Stimulus-evoked synaptic currents in neurons from the rat medial preoptic nucleus

2000 ◽  
Vol 32 (3) ◽  
pp. 190-190
Author(s):  
E. Malinina ◽  
S. Johansson
Keyword(s):  
Preoptic Nucleus ◽  
Synaptic Currents ◽  
Medial Preoptic Nucleus

Neurosteroid Modulation of Synaptic and GABA-Evoked Currents in Neurons From the Rat Medial Preoptic Nucleus

1999 ◽  
Vol 82 (1) ◽  
pp. 143-151 ◽  
Author(s):  
David Haage ◽  
Staffan Johansson
Keyword(s):  
Voltage Clamp ◽  
Gaba Release ◽  
Decay Phase ◽  
Maximal Effect ◽  
Preoptic Nucleus ◽  
Gaba Concentration ◽  
Synaptic Currents ◽  
Perforated Patch ◽  
Medial Preoptic Nucleus ◽  
Synaptic Terminals

The effects of the neurosteroid 3α-hydroxy-5α-pregnane-20-one (allopregnanolone) on synaptic and GABA-evoked currents in acutely dissociated neurons from the medial preoptic nucleus of rat were investigated by perforated-patch recordings under voltage-clamp conditions. The effect of 2.0 μM allopregnanolone on GABA-evoked currents depended strongly on the GABA concentration: the currents evoked by 100 μM GABA were markedly depressed and the desensitization was faster, but the decay after GABA application was prolonged. In contrast, the currents evoked by 1.0 μM GABA were markedly potentiated, the activation was faster, a prominent desensitization was induced, and the decay after GABA application was prolonged. In the absence of externally applied GABA, 2.0 μM allopregnanolone induced a slow current that could be attributed to Cl−. Allopregnanolone did not significantly affect the amplitude of spontaneous tetrodotoxin-insensitive (miniature) synaptic currents (mIPSCs) originating from synaptic terminals releasing GABA onto the dissociated neurons. However, the mIPSC decay phase was dramatically prolonged, with half-maximal effect at ∼50 nM allopregnanolone. A qualitatively similar effect of allopregnanolone was seen when KCl was used to evoke synchronous GABA release. The frequency of mIPSCs was also affected, on average increased 3.5-fold, by 2.0 μM allopregnanolone, suggesting a presynaptic steroid action.

The medial preoptic nucleus receives vasotocinergic inputs in male quail: a tract-tracing and immunocytochemical study

2002 ◽  
Vol 24 (1) ◽  
pp. 27-39 ◽  
Author(s):  
Philippe Absil ◽  
Monica Papello ◽  
Carla Viglietti-Panzica ◽  
Jacques Balthazart ◽  
GianCarlo Panzica
Keyword(s):  
Immunocytochemical Study ◽  
Preoptic Nucleus ◽  
Tract Tracing ◽  
Medial Preoptic Nucleus

Differential Control of Spontaneous and Evoked GABA Release by Presynaptic L-Type Ca2+ Channels in the Rat Medial Preoptic Nucleus

2010 ◽  
Vol 104 (1) ◽  
pp. 200-209 ◽  
Author(s):  
Evgenya Malinina ◽  
Michael Druzin ◽  
Staffan Johansson
Keyword(s):  
Time Course ◽  
Stimulus Frequency ◽  
Gaba Release ◽  
High Frequency Stimulation ◽  
Functional Coupling ◽  
Channel Blockers ◽  
Preoptic Nucleus ◽  
External Stimulation ◽  
Medial Preoptic Nucleus ◽  
Differential Control

To clarify the role of presynaptic L-type Ca2+ channels in GABA-mediated transmission in the medial preoptic nucleus (MPN), spontaneous, miniature, and impulse-evoked inhibitory postsynaptic currents (sIPSCs, mIPSCs, and eIPSCs, respectively) were recorded from MPN neurons in a slice preparation from rat brain. The effects of different stimulus protocols and pharmacological tools to detect contributions of L-type Ca2+ channels and of Ca2+-activated K+ (KCa) channels were analyzed. Block of L-type channels did not affect the sIPSC and mIPSC properties (frequency, amplitude, decay time course) in the absence of external stimulation but unexpectedly potentiated the eIPSCs evoked at low stimulus frequency (0.1–2.0 Hz). This effect was similar to and overlapping with the effect of KCa-channel blockers. High-frequency stimulation (50 Hz for 10 s) induced a substantial posttetanic potentiation (PTP) of the eIPSC amplitude and of the sIPSC frequency. Block of L-type channels still potentiated the eIPSC during PTP, but in contrast, reduced the sIPSC frequency during PTP. It was concluded that L-type channels provide a means for differential control of spontaneous and impulse-evoked GABA release and that this differential control is prominent during short-term synaptic plasticity. Functional coupling of the presynaptic L-type channels to KCa channels explains the observed effects on eIPSCs.

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