Effects of crack cocaine on anxiety and panic behavior in the high T-labyrinth and involved neural substrates

• Grant number: 17/23262-1
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: May 01, 2018
• End date: April 30, 2020
• Field of knowledge: Biological Sciences - Biology
• Principal Investigator: Milena de Barros Viana
• Grantee: Maria de Fátima Santana de Nazaré
• Host Institution: Instituto de Saúde e Sociedade (ISS). Universidade Federal de São Paulo (UNIFESP). Campus Baixada Santista. Santos , SP, Brazil

Abstract

Crack cocaine was introduced in Brazil in the late 1980s or early 1990s, and its use has dramatically increased in recent decades for all socioeconomic groups. Today, Brazil is also the largest world market for crack cocaine. Crack users have a worse prognosis when compared to users of other illicit drugs because the drug causes a more serious dependency. Drug dependence is a chronic and recurrent disease that is characterized by a compulsion in the search and use of drugs, lack of control of use and an emergent negative emotional state, among which the symptoms of anxiety and irritability that define a motivational deprivation syndrome when the access to drugs is impossible. Repeated exposure to addictive drugs produces neural adaptations in reward-related brain regions that modulate both the development of compulsive drug use and the persistence of craving, and the relapse to the search for drugs in abstinence. Many of these neural adaptations result from the induction of transcription factors and subsequent regulation of gene expression, which may have potentially long lasting effects on neuronal structure and function. The Fos family of transcription factors is of particular interest, since members of this family show pattern of differential induction in brain regions after acute and chronic exposure to cocaine. During abstinence, acute withdrawal of different types of drugs of abuse produces increase in reward thresholds, increase in anxiety type responses, and increase in extracellular CRF levels in the central nucleus of the amygdala. The present work will investigate the effects of exposure to crack cocaine after acute, chronic and abstinence treatment on behavioral patterns associated with anxiety and panic attacks in male Wistar rats using the LTE model. To measure the motor activity of these animals, after the LTE tasks the animals will be tested in an open field. In addition, the activation of the neural substrates involved in these behaviors for each of the three groups will be evaluated through the immunohistochemically analysis of the c-Fos protein for the acute treatment group, Delta-FosB for the chronic treatment group and an analysis of double immunohistochemically labeling for CRF peptide for the abstinence group. (AU)