title: Age and monosodium glutamate treatment cause changes in the stimulation-induced [3H]-norepinephrine release from rat nucleus tractus solitarii-dorsal vagal nucleus slices.
abstract: 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 [3H]-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.
authors.affiliation: Department of Pharmacology and Pharmacotherapy, Semmelweis University, P.O. Box 370, H-1445 Budapest, Hungary. ronand@pharma.sote.hu
authors.forename: András Z
authors.initials: AZ
authors.lastname: Rónai
authors.forename: Erzsébet
authors.initials: E
authors.lastname: Kató
authors.forename: Mahmoud
authors.initials: M
authors.lastname: Al-Khrasani
authors.forename: Melinda
authors.initials: M
authors.lastname: Hajdú
authors.forename: Katalin
authors.initials: K
authors.lastname: Müllner
authors.forename: Guy
authors.initials: G
authors.lastname: Elor
authors.forename: Klára
authors.initials: K
authors.lastname: Gyires
authors.forename: Suzanne
authors.initials: S
authors.lastname: Fürst
authors.forename: Miklós
authors.initials: M
authors.lastname: Palkovits
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000737:chemistry / Q000378:metabolism*; D000375:Aging / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn; D001418:Baclofen / Q000378:metabolism; D018755:GABA Agonists / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D066298:In Vitro Techniques; D009638:Norepinephrine / Q000737:chemistry / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D018080:Receptors, GABA-B / Q000378:metabolism; D012970:Sodium Glutamate / Q000494:pharmacology*; D017552:Solitary Nucleus / Q000187:drug effects* / Q000378:metabolism; D014316:Tritium / Q000378:metabolism
chemical_list: D000316:Adrenergic alpha-Agonists; D018755:GABA Agonists; D018080:Receptors, GABA-B; D014316:Tritium; D018698:Glutamic Acid; D001418:Baclofen; D012970:Sodium Glutamate; D009638:Norepinephrine