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Updated: Oct 10, 2025
The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders
Published on: August 5, 2017
Prenatal alcohol exposure affects developmental differentiation of interictal discharges in septal and temporal
Maria-Eleni Evangelaki1, Caterina Psarropoulou1
1Laboratory of Animal and Human Physiology, Dept. of Biological Applications and Technology, Faculty of Health Sciences, University of Ioannina, Ioannina, Greece.
Insights
Prenatal alcohol exposure (PAE) alters hippocampal network function, increasing seizure susceptibility. This study reveals how PAE affects neuronal excitability and its development in offspring, offering insights into CNS dysfunction.
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Neuropharmacology
Background:
- Prenatal alcohol exposure (PAE) is a leading cause of lifelong central nervous system (CNS) dysfunction.
- PAE is associated with an increased risk of seizure disorders.
- Understanding the mechanisms underlying PAE-induced neurodevelopmental alterations is crucial.
Purpose of the Study:
- To investigate the effects of PAE on hippocampal excitability in vitro.
- To examine the developmental trajectory of hippocampal network function following PAE.
- To identify potential mechanisms for aberrant neuronal network function in PAE offspring.
Main Methods:
- Hippocampal slices were prepared from young and adult offspring of dams exposed to ethanol during pregnancy.
- Interictal-like epileptiform discharges (IEDs) were induced using Mg2+-free artificial cerebrospinal fluid (ACSF) or 4-Aminopyridine (4-AP).
- Electrophysiological recordings were performed in CA1 pyramidal neurons of temporal and septal slices.
Main Results:
- PAE altered the control of synchronous discharges by NMDA receptors and K+ conductances.
- IED frequency and duration varied by brain region (temporal vs. septal), age, and induction method.
- A temporal-to-septal excitability gradient emerged later in development and was influenced by PAE.
Conclusions:
- PAE significantly impacts hippocampal neuronal network function and its developmental maturation.
- Alterations in excitability and discharge patterns suggest mechanisms for increased seizure susceptibility.
- Findings provide insights into the long-term neurological consequences of prenatal ethanol exposure.
Abstract:
Prenatal alcohol exposure (PAE) provokes lifelong CNS dysfunction, including an increased susceptibility to seizure disorders. We investigated hippocampal excitability in vitro in the offspring of dams exposed to a mild ethanol concentration throughout pregnancy (ethanol 15%v/v in drinking water). Hippocampal slices were prepared from the offspring at a young (Y, 21-30 postnatal days, PND) or adult (A, 60 PND) age, with controls from same age normal rats (N). Synchronous spontaneous interictal-type epileptiform discharges (IEDs) were induced by bathing the slices in Mg2+-free ACSF or in 4-Aminopyridine (4-AP, 50µΜ) and were recorded from CA1 pyramidal layer of temporal (T) and septal slices (S). Hippocampal slices readily generated IEDs following NMDA receptor activation or K+ conductance block, with frequency and duration depending on location (septal or temporal), age, the activating mechanism, and prior conditioning (N or PAE). From the two media, 4-AP induced higher frequency (always), shorter duration (mostly) IEDs compared to Mg 2+-free ACSF. Temporal IED frequency increased with age, whereas septal was stable, indicating an earlier maturation of the latter part. The hippocampal "T to S" (high to low) excitability gradient appeared at/later than the end of the first postnatal month and mostly concerned discharge frequency. Discharge duration generally decreased with maturation but appeared to depend on many factors, including conditioning. Prenatal alcohol exposure differentiated the control of synchronous discharges by NMDA receptors and K+ conductances, and their developmental evolution, thus suggesting potential mechanisms for aberrant hippocampal neuronal network function.
