Title

MICROGLIA ACTIVATION AFTER EXPOSURE TO METHAMPHETAMINE

Faculty Mentor(s)

Steven Lloyd, Ryan Shanks

Proposal Type

Poster

Location

Open 3rd Floor

Start Date

4-4-2013 4:30 PM

End Date

4-4-2013 6:00 PM

Description/Abstract

Methamphetamine (METH) is a stimulant that can cause severe damage to the dopaminergic regions of the brain. METH is linked with excess microglia activation and neurotoxicity in dopaminergic brain regions. METH is an indirect agonist for dopamine and affects several systems of the brain. Previous studies in our lab revealed an inverse relationship between METH exposure and microglial activation in the tuberoinfundibular TIDA pathway. This study was conducted to: 1) replicate previous studies conducted by other labs using different methodology; and 2) provide relative measurements of data previously collected from the TIDA pathway. Both studies examine the localization of neurotoxicity caused by microglia activation. Six C57Bl/6J mice received either 5 mg/kg METH (3) or an equal volume of saline (3) for ten days. After the final injections brains were extracted and processed for paraffin embedding, then serially sectioned at 5 µm. Activation was assessed using a biotinylated lection and visualized with an ABC technique and the chromogen DAB. Analyses were conducted under the light microscope using NIH Image J. Activation required cell bodies >7.5 µm, relatively short processes, and lectin-positive staining. Cell counts were performed on three slides per brain using three sections from each slide.

This document is currently not available here.

Share

COinS
 
Apr 4th, 4:30 PM Apr 4th, 6:00 PM

MICROGLIA ACTIVATION AFTER EXPOSURE TO METHAMPHETAMINE

Open 3rd Floor

Methamphetamine (METH) is a stimulant that can cause severe damage to the dopaminergic regions of the brain. METH is linked with excess microglia activation and neurotoxicity in dopaminergic brain regions. METH is an indirect agonist for dopamine and affects several systems of the brain. Previous studies in our lab revealed an inverse relationship between METH exposure and microglial activation in the tuberoinfundibular TIDA pathway. This study was conducted to: 1) replicate previous studies conducted by other labs using different methodology; and 2) provide relative measurements of data previously collected from the TIDA pathway. Both studies examine the localization of neurotoxicity caused by microglia activation. Six C57Bl/6J mice received either 5 mg/kg METH (3) or an equal volume of saline (3) for ten days. After the final injections brains were extracted and processed for paraffin embedding, then serially sectioned at 5 µm. Activation was assessed using a biotinylated lection and visualized with an ABC technique and the chromogen DAB. Analyses were conducted under the light microscope using NIH Image J. Activation required cell bodies >7.5 µm, relatively short processes, and lectin-positive staining. Cell counts were performed on three slides per brain using three sections from each slide.