A presente dissertação teve como objetivo investigar a toxicomania a partir da clínica psicanalítica com usuários de álcool e/ou drogas. Empreendeu-se para tanto, uma revisão teórica do campo psicanalítico orientado pela obra freudiana e pelo ensino de Lacan, articulada a uma análise de cinco casos clínicos. O tema e questões relacionadas surgiram dos desafios ante a prática e de uma atitude investigativa, por parte da autora, diante do serviço público assistencial, além de perceber a relevância atribuída ao tema pela sociedade contemporânea em virtude de seu expressivo crescimento como problema de saúde pública. As questões que se colocam no texto podem ser propostas a partir das perguntas: o que é toxicomania? Qual a influência desse signo? __ uma vez que o termo toxicomania significa alguma coisa para alguém, para a medicina, por exemplo, o sintoma é um signo. Quais as consequências para a direção do tratamento de fazer da toxicomania umsintoma, signo da doença? É possível que a toxicomania seja um sintoma, não como signo, mas, como significante, e, como tal, passível de ser decifrado? Portanto, a linha de trabalho segue, inicialmente, a ética da psicanálise e o lugar do psicanalista na instituição pública de saúde; destaca a toxicomania articulada aos discursos, tal como propostos por Jacques Lacan, e suas modalidades de tratamento; aponta os avatares da toxicomania na contemporaneidade; e, por fim, levanta a questão sobre a toxicomania à luz da psicanálise, bem como seu papel no diagnóstico clínico. Nessa perspectiva, foram verificadas duas hipóteses: a toxicomania como um fenômeno clínico e no caso de pacientes cuja estrutura clínica seja neurótica, a toxicomania ser um sintoma. Para Freud, o sintoma é uma formação de compromisso que promove uma satisfação substitutiva. Ao longo do trabalho, verificou-se que, por vezes, a toxicomania também pode ser uma substituição desse tipo. / This dissertation aimed to investigate the drug addiction from the psychoanalytic clinic with users of alcohol and /or drugs. Taken up for both, a theoretical review of the field work guided by Freudian work and the teaching of Lacan, articulated to an analysis of five cases. The topic and issues were the challenges before the practice and attitude research by the author, before the public welfare, and understand the importance given to the subject by contemporary society because of their significant growth as a health problem. The issues that arise in the text may be proposed from the questions: what is drug addiction? What is the influence of this sign? since the sentence drug addiction means something to someone, because, for medicine, for example, the symptom is a sign. What are the consequences for the direction of the treatment to make the drug addiction a symptom, sign of the disease? Is it possible that the drug addition is a symptom, not like a sign, but like a significant and therefore able to be deciphered? So the line of work follow, initially, the ethics of psychoanalysis and the place of the psychoanalyst in the institution of public health, highlights the drug addiction linked to discourses, as proposed by Jacques Lacan, and their modalits of treatment, as the avatars of drug addiction in contemporaneity, and, finally, raises the question about drug addiction in the light of psychoanalysis, and its role in clinical diagnosis. Accordingly, two hypotheses were verified: the drug addiction as a clinical phenomenon and in the case of patients whose clinical structure is neurotic, the addiction is a symptom. For Freud, the symptom is a formation of compromise that promotes a substitutive satisfaction. Throughout the work, it was found that sometimes the drug addiction can also be a replacement of this type.

published_or_final_version / Social Work / Master / Master of Social Sciences

This thesis aims to investigate and deconstruct the relationship between the narcotic, its narrative, and western modernity. To reveal the relationship, this thesis argues that it is possible to understand the philosophical, political, cultural and ethical dimensions of western modernity through the ulterior lens of the narcotic. As such, this thesis investigates western modernity's relationship to (a) cocaine as a specific narcotic, and (b) the concept of the narcotic with all its attendant connotations of addictions, illegitimacy, transgression, illegality, and so on. Accordingly, the thesis is both interpretive of the historical narrative of the narcotic of cocaine, and generative in its deconstruction of the relationship between western modernity and the concept of the narcotic. The deconstruction of this relationship ultimately reveals both prior narratives not as oppositional, but as supplementary. This has radical consequences for the manner in which we engage with narcotic use and the user - if the narcotic is supplement to the logic of western modernity, at each attempt to expel the use and user of the narcotic, rather then create difference, we self implicate ourselves in that expulsion and distance. To seek a new and more just means of dealing with the concept of the narcotic, and its use, therefore requires a new epistemological framework which can at once contemplate both narratives at the same time. To this end, the thesis suggests the use of critical complexity theory as one such methodological tool, if supplemented by the thoughts and strategies of Derridian deconstruction and Foucauldian discourse analysis.

published_or_final_version / Social Work / Master / Master of Social Work

My work investigates a lifelong passion for buildings, homes, and architecture. Buildings are more then shelters made of wood and screws; I personify them as if they were living breathing creatures. I’m particularly drawn to rundown and abandoned structures because I empathize with these sad looking buildings that were once majestic. This personal connection exists because I view them as versions of my former self, rough around the edges with a promising interior. Expanding beyond vacant and decaying buildings, I portray my experiences within fabricated architectural systems. I communicate with building materials and architecture through their many layers of physical and socially constructed histories. Drawing from my memories and feelings surrounding my brother’s death and subsequent drug addiction, I’ve focused on the emotions of abandonment, isolation, absence, and loneliness.

Cocaine (CA) exposure during pregnancy causes long-lasting negative effects on fetal brain development and eventually results in motor dysfunction or changes in learning and memory performance. £^-amino-butyric acid (GABA) is the primary inhibitory neurotransmitter in the adult brain and undergo a switch from excitatory to inhibitory during early postnatal period. The excitatory/inhibitory switch is resulted in the relative temporal expression of K+-Cl- cotransporter 2 (KCC2). GABA is the neurotransmitter in the rat was born from excitement to inhibition and until the growth of thirty days have completely inhibitory. Here we test the effect of CA prenatal exposure on the expression of KCC2 in prefrontal cortex (recognition), hippocampus (memory), VTA (reward) and nucleus accumbens (reward). Protein expression profile of control or prenatal CA treated groups were evaluated by western blot in 2 days interval from postnatal day (PND) 8 to 30. The expression of KCC2 was time-dependently enhanced from PND 8 and reaches its maximal expression around PND 18 in prenatal CA exposure groups. The time-dependent profile of KCC2 expression in prefrontal cortex and NAc was significantly delayed in prenatal CA exposure group. We then correlate the KCC2 expression and the cocaine sensitivity by locomotor activity assay. We found group A shows a higher sensitivity to cocaine than group B in control rats. Surprisingly, group A of prenatal cocaine reduce the sensitive to cocaine to a similar extend like group B in control rats, suggesting prenatal exposure of cocaine might enhance the KCC2 expression. Furthermore, age range of A group (PND 22~27) and B group (PND 29~34) to repeated cocaine exposure resulted in up-regulation of KCC2 expression in B group earlier than A group. We found that the KCC2 expressions of repeated cocaine exposure in B group were higher than A group. In other words, in the B group, the inhibitory effect of GABA was significant and the locomotor activity was relatively slow. Therefore, the A group was more easy be cocaine addiction than B group. We next explore the signaling mechanism underlying cocaine exposure-induced KCC2 expression inhibition. Brain slices were incubated with cocaine with or without dopamine receptor antagonists and KCC2 expression was evaluated by western blot. Either SCH23390 (dopamine D1-receptor inhibitor) or eticlopride (dopamine D2-receptor inhibitor) significantly hamper the inhibition of KCC2 expression by cocaine in normal slices. However, only D2 antagonist eticlopride but not SCH23390 is effective reverse cocaine-induced KCC2 expression inhibition. Overall, results from our current studies provide a further insight into the molecular mechanism of cocaine-induced synaptic modification.

published_or_final_version / Public Administration / Master / Master of Social Sciences

Thesis (Ph. D. in Molecular Physiology and Biophysics)--Vanderbilt University, Aug. 2009. / Title from title screen. Includes bibliographical references.

Thesis (Ph. D. in Neuroscience)--Vanderbilt University, Aug. 2009. / Title from title screen. Includes bibliographical references.

Thesis (J.C.L.)--Catholic University of America, 2003. / Includes bibliographical references (leaves 47-52).