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Prenatal stress enhances excitatory synaptic transmission and impairs long-term potentiation in the frontal cortex of adult offspring rats.

Sowa J, Bobula B, Glombik K, Slusarczyk J, Basta-Kaim A, Hess G - PLoS ONE (2015)

Bottom Line: In ex vivo frontal cortex slices originating from prenatally stressed animals, the amplitude of extracellular field potentials (FPs) recorded in cortical layer II/III was larger, and the mean amplitude ratio of pharmacologically-isolated NMDA to the AMPA/kainate component of the field potential--smaller than in control preparations.These effects were accompanied by an increase in the mean frequency, but not the mean amplitude, of spontaneous excitatory postsynaptic currents (sEPSCs) in layer II/III pyramidal neurons.These data demonstrate that stress during pregnancy may lead not only to behavioral disturbances, but also impairs the glutamatergic transmission and long-term synaptic plasticity in the frontal cortex of the adult offspring.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland.

ABSTRACT
The effects of prenatal stress procedure were investigated in 3 months old male rats. Prenatally stressed rats showed depressive-like behavior in the forced swim test, including increased immobility, decreased mobility and decreased climbing. In ex vivo frontal cortex slices originating from prenatally stressed animals, the amplitude of extracellular field potentials (FPs) recorded in cortical layer II/III was larger, and the mean amplitude ratio of pharmacologically-isolated NMDA to the AMPA/kainate component of the field potential--smaller than in control preparations. Prenatal stress also resulted in a reduced magnitude of long-term potentiation (LTP). These effects were accompanied by an increase in the mean frequency, but not the mean amplitude, of spontaneous excitatory postsynaptic currents (sEPSCs) in layer II/III pyramidal neurons. These data demonstrate that stress during pregnancy may lead not only to behavioral disturbances, but also impairs the glutamatergic transmission and long-term synaptic plasticity in the frontal cortex of the adult offspring.

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Prenatal stress does not modify the intrinsic excitability of layer II/III pyramidal neurons.(A) Example of a response of a cell from a stressed rat (upper trace) to a depolarizing current pulse (lower trace). (B) Example of an injected current vs. spiking rate relationship in a cell shown in (A). (C) The mean firing threshold (± SEM) and (D) the mean gain (a slope of injected current vs. spiking rate relationship; ± SEM) of pyramidal neurons prepared from control (white bars; 19 cells from 5 rats) and prenatally stressed animals (black bars; 16 cells from 5 rats). The differences are not significant.
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pone.0119407.g003: Prenatal stress does not modify the intrinsic excitability of layer II/III pyramidal neurons.(A) Example of a response of a cell from a stressed rat (upper trace) to a depolarizing current pulse (lower trace). (B) Example of an injected current vs. spiking rate relationship in a cell shown in (A). (C) The mean firing threshold (± SEM) and (D) the mean gain (a slope of injected current vs. spiking rate relationship; ± SEM) of pyramidal neurons prepared from control (white bars; 19 cells from 5 rats) and prenatally stressed animals (black bars; 16 cells from 5 rats). The differences are not significant.

Mentions: Whole-cell recordings were obtained from layer II/III neurons exhibiting a regular spiking firing pattern in response to a depolarizing current pulse (Fig. 3A) and no spontaneous spiking activity at the resting membrane potential. There were no significant differences between neurons originating from prenatally stressed and control animals either in the resting membrane potential (−74.9 ± 0.7 vs. −75.3 ±0.6 mV, respectively, p = 0.684) or the input resistance (44.9 ± 3.2 vs. 42.3 ± 3.1 MΩ, respectively, p = 0.563). Analyses of the relationship between injected current and firing rate (Fig. 3B) demonstrated that prenatal stress did not modify the intrinsic excitability of frontal cortical pyramidal neurons (Fig. 3C, D).


Prenatal stress enhances excitatory synaptic transmission and impairs long-term potentiation in the frontal cortex of adult offspring rats.

Sowa J, Bobula B, Glombik K, Slusarczyk J, Basta-Kaim A, Hess G - PLoS ONE (2015)

Prenatal stress does not modify the intrinsic excitability of layer II/III pyramidal neurons.(A) Example of a response of a cell from a stressed rat (upper trace) to a depolarizing current pulse (lower trace). (B) Example of an injected current vs. spiking rate relationship in a cell shown in (A). (C) The mean firing threshold (± SEM) and (D) the mean gain (a slope of injected current vs. spiking rate relationship; ± SEM) of pyramidal neurons prepared from control (white bars; 19 cells from 5 rats) and prenatally stressed animals (black bars; 16 cells from 5 rats). The differences are not significant.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4352064&req=5

pone.0119407.g003: Prenatal stress does not modify the intrinsic excitability of layer II/III pyramidal neurons.(A) Example of a response of a cell from a stressed rat (upper trace) to a depolarizing current pulse (lower trace). (B) Example of an injected current vs. spiking rate relationship in a cell shown in (A). (C) The mean firing threshold (± SEM) and (D) the mean gain (a slope of injected current vs. spiking rate relationship; ± SEM) of pyramidal neurons prepared from control (white bars; 19 cells from 5 rats) and prenatally stressed animals (black bars; 16 cells from 5 rats). The differences are not significant.
Mentions: Whole-cell recordings were obtained from layer II/III neurons exhibiting a regular spiking firing pattern in response to a depolarizing current pulse (Fig. 3A) and no spontaneous spiking activity at the resting membrane potential. There were no significant differences between neurons originating from prenatally stressed and control animals either in the resting membrane potential (−74.9 ± 0.7 vs. −75.3 ±0.6 mV, respectively, p = 0.684) or the input resistance (44.9 ± 3.2 vs. 42.3 ± 3.1 MΩ, respectively, p = 0.563). Analyses of the relationship between injected current and firing rate (Fig. 3B) demonstrated that prenatal stress did not modify the intrinsic excitability of frontal cortical pyramidal neurons (Fig. 3C, D).

Bottom Line: In ex vivo frontal cortex slices originating from prenatally stressed animals, the amplitude of extracellular field potentials (FPs) recorded in cortical layer II/III was larger, and the mean amplitude ratio of pharmacologically-isolated NMDA to the AMPA/kainate component of the field potential--smaller than in control preparations.These effects were accompanied by an increase in the mean frequency, but not the mean amplitude, of spontaneous excitatory postsynaptic currents (sEPSCs) in layer II/III pyramidal neurons.These data demonstrate that stress during pregnancy may lead not only to behavioral disturbances, but also impairs the glutamatergic transmission and long-term synaptic plasticity in the frontal cortex of the adult offspring.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland.

ABSTRACT
The effects of prenatal stress procedure were investigated in 3 months old male rats. Prenatally stressed rats showed depressive-like behavior in the forced swim test, including increased immobility, decreased mobility and decreased climbing. In ex vivo frontal cortex slices originating from prenatally stressed animals, the amplitude of extracellular field potentials (FPs) recorded in cortical layer II/III was larger, and the mean amplitude ratio of pharmacologically-isolated NMDA to the AMPA/kainate component of the field potential--smaller than in control preparations. Prenatal stress also resulted in a reduced magnitude of long-term potentiation (LTP). These effects were accompanied by an increase in the mean frequency, but not the mean amplitude, of spontaneous excitatory postsynaptic currents (sEPSCs) in layer II/III pyramidal neurons. These data demonstrate that stress during pregnancy may lead not only to behavioral disturbances, but also impairs the glutamatergic transmission and long-term synaptic plasticity in the frontal cortex of the adult offspring.

Show MeSH
Related in: MedlinePlus