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Age and monosodium glutamate treatment cause changes in the stimulation-induced [3H]-norepinephrine release from rat nucleus tractus solitarii-dorsal vagal nucleus slices
被引:1
|作者:
Rónai, AZ
Kató, E
Al-Khrasani, M
Hajdú, M
Müllner, K
Elor, G
Gyires, K
Fürst, S
Palkovits, M
机构:
[1] Semmelweis Univ, Dept Pharmacol & Pharmacotherapy, H-1445 Budapest, Hungary
[2] Med & Pharmaceut Univ, Targu Mures, Romania
[3] Semmelweis Univ, Dept Anat, H-1085 Budapest, Hungary
基金:
匈牙利科学研究基金会;
关键词:
nucleus tractus solitarii-dorsal motor vagal nucleus;
norepinephrine release;
rat age;
neonatal monosodium glutamate;
L-glutamate;
Baclofen;
D O I:
10.1016/j.lfs.2003.05.012
中图分类号:
R-3 [医学研究方法];
R3 [基础医学];
学科分类号:
1001 ;
摘要:
In nucleus tractus solitarii-dorsal vagal nucleus slices prepared from young adult rats (180-260 g) 10(-3) M L-glutamate and 10(-5) M baclofen caused a 2-3-fold increase of field stimulation-induced [H-3]-norepinephrine release without affecting the resting release. In slices prepared from rats treated neonatally with monosodium glutamate neither L-glutamate nor baclofen had any effect on stimulation-induced norepinephrine release, tested between postnatal days 74-99 (350-530 g). In untreated littermates used in the same period (460-580 g) L-glutamate was fully effective whereas baclofen was ineffective. The tritium content in tissue extracts did not differ significantly in the three experimental groups. It is concluded that i) the loss of GABA(B) receptor-mediated disinhibitory stimulation of norepinephrine release is an age-related phenomenon and ii) neonatal monosodium glutamate treatment causes a damage in the local neural circuitry characterized by the loss of glutamate receptor-mediated mechanism that stimulates the release of norepinephrine. (C) 2003 Elsevier Inc. All rights reserved.
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页码:1573 / 1580
页数:8
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