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Alterations in the functions of glutamatergic and GABAergic systems, as well as disturbances in synaptic plasticity related to cognitive functions have been linked to the patophysiology of mood disorders. High level of glucocorticoids in the circulatory system observed after prolonged exposure to stress is considered as major cause of depression. Repeated corticosterone administration represents an animal model to study the effects of non-adaptative stress. The aim of the present study was to examine the influence of repeated corticosterone administration on excitatory and inhibitory synaptic transmission as well as long-term potentiation (LTP) in ex vivo slices of the frontal cortex. Male Wistar rats were treated with corticosterone (10 mg/kg s.c.; suspended in 1% Tween 80) twice daily, for 7 or 21 days. Frontal cortical slices were prepared 48 hours after last drug administration. Whole-cell recordings of spontaneous excitatory postsynaptic currents (sEPSCs) and spontaneous inhibitory postsynaptic currents (sIPSCs) were made from layer II/III pyramidal cells at the holding membrane potential of -78 mV and 0 mV, respectively. Extracellular recordings of field potentials evoked by stimulation of layer V were made from layer II/III. We observed an increase of the mean sEPSCs frequency in slices prepared from animals treated with corticosterone for 7 and 21 days while the mean sEPSCs amplitude remained unchanged. In contrast, no corticosterone-induced changes in parameters characterizing sIPSCs were evident. After 7 and 21 days of stress hormone administration LTP was reduced. These data demonstrate that repeated corticosterone treatment enhances basal glutamatergic transmission and concurrently attenuates LTP. In contrast, GABAergic transmission remained unaffected by corticosterone.
Wistar rats were subjected to restraint lasting 10 min and repeated twice daily for 3, 7 and 14 days. Brain slices were prepared 24 h after the last restraint session and studied ex vivo. In slices of the frontal cortex field potentials (FPs) were evoked by electrical stimulation of underlying sites in the cortical layer V and recorded in layer II/III. In the hippocampal slices field excitatory postsynaptic potentials were evoked by stimulation of Schaffer collaterals and recorded in the stratum radiatum of the CA1 area. In cortical preparations significant differences between experimental and control groups were evident already after 3 days of restraint stress and consisted of an increase in the maximum FP amplitude (3.0 mV vs. 2.2 mV, respectively) as well as a reduced long-term potentiation (LTP; 112 % vs. 139 % of baseline, respectively). While in the frontal cortex there were no differences after 7 or 14 days of restraint, in the hippocampus a significant effect of restraint stress, namely a reduction of LTP (from 146 % to 120 % of baseline) was observed only after 14 days of restraint. These results indicate that repeated restraint stress differentially modulates synaptic transmission and plasticity in the two brain areas studied. Support: “DeMeTer” and statutory funds from the Institute of Pharmacology.
BACKGROUNDANDAIMS: Repeated exposure of experimental animalsto stressinduces a spectrumof depression-like symptomsincluding anorexia, weight loss, anhedonia, fatigue, impaired social interactions and memory dysfunctions. However, the mechanisms of the influence of stress on glutamatergic transmission and synaptic plasticity in the cerebral cortex remain poorly understood. The vagus nerve appears to be an important neural pathway for communicating immune signals originating in the periphery to the brain. Subdiaphragmatic vagotomy (SV) had earlier been shown to inhibit behavioral and neural effects of peripheral interleukin-1beta (IL-1β). We have previously demonstrated that peripherally produced IL-1β may mediate the influence of repeated restraintstress on the functions of the frontal cortex. The purpose of this study was to determine whether the vagus nerve mediates the effects of repeated restraint stress on excitatory synaptic transmission and longterm potentiation (LTP) in the rat frontal cortex. METHODS: Subdiaphragmatic vagotomy or sham surgery was performed 10 days before restraint stress and electrophysiological measurements. The effects of 10 min restraint stress, repeated twice daily for 3 consecutive days were studied ex vivo in the rat frontal cortex slices prepared 24 h after the last stress session. RESULTS: In slices originating from stressed animals, the amplitude of field potentials was increased, compared to control preparations. Consistent with the previous studies, restraint stress resulted in a reduced magnitude of LTP. Stress-induced modifications of the glutamatergic transmission and synaptic plasticity were prevented by SV procedure. CONCLUSION: These data suggest that the vagus nerve may mediate the influence of repeated restraint stress on the rat frontal cortex.
Chronic stress and elevated level of corticosterone have been implicated in a variety of pathophysiological processes including mood disorders. A growing body of evidence links cognitive dysfunctions with abnormalities of excitatory transmission in the brain. We studied glutamatergic transmission and synaptic plasticity in the frontal cortex after exposure of rats to two different types of stress: crowding and restraint. Additionally, repeated corticosterone administration was employed as a model of non-adaptive stress. Electrophysiological experiments were performed on ex vivo frontal cortical slices prepared 24 h after last stress session. In slices originating from stressed and corticosterone-treated animals the amplitude of extracellular field potentials recorded in cortical layer II/III was increased and the magnitude of long-term potentiation (LTP) was decreased. Whole-cell recoding from layer II/III pyramidal neurons demonstrated corticosterone treatment-induced increase in the frequency of spontaneous excitatory postsynaptic currents (sEPSCs). These data point to an enhancement of excitatory transmission in the frontal cortex resulting from an increased glutamate release as a common effect of different types of stress. Support: grant POIG 01.01.02-12-004/09-00 from the European Regional Development Fund
The paraventricular nucleus of the hypothalamus (PVN) is the main regulatory center of the hypothalamic-pituitary-adrenal (HPA) axis. One important function of PVN neurosecretory neurons is the release of corticotropin releasing hormone (CRH) to the pituitary gland. This study was aimed at establishing the effects of restraint stress on GABAergic and glutamatergic inputs to parvocellular neurons of the PVN. Male adult rats were subjected to restraint in metal tubes lasting for 10 min, 2 times daily (repeated for 3 consecutive days). Whole-cell recording were performed from parvocellular neurons. Spontaneous inhibitory postsynaptic currents (sIPSCs) were recorded from cells which were voltage clamped at 0 mV and spontaneous excitatory postsynaptic currents (sEPSCs) were recorded at −76 mV. The amplitude and the frequency of sIPSCs and sEPSCs were measured. Restraint stress resulted in an increase in the frequency of sEPSCs while the amplitude of sEPSCs was not altered. Also the parameters characterizing sIPSCs remained unaltered. Thus, restraint stress selectively enhances excitatory input to the paraventricular nucleus of the rat, most likely via a presynaptic mechanism. Support: POIG 01.01.02-12-004/09-00 awarded by the European Regional Development Fund
Chronic stress and resulting from it, prolonged hyperactivation of the hypothalamic–pituitary–adrenal (HPA) axis and elevated level of glucocorticoids in the circulatory system, have been linked to the pathophysiology of depressive disorders. Dysregulation of the HPA axix is characteristic for individuals with depression. The paraventricular nucleus of the hypothalamus (PVN) is a major regulator of stress responses acting via the release of corticotropin releasing hormone (CRH) to the pituitary gland. This study was aimed at establishing the effects of restraint stress on GABAergic and glutamatergic inputs to the paraventricular nucleus of the rat. Male adult rats were subjected to restraint in metal tubes lasting for 10 min (2 times daily, repeated for 3 consecutive days). Control animals were kept in home cages. Twenty-four hour after the last stress session rats were decapitated, their brains were removed and slices containing a part of PVN (420 µm thick) were cut using a vibrating microtome. Neurons were visualized using Zeiss Axioskop upright microscope using Nomarski optics, a 40× water immersion lens and an infrared camera parvocellular neurons of PVN were selected based on the morphology of the soma and on the response to depolarizing current pulses. Spontaneous IPSCs were recorded from parvocellular neurons which were voltage clamped at 0 mV and sEPSCs were recorded at -76 mV. The amplitude and the frequency of sIPSCs and sEPSCs were recorded. Obtained data indicate that the restraint stress resulted in an increase in the mean frequency of sEPSCs while the mean amplitude of sEPSCs was not altered. The restraint stress had no effect on frequency and amplitude of sIPSCs. Thus, restraint stress enhances glutamatergic, but not GABAergic, inputs to the paraventricular nucleus of the rat. Grant: POIG 01.01.02-12-004/09-00 financed by European Regional Development Fund.
The effects of a repeated treatment with antipsychotic drugs, clozapine and haloperidol, on the modulation of network activity ex vivo by 5-HT receptors were examined in rat frontal cortical slices using extracellular recording. Rats were treated for 21 days with clozapine (30 mg/kg p.o.), or haloperidol (1 mg/kg p.o.). Spontaneous bursting activity was induced in slices prepared 3 days after the last drug administration by perfusion with a medium devoid of Mg2+ ions and with added picrotoxin (30 mM). The application of 2-3 µM 8-OH-DPAT, acting through 5-HT1A receptors, resulted in a reversible decrease of bursting frequency. In the presence of 1 µM DOI, the 5-HT2 agonist, or 5 µM zacopride, the 5-HT4 agonist, bursting frequency increased. Chronic clozapine treatment resulted in an attenuation of the effect of the activation of 5-HT2 receptors, while the effects related to 5-HT1A and 5-HT4 receptor activation were unchanged. Treatment with haloperidol did not influence the reactivity to the activation of any of the three 5-HT receptor subtypes. These data are consistent with earlier findings demonstrating a selective downregulation of 5-HT2A receptors by clozapine and indicate that chronic clozapine selectively attenuates the 5-HT-mediated excitation in neuronal circuitry of the frontal cortex while leaving the 5-HT-mediated inhibition intact.
Adaptive behavior, such as regulation of appetitive motivation or reward processing, is associated with plasticity of the brain’s dopamine system. We examined different types of adaptive behavior in the transgenic mouse line (NR1D1CreERT2) where the GluN1 subunit is selectively inactivated in dopaminoceptive neurons. We used electrophysiological recordings to investigate if functions of D1-expressing neurons are modified. In transgenic animals the amplitude of field potentials in the NAcc was not different form controls, however, LTP was reduced from 138% in control to 118% in D1ERT2 [Tg-N/0-N] animals. Recordings of spontaneous EPSCs from medium spiny neurons of the NAcc demonstrated that approximately 50% of the cells lacked the NMDAR-dependent component of sEPSCs. These results suggest that the mutation significantly alters functions of dopaminoceptive neurons.
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