Corticosterone Reduces Synaptic Inhibition in Rat Hippocampal and Neocortical Neurons in vitro
M L Zeise1, A Teschemacher, J Arriagada
1Max-Planck-lnstitute for Psychiatry, Clinical Neuropharmacology, Munich, FRG.
Journal of Neuroendocrinology
|May 11, 2011
Summary
Corticosterone, a stress hormone, reduces synaptic inhibition in rat brain neurons. This effect, particularly in the hippocampus, alters neuronal response patterns, potentially impacting information processing.
Area of Science:
- Neuroscience
- Endocrinology
- Cellular Electrophysiology
Background:
- Corticosterone is a primary glucocorticoid hormone involved in stress response.
- Glucocorticoids are known to influence neuronal function, but their specific effects on synaptic inhibition and excitability require detailed investigation.
Purpose of the Study:
- To investigate the impact of corticosterone on postsynaptic potentials and membrane properties in rat neocortical and hippocampal pyramidal neurons.
- To determine the role of glucocorticoid receptors in mediating these effects.
Main Methods:
- Intracellular recordings were performed on neocortical and hippocampal CA1 pyramidal neurons from adult rats in vitro.
- Neurons were exposed to varying concentrations of corticosterone (10(-7) to 10(-5) M).
- The effects were assessed using depolarizing current steps and orthodromic stimulation, with and without the glucocorticoid receptor antagonist RU 38486.
Main Results:
- Corticosterone significantly reduced both early and late components of inhibitory postsynaptic potentials in both neocortical and hippocampal neurons.
- The glucocorticoid receptor antagonist RU 38486 blocked this effect in the hippocampus.
- In hippocampal neurons, corticosterone decreased a depolarizing membrane transient and increased action potential threshold, while neocortical neurons showed no change in these parameters.
- No significant alterations were observed in excitatory postsynaptic potentials, action potentials, membrane potential, input resistance, or afterhyperpolarization.
Conclusions:
- Corticosterone modulates synaptic inhibition and neuronal excitability, with distinct effects in the hippocampus versus the neocortex.
- Reduced synaptic inhibition and altered excitability in the hippocampus suggest a mechanism for enhanced response to repeated synaptic inputs and blunted low-frequency responses.
