Comments

To identify differences between OT and VP neurons in membrane and synaptic properties, firing patterns, and plasticity during pregnancy and lactation, the authors summarized some previous findings from the following approach: 1) VP neuronal excitability is influenced by slow (sDAP) and fast (fDAP) depolarizing afterpotentials that underlie phasic bursting activity. The fDAP may relate to a transient receptor potential (TRP) channel, type melastatin (TRPM4 and/or TRPM5), both of which are immunochemically localized more to VP neurons, and especially, to their dendrites. Both TRPM4 and TRPM5 mRNAs are found in the SON, but single cell RT-PCR suggestsTRPM4 might be the more prominent channel. Phasic bursting in VP neurons is little influenced by spontaneous synaptic activity in slices, being shaped largely by intrinsic currents. 2) The firing pattern of OT neurons ranges from irregular to continuous, with the coefficient of variation determined by randomly distributed, spontaneous GABAergic, inhibitory synaptic currents (sIPSCs). These sIPSCs are 4–5 fold more frequent in OT vs. VP neurons, and much more frequent than spontaneous excitatory synaptic currents. 3) Both cell types express Ca2+-dependent afterhyperpolarisations (AHPs), including an apamin-sensitive, medium duration AHP and a slower, apamin-insensitive AHP (sAHP). In OT neurons, both AHPs are enhanced during pregnancy and lactation. During pregnancy, the plasticity of the sAHP is blocked by antagonism of central OT receptors. AHP enhancement is mimicked by exposing slices from Day 19 pregnant rats to OT and estradiol, suggesting central OT and sex steroids program this plasticity during pregnancy by direct hypothalamic actions. They believe that the differences in VP and OT neuronal function are underlain by differences in both membrane and synaptic properties, and differentially modulated by reproductive state. Although this work was published 8 years ago, it is still very important reference for researchers in the field of hypothalamo-neurohypophysial system.

 

Questions and discussions:

1) How to differentiate slow (sDAP) and fast (fDAP) depolarizing afterpotentials that underlie phasic bursting activity.

2) What is the relative contribution of TRPM4 and TRPV1 to VP neuronal activity?

3) What is the difference in the distribution between TRPM4 and TRPV1 in VP neurons?

4) How to understand the description of “Phasic bursting in VP neurons is little influenced by spontaneous synaptic activity in slices, being shaped largely by intrinsic currents”?

5) In addition to the “randomly distributed, spontaneous GABAergic, inhibitory synaptic currents”, what other factors determine the firing pattern of OT neurons?

6) What are the sources of IPSCs on OT vs. VP neurons?

7) What factors cause AHPs enhancement during pregnancy and lactation?

8) How do you understand the “plasticity of the sAHP”?

9) How do OT and estradiol interact to shape the sAHP during pregnancy?

10) What is the time course of AHP plastic change under OT and estradiol challenge?


2019年01月02日

2018-11-21 Literature Analysis

Armstrong, WE., et al. Performance, properties, and plasticity of identified oxytocin and vasopressin neurones in vitro, J Neuroendocrinol. 2010, 22(5): 330–342. Presented by Tong LI.

Add Time:

本网站由阿里云提供云计算及安全服务