Defense Date


Document Type


Degree Name

Master of Science


Anatomy & Neurobiology

First Advisor

M. Alex Meredith


Dendritic spines are the major site of excitatory synapses in cortex, and factors that reduce dendritic spine numbers will produce serious cortical processing deficits, such as has been demonstrated for mental retardation and other psychiatric disorders. Prenatal alcohol exposure also has detrimental effects on brain development that lead to Fetal Alcohol Spectrum Disorder (FASD), which results in reduction of dendritic spine numbers in the hippocampus, prefrontal cortex and somatosensory cortex. FASD also is associated with temporal processing disorders involving sequential auditory stimuli that would be processed in auditory cortical areas. However, it is unknown if the reduction of spine density following prenatal alcohol exposure occurs at auditory cortex, or is generally reduced across the different sensory cortices. This present study examined that question. Young adult ferrets (176 days old, 1 male, 1 female), that were exposed to alcohol during the equivalent of third-trimester development, were used to prepare Golgi-Cox stained sections through primary auditory cortex (A1). Other cortical regions examined included primary somatosensory (S1), and higher-level multisensory cortices of lateral rostral suprasylvian (LRSS) and rostral posterior parietal (PPr) areas. Control values from normal animals (n=3) were derived from a previous study. The results of this present study demonstrated that, dendritic spine density was significantly (Student's t-test, P < 0.05) lower in the alcohol treated group than in normal controls in all the cortical regions examined. These data indicate that although reduced spine density in auditory cortex may underlie temporal processing disorders in FASD, pre-natal alcohol exposure has widespread consequences for sensory cortical processing in general.


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Date of Submission

May 2011