• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• 제5권1호
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• pp.93-101
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• 1994

반복적으로 공격적인 행동 양상을 보이는 사람들의 세로토닌 반응(serotonergic responsivity)이 정상인과 비교하여 차이가 있을 것인지를 알아보고자 연구를 실시하였다. 나이를 대조하여 공격성군(소년원 재소자 16명)과 대조군(의과대학생 17명)으로 구분한 연구대상에게, 여러 심리검사 척도를 이용하여 공격성의 심한 정도를 정의하고, 두뇌의 세로토닌 기능과 일치하는 것으로 알려진 혈소판의 이미프라민 결합을 측정하여 다음과 같은 결과를 얻었다. 1) 공격성군은 대조군에 비하여 공격척도상 신체적 공격성(physical aggression)의 평균이 모두 유의하게 높은 값을 나타내었다. 이외에도 공격성군은 대조군에 비해 충동성(impulsivity), 적대감(hostility), 정신증(psychoticism)등이 통계적으로 유의하게 높은 평균값을 보였다. 2) 공격성군은 대조군에 비하여 혈소판 이미프라민 최대결합부위 밀도(Bmax)가 낮은 경향을 보였다. 3) 공격성군과 대조군의 혈소판 이미프라민 결합의 결합상수(Kd) 값은 통계적으로 유의한 차이를 보이지 않았다. 4) 연구대상군을 전체로 하였을 때, 공격성척도(PFAV)와 갈등해결 척도(CTS)의 신체적 공격성의 심한 정도는 혈소판 이미프라민 최대결합부위 밀도(Bmax)와 통계적으로 유의한 정도의 역비례 상관관계를 보였다.

• 생물정신의학
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• 제1권1호
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• pp.88-97
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• 1994

Many evidences are compatible with the correlation between the inhibition of [$^3H$] imipramine([$^3H$]IMI) and [$^3H$]paroxetine([$^3H$]PAT) binding to the 5-hydroxytryptamine(5-HT) transporter complex and the 5-HT uptake of 5-HT neurons and platelets, and most antidepressants have been shown to inhibit the [$^3H$]IMI and [$^3H$]PAT binding and the neuronal 5-HT uptake. However, several paradoxical research findings led to doubt about the pharmacological significance of the [$^3H$]IMI and [$^3H$]PAT binding sites. This study was carried to clarify the correlation between the [$^3H$]IMI and [$^3H$]PAT binding parameters and the tissue 5-HT content or/and [$^3H$]5-HT uptake in the rabbit platelet, which contains 40 times ad much 5-HT as that of human platelet and shows the 10 fold higher $B_{max}$ of the 5-HT transporter binding to a 5-HT uptake inhibitor. The rabbits were treated for 28 days with amitriptyline(4mg/kg/day : AP), fluoxetine(0.5mg/kg/day : FO), and sertraline(0.5mg/kg/day : SA) via an Alzet osmotic pump implanted for constant infusion. The [$^3H$]IMI binding $B_{max}$ and $K_d$ of the rabbit platelets were $6.4{\pm}1.2$pmol/mg protein and $10.9{\pm}2.1$nM and those in the [$^3H$]PAT binding were $8.6{\pm}1.1$pmol/mg protein and $1.6{\pm}0.3$nM, respectively. AP slightly increased $B_{max}$ of [$^3H$]IMI binding and both [$^3H$]IMI binding and [$^3H$]PAT binding $K_d$, and i contrast, it slightly decreased $B_{max}$ of [$^3H$]PAT binding. FO Slightly increased $K_d$ of both and [$^3H$]IMI and [$^3H$]PAT binding and slightly decreased $B_{max}$ of [$^3H$]IMI and [$^3H$]PAT binding. SA produced the significant increase of [$^3H$]PAT binding $B_{max}$ and the slight increase of both [$^3H$]IMI and [$^3H$]PAT binding $K_d$ and in contrast, it slightly decreased $B_{max}$ and of [$^3H$]IMI binding. And, the $V_{max}$ and $K_m$ of platelet [$^3H$]5-HT uptake were $24.2{\pm}2.4$pmol/$10^8$ platelets/min and $3.3{\pm}0.3$nM, respectively. The $V_{max}$ was little affected by AP, FO, or SA, but the [$^3H$]5-HT uptake $K_m$ value was moderately increased by FO. However, the platelet 5-HT content was moderately decreased by all of the 5-HT uptake inhibitors used in this study. These results seem to be consistent with the allosterical and competitive interaction of 5-HT uptake inhibiting antidepressants with each other as well as 5-HT in the 5-HT transporter binding, and provide no support for the view that the potencies of 5-HT uptake inhibitors to inhibit the [$^3H$]IMI or [$^3H$]PAT binding with 5-HT transporter complex correlate with their antidepressant potencies.