffer from depression are regarding noradrenergic function in depres-more likely quit school (Kandel & Davies, sion. This most likely reflects diagnostic het-1986) and to have difficulty adjusting to adult erogeneity and the fact that studies have mea-roles. Specifically, Kandel and Davies (1986) sured CSF NE at a single time point. On the found that women who had suffered from ad-other hand, we recently measured CSF NE ev-olescent depression were more likely to di-ery hour for 24 hr in patients with melan-vorce than were their never-depressed peers, cholic depression. Results indicated that these and men who were depressed in adolescence patients exhibit chronic elevations in NE, experienced more periods of unemployment even during sleep (Wong, Kling, Munson, than did their never-depressed counterparts. In Listwak, Licinio, Prolo, Karp, McCutcheon, terms of direction of causality, Cole and Geracioti, De Bellis, Rice, Goldstein, Veld-Milstead (1989) showed that, in children, de-huis, Chrousos, Oldfield, McCann, & Gold, pression preceded social skill deficits, as well 2000). The elevated NE levels in melancholic a decline in self-perceived competence. patients are compatible with their pathological Granger, Weisz, McCracken, Ikeda, and hyperarousal, anxiety, and physiological hy-Douglas (1996) found evidence that the stress perreactivity. As noted, NE serves as an alarm system may play a role in this association. system in the brain and inhibits neurovegeta-Specifically, they showed that, among chil-tive functions such as sleep, feeding, and sex-dren who had been referred for treatment, ual behavior. NE also activates the amygdala continuity of internalizing problems predicted fear system Doux, 1992) and inhibits the subsequent HPA axis reactivity to psychoso-medial prefrontal cortex, which ordinarily cial challenge, which turn predicted a sig-
cortex CRH receptors (Nemeroff, Owens, changes mood from one state to another based Bissette, Andorn, ing was interpreted to reflect increased CRH thew, Ubriani, Tayfor, release in the frontal cortex resulting in a recent data indicate that the increase in avail-down-regulation of CRH receptors. Finally, able NE that results from antidepressant use Brady, Whitfield, Fox, Gold, and Herkenham gradually results a decrease in the firing (1991) found evidence that antidepressants rate of the LC, which then reduces anxiety produce a down-regulation of the CRH sys-and arousal (Wong et al., 2000). tem. Specifically, they showed that chronic, but not short-term, administration of an anti-depressant (imipramine) Developmental Sequelae to rats caused a sig-nificant decrease in PVN CRH of Major Depression mRNA levels association with a significant increase in At any age, the onset of depression appears Type I glucocorticoid receptor mRNA levels to result in longlasting functional impairment, the hippocampus, which are thought to play even beyond that associated with chronic ill-an important role in restraining the HPA axis. ness (Judd, Akiskal, Zeller, Paulus, Leon, Norepinephrine is perhaps the more widely Maser, Endicott, Coryell, Kunovac, Mueller, studied neurotransmitter biological studies Rice, & Keller, 2000; Wells, Stewart, Hays, of major depression. The first significant bio-Burnam, Rogers, Daniels, Berry, Green-logical hypothesis regarding major depres-field, sion, the catecholamine hypothesis, stated that ler, Endicott, Maser and Klerman (1993) re-major depression resulted from reduced levels ported that adults with unipolar depression of available NE (Schildkraut, 1965). This the-were less likely get married, and those who ory was based on clinical observations that did get married were twice likely to get drugs, such tricyclic antidepressants and separated or divorced. Furthermore, the au-monoamine oxidase inhibitors, which appar-thors found that psychosocial impairments ently increased NE the synapse, had antide-that were associated with depression persisted pressant effects. More recently, many con-even after a significant period of remission. flicting studies have appeared in the literature Adolescents who suffer from depression are regarding noradrenergic function in depres-more likely quit school (Kandel & Davies, sion. This most likely reflects diagnostic het-1986) and to have difficulty adjusting to adult erogeneity and the fact that studies have mea-roles. Specifically, Kandel and Davies (1986) sured CSF NE at a single time point. On the found that women who had suffered from ad-other hand, we recently measured CSF NE ev-olescent depression were more likely to di-ery hour for 24 hr in patients with melan-vorce than were their never-depressed peers, cholic depression. Results indicated that these and men who were depressed in adolescence patients exhibit chronic elevations in NE, experienced more periods of unemployment even during sleep (Wong, Kling, Munson, than did their never-depressed counterparts. In Listwak, Licinio, Prolo, Karp, McCutcheon, terms of direction of causality, Cole and Geracioti, De Bellis, Rice, Goldstein, Veld-Milstead (1989) showed that, in children, de-huis, Chrousos, Oldfield, McCann, & Gold, pression preceded social skill deficits, as well 2000). The elevated NE levels in melancholic a decline in self-perceived competence. patients are compatible with their pathological Granger, Weisz, McCracken, Ikeda, and hyperarousal, anxiety, and physiological hy-Douglas (1996) found evidence that the stress perreactivity. As noted, NE serves as an alarm system may play a role in this association. system in the brain and inhibits neurovegeta-Specifically, they showed that, among chil-tive functions such as sleep, feeding, and sex-dren who had been referred for treatment, ual behavior. NE also activates the amygdala continuity of internalizing problems predicted fear system Doux, 1992) and inhibits the subsequent HPA axis reactivity to psychoso-medial prefrontal cortex, which ordinarily cial challenge, which turn predicted a sig-
ABSTRACT
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