Neocortical infarction in subhuman primates leads to restricted morphological damage of the cholinergic neurons in the nucleus basalis of Meynert.
The aim of the present study was to investigate the long-term effect of cortical infarction on the subhuman primate (Cercopithecus aethiops) basal forebrain. The lesion, carried out by cauterizing the pial blood vessels supplying the left fronto-parieto-temporal neocortex, induced retrograde degenerative processes within the ipsilateral nucleus basalis of Meynert. The morphometrical analysis revealed that significant shrinkage of cholinergic neurons and loss of neuritic processes were localized within the intermediate regions of the nucleus basalis. The average cross-sectional areas of choline acetyltransferase-immunoreactive neurons in the intermedio-ventral (Ch4iv) and intermedio-dorsal (Ch4id) nucleus basalis were decreased to 62.5 +/- 9.5 and 58.0 +/- 8.6%, respectively, of the sham-operated values. Although an apparent loss of Nissl-stained magnocellular neurons in Ch4iv and Ch4id was found by applying a quantitative analysis based on a perikaryal-size criterion, data obtained by the quantification of immunostained material failed to reveal any significant decrease of cholinergic cell density. Results are discussed in view of future application of this ischemic model to study processes of retrograde degeneration following cortical target removal and to assess potential neurotrophic and neuroprotective properties of pharmacologic agents.
Liberini
P
P
Department of Pharmacology and Therapeutics, McGill University, Montreal, Que., Canada.
Pioro
E P
EP
Maysinger
D
D
Cuello
A C
AC
D000818:Animals; D002544:Cerebral Infarction / Q000201:enzymology / Q000473:pathology*; D002522:Chlorocebus aethiops; D002795:Choline O-Acetyltransferase / Q000276:immunology / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D009410:Nerve Degeneration / Q000502:physiology; D009474:Neurons / Q000201:enzymology / Q000502:physiology*; D010275:Parasympathetic Nervous System / Q000201:enzymology / Q000473:pathology*; D010641:Phenotype; D016548:Prosencephalon / Q000473:pathology; D017475:Receptors, Nerve Growth Factor / Q000276:immunology / Q000378:metabolism; D013377:Substantia Innominata / Q000201:enzymology / Q000473:pathology*
D017475:Receptors, Nerve Growth Factor; D002795:Choline O-Acetyltransferase