Noradrenergic Modulation of Spontaneous Inhibitory Postsynaptic Currents in the Hypothalamic Paraventricular Nucleus.
- Author:
Long Hwa LEE
1
;
Wonee CHONG
;
Kiho LEE
;
Jin Bong PARK
;
Pan Dong RYU
Author Information
1. Department of Pharmacology, College of Veterinary Medicine and School of Agricultural Biotechnology, Seoul National University, Suwon, Korea. pandryu@plaza.snu.ac.kr
- Publication Type:Original Article
- Keywords:
Paraventricular nucleus;
Norepinephrine;
IPSC;
Alpha adrenoceptor;
Clonidine;
Yohimbine
- MeSH:
Brain Stem;
Clonidine;
Inhibitory Postsynaptic Potentials*;
Membranes;
Neurons;
Norepinephrine;
Paraventricular Hypothalamic Nucleus*;
Synaptic Transmission;
Yohimbine
- From:The Korean Journal of Physiology and Pharmacology
2002;6(2):71-80
- CountryRepublic of Korea
- Language:English
-
Abstract:
Previous studies have suggested that brain stem noradrenergic inputs differentially modulate neurons in the paraventricular nucleus (PVN). Here, we compared the effects of norepinephrine (NE) on spontaneous GABAergic inhibitory postsynaptic currents (sIPSCs) in identified PVN neurons using slice patch technique. In 17 of 18 type I neurons, NE (30-100microM) reversibly decreased sIPSC frequency to 41+/-7% of the baseline value (4.4+/-0.8 Hz, p<0.001). This effect was blocked by yohimbine (2-20microM), an alpha2-adrenoceptor antagonist and mimicked by clonidine (50 microM), an alpha2-adrenoceptor agonist. In contrast, NE increased sIPSC frequency to 248+/-32% of the control (3.06+/-0.37 Hz, p<0.001) in 31 of 54 type II neurons, but decreased the frequency to 41+/-7% of the control (5.5+/-1.3 Hz) in the rest of type II neurons (p<0.001). In both types of PVN neurons, NE did not affect the mean amplitude and decay time constant of sIPSCs. In addition, membrane input resistance and amplitude of sIPSC of type I neurons were larger than those of type II neurons tested (1209 vs. 736 M omega, p<0.001; 110 vs. 81 pS, p<0.001). The results suggest that noradrenergic modulation of inhibitory synaptic transmission in the PVN decreases the neuronal excitability in most type I neurons via alpha2-adrenoceptor, however, either increases in about 60% or decreases in 40% of type II neurons.
