It has been reported that endogenous steroids synthesized de novo in neurons of the central nervous system (CNS) modulate the neuronal activity of neurons in the CNS in terms of a nongenomic way [1][2][3][4][5][6][7]. Histological and binding studies revealed receptors or binding sites for neuroactive steroids in the membrane of neurons of the limbic structures such as hippocampus, septal nuclei and amygdala [8][9][10]. However, there are some differences in the actions of corticosteroids on synaptic transmission in the hippocampus. Neuronal excitability was reduced by corticosterone in hippocampal pyramidal neurons [4]. Zeise et al. [7] showed that corticosterone depressed inhibitory postsynaptic potentials (IPSPs) without affecting the fast excitatory postsynaptic potential (EPSP) in hippocampal and neocortical neurons. On the other hand, dehydroepiandrosterone, a neurosteroid, enhanced the EPSP in hippocampal CA1 pyramidal neurons [11].The lateral septum belongs to the limbic system that participates in a variety of physiological and behavioral functions related to learning, memory and emotions (fear and aggression), as well as autonomic regulation. Neurons in the dorsolateral nucleus (DLSN) receive massive glutamatergic nerve inputs from hippocampal CA1 and CA3 pyramidal neurons through the fimbria/fornix pathway [12,13]. Stimulation of these neurons evokes EPSP in the DLSN neurons [14,15]. Principal neurons in the DLSN which contain ␥-aminobutyric acid (GABA) not only send afferents to hypothalamic and amygdaloid areas but also participate in local inhibitory circuits within the lateral septum mediating the IPSP via their local axon Key words: corticosteroids, lateral septum, presynaptic inhibition, IPSP, GABA-release.
Abstract:The effects of corticosteroids on synaptic transmission in the rat dorsolateral septal nucleus (DLSN) were examined, in vitro, by using intracellular and voltage-clamp recording methods. Prednisolone (100 M) increased the amplitude of excitatory postsynaptic potential (EPSP) and depressed both fast and slow inhibitory postsynaptic potentials (IPSP). Under voltage-clamp conditions, prednisolone (100 M) increased the amplitude of excitatory postsynaptic current (EPSC) and depressed the fast and slow inhibitory postsynaptic currents (IPSCs). Corticosterone (100 M) mimicked the effects of prednisolone on the postsynaptic currents (PSCs). To examine the direct effects of prednisolone on the EPSC and slow IPSC, the fast IPSC was blocked by bicuculline (20 M). Under these experimental conditions, prednisolone (100 M) did not alter the isolated EPSC but depressed slow IPSC by 22Ϯ3% (nϭ10). The fast IPSC was isolated by pretreatment with kynurenic acid and CGP55845A, where the EPSC and slow IPSC were blocked. Prednisolone (100 M) depressed the isolated fast IPSC in DLSN neurons. Prednisolone (100 M) did not change either the inward current produced by glutamate or the outward current produced by ␥-aminobutyric acid (GABA). The results suggest that corticosteroids facilitate excitatory synapti...