Abstract
BackgroundEthanol exposure during the rodent equivalent to the 3rd trimester of human pregnancy (i.e., first 1–2 weeks of neonatal life) has been shown to produce structural and functional alterations in the CA3 hippocampal sub-region, which is involved in associative memory. Synaptic plasticity mechanisms dependent on retrograde release of brain-derived neurotrophic factor (BDNF) driven by activation of L-type voltage-gated Ca2+ channels (L-VGCCs) are thought to play a role in stabilization of both GABAergic and glutamatergic synapses in CA3 pyramidal neurons. We previously showed that ethanol exposure during the first week of life blocks BDNF/L-VGCC-dependent long-term potentiation of GABAA receptor-mediated synaptic transmission in these neurons. Here, we tested whether this effect is associated with lasting alterations in GABAergic and glutamatergic transmission.MethodsRats were exposed to air or ethanol for 3 h/day between postnatal days three and five in vapor inhalation chambers, a paradigm that produces peak serum ethanol levels near 0.3 g/dl. Whole-cell patch-clamp electrophysiological recordings of spontaneous inhibitory and excitatory postsynaptic currents (sIPSCs and sEPSCs, respectively) were obtained from CA3 pyramidal neurons in coronal brain slices prepared at postnatal days 13–17.ResultsEthanol exposure did not significantly affect the frequency, amplitude, rise-time and half-width of either sIPSCs or sEPSCs.ConclusionsWe show that an ethanol exposure paradigm known to inhibit synaptic plasticity mechanisms that may participate in the stabilization of GABAergic and glutamatergic synapses in CA3 pyramidal neurons does not produce lasting functional alterations in these synapses, suggesting that compensatory mechanisms restored the balance of excitatory and inhibitory synaptic transmission.
Highlights
Ethanol exposure during the rodent equivalent to the 3rd trimester of human pregnancy has been shown to produce structural and functional alterations in the CA3 hippocampal sub-region, which is involved in associative memory
We evaluated the impact of this ethanol exposure paradigm on γ-amino butyric acid receptor (GABAA) receptor-mediated spontaneous inhibitory postsynaptic currents
Our ethanol exposure paradigm did not significantly affect the properties of spontaneous inhibitory postsynaptic current (sIPSC), a finding that does not support the hypothesis that ethanol exposure during this critical period, when CA3 pyramidal neurons express brain-derived neurotrophic factor (BDNF)/L-type voltage-gated Ca2+ channel (L-VGCC)-dependent synaptic plasticity, produces a lasting impairment in GABAA receptor-dependent synaptic transmission
Summary
Ethanol exposure during the rodent equivalent to the 3rd trimester of human pregnancy (i.e., first 1–2 weeks of neonatal life) has been shown to produce structural and functional alterations in the CA3 hippocampal sub-region, which is involved in associative memory. Synaptic plasticity mechanisms dependent on retrograde release of brain-derived neurotrophic factor (BDNF) driven by activation of L-type voltage-gated Ca2+ channels (L-VGCCs) are thought to play a role in stabilization of both GABAergic and glutamatergic synapses in CA3 pyramidal neurons. The mechanisms responsible for the hippocampal alterations associated with developmental alcohol exposure are not well understood, several studies suggest that these are, in part, a consequence of damage to neurons located in the CA3 sub-region, which is involved in associative memory [1, 4]. Gestational exposure to ethanol triggered the formation of a hypertrophic infra-pyramidal mossy fiber
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