Effects of suicide transport lesions of the striatopallidal or striatonigral pathways on striatal ultrastructure.
In the basal ganglia, centrally active suicide transport agents produce selective lesions of the striatopallidal and striatonigral pathways based on receptor binding and neuropeptide mRNA studies. Anatomical analyses indicate a selective, albeit modest, loss of projection neurons. In the present study, we sought to determine the ultrastructural sequelae in the striatum of suicide transport injections of the globus pallidus (GP) or substantia nigra (SN). Neostriata of adult rats were examined 10 days after lesions of the striatopallidal or striatonigral pathways with OX7-saporin or volkensin. Controls consisted of normal unoperated rats and animals injected into either target with ricin, a toxic lectin that is not transported in the central nervous system. Injections with OX7-saporin or volkensin into the GP or SN produced a decrease in striatal synaptic density of approximately 20%, relative to the contralateral side. Dark degenerating profiles, though very rare in the contralateral striata, were present throughout the neuropil in the ipsilateral striata. In animals with striatopallidal lesions, axospinous synapses of both the asymmetric and symmetric type were decreased in density, while the number of synapses formed with dendritic shafts was unaffected. In addition, the number of striatal mitochondrial profiles was decreased ipsilateral to the lesions. In animals with striatonigral lesions, the number of axospinous and axodendritic synapses of the asymmetric type was decreased ipsilateral to the lesions. Synaptic density and ultrastructural integrity remained unaffected in the striata of animals receiving ricin injections and in the contralateral striata of animals receiving OX7-saporin or volkensin injections. Our results, taken together with previous studies showing marked loss of receptors, uptake sites and mRNA, suggest that while most synapses are present and intact, the efficacy of synaptic transmission may be altered.
Roberts
R C
RC
Maryland Psychiatric Research Center, University of Maryland School of Medicine, Baltimore 21228, USA.
Strain-Saloum
C
C
Wiley
R G
RG
D000818:Animals; D000911:Antibodies, Monoclonal; D001369:Axons / Q000187:drug effects / Q000648:ultrastructure; D001479:Basal Ganglia / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D005917:Globus Pallidus / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D006023:Glycoproteins; D018796:Immunoconjugates; D000922:Immunotoxins / Q000633:toxicity; D008297:Male; D008854:Microscopy, Electron; D009699:N-Glycosyl Hydrolases; D017072:Neostriatum / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D009434:Neural Pathways / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D009498:Neurotoxins / Q000302:isolation & purification / Q000633:toxicity*; D037121:Plant Lectins; D010940:Plant Proteins / Q000302:isolation & purification / Q000633:toxicity*; D010947:Plants, Toxic / Q000737:chemistry; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D054789:Ribosome Inactivating Proteins, Type 1; D054790:Ribosome Inactivating Proteins, Type 2; D012270:Ribosomes / Q000187:drug effects; D000076985:Saporins; D013378:Substantia Nigra / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D013569:Synapses / Q000187:drug effects / Q000648:ultrastructure
D000911:Antibodies, Monoclonal; D006023:Glycoproteins; D018796:Immunoconjugates; D000922:Immunotoxins; D009498:Neurotoxins; C085346:OX7-saporin; D037121:Plant Lectins; D010940:Plant Proteins; D012333:RNA, Messenger; D054789:Ribosome Inactivating Proteins, Type 1; D054790:Ribosome Inactivating Proteins, Type 2; C049134:volkensin; D009699:N-Glycosyl Hydrolases; D000076985:Saporins