Gestational and postnatal malnutrition affects sensitivity of young rats to picrotoxin and quinolinic acid and uptake of GABA by cortical and hippocampal slices.
It is widely known that a complex interaction between excitatory and inhibitory systems is required to support the adequate functioning of the brain and that significant alterations induced by early protein restriction are complex, involving many systems. Based on such assumptions, we investigated the effects of maternal protein restriction during pregnancy and lactation followed by offspring protein restriction on some GABAergic and glutamatergic parameters, which mediate inhibitory and excitatory transmission, respectively. The sensitivity of young malnourished rats to convulsant actions of the GABA(A) receptor antagonist picrotoxin (PCT; s.c.) and to N-methyl-d-aspartate (NMDA) receptor agonist quinolinic acid (QA; i.c.v) and also gamma-amino-n-butyric acid (GABA) and glutamate uptake by cortical and hippocampal slices were evaluated in P25 old rats. Early protein malnutrition induced higher sensitivity to picrotoxin, which could be associated with the observed higher GABA uptake by cortical, and hippocampal slices in malnourished rats. In contrast, we observed lower sensitivity to quinolinic acid in spite of unaltered glutamate uptake by the same cerebral structures. Picrotoxin enhanced GABA uptake in hippocampus in well- and malnourished rats; however, it did not affect cortical GABA uptake. Our data corroborate our previous report, showing that malnutrition depresses the glutamatergic activity, and point to altered modulation of GABAergic neurotransmission. Such findings allow us to speculate that malnutrition may affect the excitatory and inhibitory interaction.
Schweigert
Ingrid D
ID
Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600 anexo, CEP 90035-003, Porto Alegre, RS, Brazil.
de Oliveira
Diogo L
DL
Scheibel
Fernando
F
da Costa
Fabiane
F
Wofchuk
Susana T
ST
Souza
Diogo O
DO
Perry
Marcos L S
ML
D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D001835:Body Weight / Q000187:drug effects; D002364:Caseins / Q000494:pharmacology; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D005260:Female; D048070:Fetal Nutrition Disorders / Q000473:pathology*; D018756:GABA Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism; D066298:In Vitro Techniques; D007774:Lactation; D008297:Male; D010852:Picrotoxin / Q000494:pharmacology*; D011247:Pregnancy; D039401:Prenatal Nutritional Physiological Phenomena; D017378:Quinolinic Acid / Q000494:pharmacology*; D051381:Rats; D012640:Seizures; D013997:Time Factors; D014316:Tritium / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D002364:Caseins; D018690:Excitatory Amino Acid Agonists; D018756:GABA Antagonists; D018698:Glutamic Acid; D010852:Picrotoxin; D017378:Quinolinic Acid; D014316:Tritium; D005680:gamma-Aminobutyric Acid