Submission Type

Poster

Start Date

4-26-2023

Abstract

The neurodevelopmental hypothesis depicts schizophrenia as a long-term consequence of aberrant development of the glutamate and dopamine neurotransmitter systems during the perinatal period. The drug MK-801 is a glutamate N-methyl-D-aspartate (NMDA) receptor antagonist that produces schizophrenia-like symptoms in laboratory rodents when administered early in development. Our laboratory has been investigating whether CDPPB, a positive allosteric modulator of the metabotropic glutamate receptor 5 (mGluR5), would reverse the effects of MK-801. To test this, mice were first administered 0.25 mg/kg MK-801 as neonates, and later given 10.0 mg/kg CDBBD or saline during their juvenile period. Previously, our lab found that MK-801 produced a series of long-term behavioral deficits, some of which were reversed with CDPPB treatment. For the current study, brains were extracted, sectioned with a cryostat, and stained with myelin-specific Luxol-Fast Blue. Brain sections were digitized and examined microscopically. Morphometric measures such as total section volume, lateral ventricle volume and corpus callosum volume were determined with ImageJ software. The goal of the current study is to determine if a reduction of myelinated structures such as the corpus callosum and/or enlargement of the cerebral ventricles are related to the behavioral deficits observed earlier.

Comments

Sponsored by Vincent Markowski

Share

COinS
 
Apr 26th, 12:00 AM

129 - Analysis of Corpus Callosum and Ventricles in Brain Tissue of MK801/CDPPB Treated C57BL6/J Mice

The neurodevelopmental hypothesis depicts schizophrenia as a long-term consequence of aberrant development of the glutamate and dopamine neurotransmitter systems during the perinatal period. The drug MK-801 is a glutamate N-methyl-D-aspartate (NMDA) receptor antagonist that produces schizophrenia-like symptoms in laboratory rodents when administered early in development. Our laboratory has been investigating whether CDPPB, a positive allosteric modulator of the metabotropic glutamate receptor 5 (mGluR5), would reverse the effects of MK-801. To test this, mice were first administered 0.25 mg/kg MK-801 as neonates, and later given 10.0 mg/kg CDBBD or saline during their juvenile period. Previously, our lab found that MK-801 produced a series of long-term behavioral deficits, some of which were reversed with CDPPB treatment. For the current study, brains were extracted, sectioned with a cryostat, and stained with myelin-specific Luxol-Fast Blue. Brain sections were digitized and examined microscopically. Morphometric measures such as total section volume, lateral ventricle volume and corpus callosum volume were determined with ImageJ software. The goal of the current study is to determine if a reduction of myelinated structures such as the corpus callosum and/or enlargement of the cerebral ventricles are related to the behavioral deficits observed earlier.

 

To view the content in your browser, please download Adobe Reader or, alternately,
you may Download the file to your hard drive.

NOTE: The latest versions of Adobe Reader do not support viewing PDF files within Firefox on Mac OS and if you are using a modern (Intel) Mac, there is no official plugin for viewing PDF files within the browser window.