Neurosteroid regulation of inhibitory synaptic transmission in the rat hippocampus in vitro

Jh, Meyer; Lee, S.; Wittenberg, George F.; Randall, Robert D.; Gruol, Donna L.

doi:10.1016/s0306-4522(98)00543-0

Cited by 36 publications

(19 citation statements)

References 42 publications

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“…Thus, the efficacy of DHEAS on recovery of spine loss of cortical pyramidal neurons may depend on the intracellular Ca 2+ transients. Some studies also indicate that DHEAS can play a neuromodulatory role and alter synaptic transmission in the hippocampus through selective postsynaptic actions on inhibitory synaptic transmission (Ffrench-Mullen and Spence, 1991;Meyer et al, 1999;Steffensen, 1995). It has been reported that DHEA binding to the androgen or estrogen receptor is lower because its affinity is at least an order of magnitude less than that of the endogenous ligand (Waterhouse et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Exogenous dehydroisoandrosterone sulfate reverses the dendritic changes of the central neurons in aging male rats

Chen

Tseng

Wang

et al. 2014

Experimental Gerontology

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Section: Discussionmentioning

confidence: 99%

Exogenous dehydroisoandrosterone sulfate reverses the dendritic changes of the central neurons in aging male rats

Chen

Tseng

Wang

et al. 2014

Experimental Gerontology

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“…Farb et al (124), using whole cell recordings from voltageclamped spinal cord neurons, have observed no enhancing effect of DHEAS (at concentrations up to 10 µM) on the basal transmembrane potential, and the spontaneous firing activity and no modulatory effect of DHEAS on the neuronal response to NMDA, that is, a direct modulatory action. However, Meyer et al (125) showed that DHEAS, in the concentration range of 10 -100 µM, weakly facilitated the activation of CA1 neurons in hippocampal slices after stimulation of the Schaffer collaterals. This enhancement was related however to a concomitant antagonistic activity of the neurosteroid on GABA-mediated inhibitory postsynaptic potentials as well as an indirect augmentation of the glutamatergic excitatory postsynaptic potentials.…”

Section: 2mentioning

confidence: 99%

The Sigma1 Protein as a Target for the Non-genomic Effects of Neuro(active)steroids: Molecular, Physiological, and Behavioral Aspects

2006

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Abstract. Steroids synthesized in the periphery or de novo in the brain, so called 'neurosteroids', exert both genomic and nongenomic actions on neurotransmission systems. Through rapid modulatory effects on neurotransmitter receptors, they influence inhibitory and excitatory neurotransmission. In particular, progesterone derivatives like 3α-hydroxy-5α-pregnan-20-one (allopregnanolone) are positive allosteric modulators of the γ-aminobutyric acid type A (GABA A ) receptor and therefore act as inhibitory steroids, while pregnenolone sulphate (PREGS) and dehydroepiandrosterone sulphate (DHEAS) are negative modulators of the GABA A receptor and positive modulators of the N-methyl-D-aspartate (NMDA) receptor, therefore acting as excitatory neurosteroids. Some steroids also interact with atypical proteins, the sigma (σ) receptors. Recent studies particularly demonstrated that the σ 1 receptor contributes effectively to their pharmacological actions. The present article will review the data demonstrating that the σ 1 receptor binds neurosteroids in physiological conditions. The physiological relevance of this interaction will be analyzed and the impact on physiopathological outcomes in memory and drug addiction will be illustrated. We will particularly highlight, first, the importance of the σ 1 -receptor activation by PREGS and DHEAS which may contribute to their modulatory effect on calcium homeostasis and, second, the importance of the steroid tonus in the pharmacological development of selective σ 1 drugs.

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“…Population spike amplitudes were measured simultaneous to recordings of fepsps at the dendritic recording site. Recurrent inhibition was evaluated as a percentage decrease in the population spike amplitude evoked by the second relative to the first stimulation pulse (Meyer et al, 1999).…”

Section: Paired-pulse Inhibition Of Somatic Population Spike Amplitudesmentioning

confidence: 99%

Steroid pregnenolone sulfate enhances NMDA‐receptor‐independent long‐term potentiation at hippocampal CA1 synapses: Role for L‐type calcium channels and sigma‐receptors

et al. 2007

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Severe stress elevates plasma and CNS levels of endogenous neuroactive steroids that can contribute to the influence of stress on memory formation. Among the neuroactive steroids, pregnenolone sulfate (PREGS) reportedly strengthens memories and is readily available as a memory-enhancing supplement. PREGS actions on memory may reflect its ability to produce changes in memory-related neuronal circuits, such as long-term potentiation (LTP) of excitatory transmission in hippocampus. Here, we report a previously undiscovered pathway by which PREGS exposure promotes activity-dependent LTP of field excitatory postsynaptic potentials at CA1 synapses in hippocampal slices. Thus, application of PREGS, but not the phosphated conjugate of the steroid, selectively facilitates the induction of a slow-developing LTP in response to high-frequency (100 Hz) afferent stimulation, which is not induced in the absence of the steroid. The slow-developing LTP is independent of NMDA-receptor function (i.e., dAP5 insensitive) but dependent on functional L-type voltage-gated calcium channels (VGCC) and sigma-receptors. By contrast, PREGS at the highest concentration tested produces a depression in NMDA-receptor-dependent LTP, which is evident when sigma-receptor function is compromised by the presence of a sigma-receptor antagonist. We found that at early times during the induction phase of L-type VGCC-dependent LTP, PREGS via sigma-receptors transiently enhances presynaptic function. As well, during the maintenance phase of L-type VGCC-dependent LTP, PREGS promotes a further increase in presynaptic function downstream of LTP induction, as evidenced by a decrease in paired-pulse facilitation. The identification of complex regulatory actions of PREGS on LTP, involving sigma-receptors, L-type VGCCs, NMDA-receptors, and inhibitory circuits will aid future research endeavors aimed at understanding the precise mechanisms by which this stress-associated steroid may engage multiple LTP-signaling pathways that alter synaptic transmission at memory-related synapses.

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Neurosteroid regulation of inhibitory synaptic transmission in the rat hippocampus in vitro

Cited by 36 publications

References 42 publications

Exogenous dehydroisoandrosterone sulfate reverses the dendritic changes of the central neurons in aging male rats

Exogenous dehydroisoandrosterone sulfate reverses the dendritic changes of the central neurons in aging male rats

The Sigma1 Protein as a Target for the Non-genomic Effects of Neuro(active)steroids: Molecular, Physiological, and Behavioral Aspects

Steroid pregnenolone sulfate enhances NMDA‐receptor‐independent long‐term potentiation at hippocampal CA1 synapses: Role for L‐type calcium channels and sigma‐receptors

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