Effects of prenatal binge‐like ethanol exposure and maternal stress on postnatal morphological development of hippocampal neurons in rats

Abstract

This study showed regional and temporal differences in the development of different morphometric features of principal hippocampal neurons in intact subjects over a protracted 2-months postnatal period. It also demonstrated an overlap in the effects of a moderate fetal ethanol intoxication and a mild maternal stress produced by the intragastric intubation, a commonly used method of ethanol administration to the pregnant dams. Fast recovery from the adverse effects on the soma size, dendritic arborization and spines density observed at birth indicates towards the fetal ethanol/stress induced developmental retardation.

The brain‐derived neurotrophic factor VAL68MET polymorphism modulates how developmental ethanol exposure impacts the hippocampus

“…112 = 10.176, P = .002, η p 2 = 0.083; DG: F 1,112 = 60.867, P < .001, η p 2 = 0.352) between P15 and P50 mice. These results are in general agreement with a recent report, which found decreases in soma area in hippocampal subfields in rats between P10 and P30/P60 34. Taken together with the P15 data, these findings show that early in development vapor chamber EtOH exposure interacts with the BDNF val68met polymorphism to reduce the volume of cell layers in some hippocampal regions, but that these effects are not static, disappearing as the animal ages.…”

Direct Intracellular Signaling by the Carboxy terminus of NMDA Receptor GluN2 Subunits Regulates Dendritic Morphology in Hippocampal CA1 Pyramidal Neurons

“…While this specific age difference could be masking potential BAc effects, it is unlikely, given that BAc animals and WT animals did not differ from one another in any dendritic measure in either methodology. Further, when comparing between animals at 30 and 60 or 70 days of age, there is no difference in relevant dendritic parameters for CA1 pyramidal cells (Jakubowska-Dogru et al, 2017; Brunette et al, 2010). In Jakubowska-Dogru et al, mean dendritic field area, apical and basal dendritic length, apical and basal number of branches, and apical and basal mean highest branch order did not differ between control animals from P30 to P60 (2017).…”

Effect of Alcohol on Hippocampal-Dependent Plasticity and Behavior: Role of Glutamatergic Synaptic Transmission

“…Nevertheless, in some models, at 2 months after birth (∼P60), the litters showed a recovery in the mature spines and the spine density (Ferrer et al, 1988;Tarelo-Acuña et al, 2000), which could be related with the differences in the time of exposure and the blood ethanol concentration reached. Two ethanol injections during E8 produce transient changes in the structure of the pyramidal neurons at P1, which are fully recovered at P10, including the dendritic spine density (Jakubowska-Dogru et al, 2017), suggesting the importance of the developmental stage in ethanol exposure and recovery. On the other hand, differences have been reported in the establishment of synapses, with a decrease in the total synapses, the simple synapses, and the symmetric synapses in the molecular layer of the DG at P30 (Hoff, 1988) as well as alterations in the mossy fiber topography at P60 (West et al, 1981).…”