Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1994-11-18
pubmed:abstractText
This study was designed to determine if there are age-related alterations in the bio-synthetic enzyme glutamic acid decarboxylase (GAD), the degradative enzyme GABA-transaminase (GABA-T), and the uptake system for GABA in the central nucleus of the inferior colliculus (CIC), the cochlear nucleus (CN), and/or nuclei of the lateral lemniscus (NLL) of Fischer-344 rats. For purposes of comparison, the cholinergic neuronal system was studied in parallel in young adult (3-7 months), mature (15-17 months) and aged (24-26 months) rats. In young adults GAD activity was highest in the CIC (219 nmol/mg protein/h; N = 5), intermediate in NLL (82 nmol/mg protein/h), and lowest in CN (34 nmol/mg protein/h). Choline acetyltransferase (ChAT) activity was highest in NLL and CN, and approximately 35-40% lower in CIC. A more uniform pattern was observed with GABA-T activity. Reductions in GAD activity were seen in the CIC of mature (-31%) and aged (-30%) rats that were not graded with age when compared to young adult, P < 0.05 (N = 5). This effect was regionally selective, since the CN did not show any loss of GAD or ChAT activity. The neurotransmitter selectivity of this deficit in CIC is supported by the non-parallel changes in ChAT activity (-22%, aged vs. mature, P < 0.05) that occurred after the changes in GAD activity. In contrast to the loss of GABAergic biosynthetic capacity in aged CIC, high affinity uptake processes (Kd and Vmax) for 14C-GABA and 3H-D-aspartate were not significantly altered (P > 0.05). Similar to the CIC, the NLL showed remarkable age-related deficits, but these deficits were more substantial for the cholinergic system (ChAT activity: -56% aged vs. young adult, P < 0.05; GAD activity: -35% aged vs. mature). None of the areas examined showed a significant loss of GABA-T activity with aging. These data suggest: 1) Age-related loss of GABA-mediated inhibition in the CIC of Fischer-344 rats is not attributable to changes in uptake or degradation of GABA, but may be related loss of biosynthetic capacity (i.e. activity or quantity) of the GAD present; 2) processing centers of the central auditory pathway (i.e. CIC and NLL), but not necessarily primary (i.e. CN) integrative nuclei, demonstrate selective, age-related neurochemical deficits; and 3) age-related neurochemical changes in central auditory structures may contribute substantially to the abnormal perception of signals in noise and loss of speech discrimination observed in neural presbycusis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0378-5955
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
77
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
221-30
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:7928735-4-Aminobutyrate Transaminase, pubmed-meshheading:7928735-Acetylcholine, pubmed-meshheading:7928735-Aging, pubmed-meshheading:7928735-Animals, pubmed-meshheading:7928735-Aspartic Acid, pubmed-meshheading:7928735-Auditory Pathways, pubmed-meshheading:7928735-Biological Transport, Active, pubmed-meshheading:7928735-Brain Stem, pubmed-meshheading:7928735-Choline O-Acetyltransferase, pubmed-meshheading:7928735-Cochlear Nucleus, pubmed-meshheading:7928735-Geniculate Bodies, pubmed-meshheading:7928735-Glutamate Decarboxylase, pubmed-meshheading:7928735-Inferior Colliculi, pubmed-meshheading:7928735-Kinetics, pubmed-meshheading:7928735-Pons, pubmed-meshheading:7928735-Presbycusis, pubmed-meshheading:7928735-Rats, pubmed-meshheading:7928735-Rats, Inbred F344, pubmed-meshheading:7928735-gamma-Aminobutyric Acid
pubmed:year
1994
pubmed:articleTitle
Age-related changes in brainstem auditory neurotransmitters: measures of GABA and acetylcholine function.
pubmed:affiliation
Department of Pharmacology, Southern Illinois University School of Medicine, Springfield 62702.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S.