Long-term alterations of striatal parvalbumin interneurons in a rat model of early exposure to alcohol

Abstract

BackgroundExposure to alcohol in utero is a known cause of mental retardation. Although a certain degree of motor impairment is always associated with fetal alcohol spectrum disorder, little is known about the neurobiological basis of the defective motor control. We have studied the striatal interneurons containing parvalbumin in a rat model of fetal alcohol spectrum disorder.MethodsNewborn rats received ethanol by inhalation from postnatal day two through six and parvalbumin striatal neurons were labeled by immunohistochemistry on postnatal day 60. The spatial distribution of parvalbumin interneurons was studied using Voronoi spatial tessellation and their dendritic trees were completely reconstructed.ResultsParvalbumin interneurons of ethanol-treated animals showed a clustered spatial distribution similar to that observed in control animals. The dendritic tree of parvalbumin interneurons was significantly reduced in ethanol-treated animals, as compared with controls.ConclusionsStriatal parvalbumin interneurons are crucial components of the brain network serving motor control. Therefore, the shrinkage of their dendrites could contribute to the motor and cognitive symptoms observed in fetal alcohol spectrum disorder.

Selective reduction of cerebral cortex GABA neurons in a late gestation model of fetal alcohol spectrum disorder

“…Whereas rodent PV cells originate from neurogenesis in the medial ganglionic eminence, CR cells originate in the caudal ganglionic eminence (Miyoshi et al, 2010; Rymar & Sadikot, 2007). Our results extend previous findings that immunolabeled PV cells are reduced in animal models of late gestational ethanol toxicity, in frontal cortex (Coleman et al, 2012), cingulate cortex (Moore, Ruygrok, Walker, & Heaton, 1997), piriform cortex and hippocampus (Sadrian et al, 2014), the medial septal area (Mitchell, Paiva, & Heaton, 2000), and striatum (De Giorgio, Comparini, Intra, & Granato, 2012). Our findings seem to contradict a finding of increased CR and unchanged PV cell density in rat cortex, after ethanol treatment at days P2–P6 (Granato, 2006).…”

Distinct neurobehavioral dysfunction based on the timing of developmental binge-like alcohol exposure

“…This hypothesized imbalance is a mechanistic foundation for many of the neurobehavioral deficits found in FASD and related cognitive disorders (Sadrian et al, 2013). How long-term synaptic imbalance is initiated by early ethanol exposure is unclear, but is likely connected to the many well-documented effects of ethanol on brain function, such as: apoptotic neurodegeneration (Ikonomidou et al, 2000, Chakraborty et al, 2008), altered synaptic transmission in specific cell populations (Sanderson et al, 2009, Wang et al, 2013), skewed neurotransmitter profiles (Sari et al, 2010), disruption of glutamatergic receptor subunit regulation (Nixon et al, 2002), dendritic tree reduction of PV+ interneurons (De Giorgio et al, 2012), and decreased neurogenesis (Burd et al, 2012); all found immediately following insult and some shown lasting into adulthood. These effects have each been demonstrated after acute or short-term ethanol exposure and are therefore often attributed to disruption of developmental processes occurring within that period.…”

The Brain and Movement: How Physical Activity Affects the Brain

“…Th e cerebral cortex (Tavian, De Giorgio & Granato, 2011;Granato, Palmer, De Giorgio, Tavian & Larkum, 2012;Granato & De Giorgio, 2014;, basal ganglia (De Giorgio, Comparini, Intra & Granato, 2012) and cerebellum are very sensitive to environmental factors during the development of the brain. However, physical activity is able to repair, at least in part, damage that has occurred during brain development (see for review, De Giorgio, 2017).…”