Limits...
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.

Show MeSH

Related in: MedlinePlus

Prenatal stress increases the frequency of sEPSCs recorded from layer II/III pyramidal neurons.(A) Typical examples of raw records from a control neuron (upper trace on the left) and a neuron originating from prenatally stressed rat (lower trace on the left). Traces to the right represent averages of all individual sEPSCs detected during 4 min recordings from a control neuron (upper trace) and a neuron originating from a stressed rat (lower trace). Bar graphs illustrate the effect of prenatal stress on (B) the mean frequency, (C) the mean amplitude, (D) the rise time and (E) the decay time constant of sEPSCs. In B-E, the error bars represent SEM; * p < 0.05. White bars represent neurons (n = 19) originating from control rats (n = 5) and black bars—neurons (n = 16) from prenatally stressed animals (n = 5).
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4352064&req=5

pone.0119407.g004: Prenatal stress increases the frequency of sEPSCs recorded from layer II/III pyramidal neurons.(A) Typical examples of raw records from a control neuron (upper trace on the left) and a neuron originating from prenatally stressed rat (lower trace on the left). Traces to the right represent averages of all individual sEPSCs detected during 4 min recordings from a control neuron (upper trace) and a neuron originating from a stressed rat (lower trace). Bar graphs illustrate the effect of prenatal stress on (B) the mean frequency, (C) the mean amplitude, (D) the rise time and (E) the decay time constant of sEPSCs. In B-E, the error bars represent SEM; * p < 0.05. White bars represent neurons (n = 19) originating from control rats (n = 5) and black bars—neurons (n = 16) from prenatally stressed animals (n = 5).

Mentions: Spontaneous EPSCs were recorded at the holding potential of −76 mV as inward currents (Fig. 4A). In the cells originating from prenatally stressed rats the mean frequency of sEPSCs was significantly higher in comparison to that in the cells from control animals (2.44 ± 0.28 vs. 1.60 ± 0.11 Hz, p = 0.022; Fig. 4B). The stress did not affect the mean amplitude, the mean rise time and the mean decay time constant of sEPSCs (Fig. 4C-E).


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 increases the frequency of sEPSCs recorded from layer II/III pyramidal neurons.(A) Typical examples of raw records from a control neuron (upper trace on the left) and a neuron originating from prenatally stressed rat (lower trace on the left). Traces to the right represent averages of all individual sEPSCs detected during 4 min recordings from a control neuron (upper trace) and a neuron originating from a stressed rat (lower trace). Bar graphs illustrate the effect of prenatal stress on (B) the mean frequency, (C) the mean amplitude, (D) the rise time and (E) the decay time constant of sEPSCs. In B-E, the error bars represent SEM; * p < 0.05. White bars represent neurons (n = 19) originating from control rats (n = 5) and black bars—neurons (n = 16) from prenatally stressed animals (n = 5).
© Copyright Policy
Related In: Results  -  Collection

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

pone.0119407.g004: Prenatal stress increases the frequency of sEPSCs recorded from layer II/III pyramidal neurons.(A) Typical examples of raw records from a control neuron (upper trace on the left) and a neuron originating from prenatally stressed rat (lower trace on the left). Traces to the right represent averages of all individual sEPSCs detected during 4 min recordings from a control neuron (upper trace) and a neuron originating from a stressed rat (lower trace). Bar graphs illustrate the effect of prenatal stress on (B) the mean frequency, (C) the mean amplitude, (D) the rise time and (E) the decay time constant of sEPSCs. In B-E, the error bars represent SEM; * p < 0.05. White bars represent neurons (n = 19) originating from control rats (n = 5) and black bars—neurons (n = 16) from prenatally stressed animals (n = 5).
Mentions: Spontaneous EPSCs were recorded at the holding potential of −76 mV as inward currents (Fig. 4A). In the cells originating from prenatally stressed rats the mean frequency of sEPSCs was significantly higher in comparison to that in the cells from control animals (2.44 ± 0.28 vs. 1.60 ± 0.11 Hz, p = 0.022; Fig. 4B). The stress did not affect the mean amplitude, the mean rise time and the mean decay time constant of sEPSCs (Fig. 4C-E).

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