Figure 1.
Bi-exponential fitting and pharmacological blockade of AHP responses in limbic pyramidal neurons.
A: AHP recording from a representative CA1 neuron (gray) and the fit (dark gray) overlaid with the extracted decay of the medium (black-dotted) and sAHP (black-continuous) recorded from the same neuron before and after Forskolin (50 µm, 15 min) application. Inset shows the current protocol used to evoke the AHPs. B: AHP recording from a representative layer 2/3 lateral OFC neuron before and after Forskolin treatment. C: The goodness of fit (R2) to the AHP response is averaged across CA1 neurons recorded from the vehicle (gray diamond) and corticosterone (black circles) groups. D: Goodness of fit to the AHP response from layer 2/3 lateral OFC neurons. E: Goodness of fit to the AHP response from layer 2/3 prelimbic neurons. F: Goodness of fit to the AHP response from layer 2/3 infralimbic neurons. Number within brackets in the legends indicates number of neurons.
Table 1.
Active and passive properties of neurons within each of the limbic brain regions were not significantly different between treatment (vehicle and corticosterone) groups.
Figure 2.
The long lasting effects of corticosterone treatment on AHPs and action potential firing of hippocampal CA1 pyramidal neurons.
A: schematic depiction of the experimental protocol. B: locations of the recorded neurons on a pictorial coronal mouse brain section. C: representative AHP responses from vehicle and corticosterone groups overlaid with the fit. Light gray: raw trace, thick dark gray: fit, dotted line: mAHP decay, thin black line: sAHP decay. Inset shows the current protocol used to evoke the AHPs. D: traces of action potentials from neurons representative of the vehicle and corticosterone groups. Marking on the trace indicate the positions of spike amplitude, half-width and threshold measurements. E: mAHP peak amplitude averaged per group and per current step. F: averaged values of sAHP peak amplitude for each current injection step. G: sAHP peak amplitude is correlated with total number of action potentials per current step. RVeh/RCort: Pearson’s correlation coefficient for vehicle and corticosterone treated groups. *: P<0.05; **: P<0.0001. H: accommodation index (% ratio of the interspike intervals of the last two spikes to the first two spikes) from vehicle and corticosterone groups. PInt: a significant interaction effect of corticosterone. Number within brackets in the legends indicates number of neurons.
Figure 3.
The long lasting effects of corticosterone treatment on AHPs and action potential firing of layer 2/3 lateral OFC pyramidal neurons.
A: locations of the recorded neurons on a pictorial coronal mouse brain section. B: representative AHP responses from vehicle and corticosterone groups overlaid with the fit. Light gray: raw trace, thick dark gray: fit, dotted line: mAHP decay, thin black line: sAHP decay. Inset shows the current protocol used to evoke the AHPs. C: traces of action potentials from neurons representative of the vehicle and corticosterone groups. Marking on the trace indicate the positions of spike amplitude, half-width and threshold measurements. D: mAHP peak amplitude averaged per group and per current step. E: averaged values of sAHP peak amplitude for each current injection step. F: Power of the sAHP interaction effect (corticosterone treatment x current steps) with increasing total sample size. Dotted vertical line indicates the sample size (∼70) required for a power of 0.8. Open square in the plot indicates the power at the actual sample size. G: accommodation index (% ratio of the interspike intervals of the last two spikes to the first two spikes) from vehicle and corticosterone groups. Number within brackets in the legends indicates number of neurons.
Figure 4.
The long lasting effects of corticosterone treatment on AHPs and action potential firing of layer 2/3 prelimbic pyramidal neurons.
A: locations of the recorded neurons on a pictorial coronal mouse brain section. B: representative AHP responses from vehicle and corticosterone groups overlaid with the fit. Light gray: raw trace, thick dark gray: fit, dotted line: mAHP decay, thin black line: sAHP decay. Inset shows the current protocol used to evoke the AHPs. C: traces of action potentials from neurons representative of the vehicle and corticosterone groups. Marking on the trace indicate the positions of spike amplitude, half-width and threshold measurements. D: mAHP peak amplitude averaged per group and per current step. E: averaged values of sAHP peak amplitude for each current injection step. F: accommodation index (% ratio of the interspike intervals of the last two spikes to the first two spikes) from vehicle and corticosterone groups. Number within brackets in the legends indicates number of neurons.
Figure 5.
The long lasting effects of corticosterone treatment on AHPs and action potential firing of layer 2/3 infralimbic pyramidal neurons.
A: left: a sample pyramidal neuron filled with fluorescent dye. Inset: zoomed image of the neuron (white arrow). Scale bar equals 20 microns. Right, locations of the recorded neurons on a pictorial coronal mouse brain section. B: representative AHP responses from vehicle and corticosterone groups overlaid with the fit. Light gray: raw trace, thick dark gray: fit, dotted line: mAHP decay, thin black line: sAHP decay. Inset shows the current protocol used to evoke the AHPs. C: traces of action potentials from neurons representative of the vehicle and corticosterone groups. Marking indicate the positions of spike amplitude, half-width and threshold measurements. D: mAHP peak amplitude averaged per group and per current step. E: averaged values of sAHP peak amplitude for each current injection step. F: accommodation index (% ratio of the interspike intervals of the last two spikes to the first two spikes) from vehicle and corticosterone groups. Number within brackets in the legends indicates number of neurons.