Cerebral metabolic consequences in the adult brain after neonatal excitotoxic lesions of the amygdala in rats.
In the present study the effects of neonatal excitotoxic lesions of the amygdala or ventral hippocampus on local cerebral glucose utilisation in the adult rat were studied by means of the [14C]2-deoxyglucose autoradiographic method. Our hypothesis was that damage to the brain during early development leads to long-term functional activity changes in brain regions outside the primary lesioned area which might underlie the behavioural deficits observed in animals with neonatal brain damage. Cerebral glucose utilisation in animals with a neonatal amygdala lesion was significantly decreased in the amygdala itself and in several other brain regions. The neonatal ventral hippocampal lesion did not cause significant changes in cerebral glucose utilisation, except for a decrease in the primary damaged region (i.e. caudal ventral hippocampus). Behaviourally, animals lesioned in the amygdala displayed increased ambulatory activity both before and after puberty when exposed to a novel open field, while neonatal ventral hippocampal lesions did not affect adult exploratory behaviour as compared to sham controls. These results support our hypothesis that neonatal brain damage leads to long-term functional activity changes in brain regions outside the primary lesioned area. Moreover, they suggest that this long-term effect depends on the primary area lesioned since only damage to the amygdala, and not to the ventral hippocampus, affects the functional organisation of the brain of the animals later in life. Additionally, the findings may suggest that the functional changes in the brain may underlie the behavioural deficits observed after neonatal amygdala lesion in the rat.
Gerrits
Mirjam A F M
MA
Rudolf Magnus Institute of Neuroscience, Department of Pharmacology and Anatomy, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG, Utrecht, The Netherlands. m.a.f.m.gerrits@med.uu.nl
Wolterink
Gerrit
G
van Ree
Jan M
JM
D000679:Amygdala / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D001923:Brain Chemistry / Q000502:physiology*; D003847:Deoxyglucose / Q000378:metabolism; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity; D005106:Exploratory Behavior / Q000502:physiology; D005260:Female; D005947:Glucose / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism; D007051:Ibotenic Acid / Q000633:toxicity; D009498:Neurotoxins / Q000633:toxicity*; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar
D018690:Excitatory Amino Acid Agonists; D009498:Neurotoxins; D007051:Ibotenic Acid; D003847:Deoxyglucose; D005947:Glucose