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Remote microglial activation in the quinolinic acid model of Huntington's disease.
Exp Neurol. 1993 Oct; 123(2):271-83.EN

Abstract

Intrastriatal injection of quinolinic acid (QA) in the rat leads to several structural and biochemical events which resemble neuropathological changes seen in the striatum of Huntington's disease patients. In the present experiment the accompanying microglial response in striatal projection areas following QA injection was studied immunocytochemically using monoclonal macrophage/microglial markers. After injection of 240 nmol of QA a marked microglial reaction was observed in the entire striatum, whereas injection of the same amount of solvent resulted only in a local microglial reaction around the injection site. Activated microglia were also found in the globus pallidus (GP), the entopeduncular nucleus (EP), the substantia nigra (SN), and the ventroanterior/ventrolateral, the ventromedial, and, in some rats, the reticular thalamic nucleus. The remote microglial reaction started in the first-order projection areas at Day 1 (GP) or Day 3 (EP, SN) and was found in the second-order projection areas (thalamic nuclei) by Day 5. Areas projecting to the striatum such as the amygdala and intralaminar thalamic nuclei remained free of activated microglia. It is concluded that a microglial response in striatal projection areas accompanies excitotoxic striatal injury. Anterograde degeneration of striatal projection neurons can explain the microglial activation in first-order projection areas but other mechanisms such as neuronal hyperexcitation following removal of inhibitory striatal input must be responsible for the rapid transsynaptic microglial activation seen in the thalamus.

Authors+Show Affiliations

Max-Planck-Institute of Psychiatry, Department of Neuromorphology, Martinsried, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

8405289

Citation

Töpper, R, et al. "Remote Microglial Activation in the Quinolinic Acid Model of Huntington's Disease." Experimental Neurology, vol. 123, no. 2, 1993, pp. 271-83.
Töpper R, Gehrmann J, Schwarz M, et al. Remote microglial activation in the quinolinic acid model of Huntington's disease. Exp Neurol. 1993;123(2):271-83.
Töpper, R., Gehrmann, J., Schwarz, M., Block, F., Noth, J., & Kreutzberg, G. W. (1993). Remote microglial activation in the quinolinic acid model of Huntington's disease. Experimental Neurology, 123(2), 271-83.
Töpper R, et al. Remote Microglial Activation in the Quinolinic Acid Model of Huntington's Disease. Exp Neurol. 1993;123(2):271-83. PubMed PMID: 8405289.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Remote microglial activation in the quinolinic acid model of Huntington's disease. AU - Töpper,R, AU - Gehrmann,J, AU - Schwarz,M, AU - Block,F, AU - Noth,J, AU - Kreutzberg,G W, PY - 1993/10/1/pubmed PY - 1993/10/1/medline PY - 1993/10/1/entrez SP - 271 EP - 83 JF - Experimental neurology JO - Exp Neurol VL - 123 IS - 2 N2 - Intrastriatal injection of quinolinic acid (QA) in the rat leads to several structural and biochemical events which resemble neuropathological changes seen in the striatum of Huntington's disease patients. In the present experiment the accompanying microglial response in striatal projection areas following QA injection was studied immunocytochemically using monoclonal macrophage/microglial markers. After injection of 240 nmol of QA a marked microglial reaction was observed in the entire striatum, whereas injection of the same amount of solvent resulted only in a local microglial reaction around the injection site. Activated microglia were also found in the globus pallidus (GP), the entopeduncular nucleus (EP), the substantia nigra (SN), and the ventroanterior/ventrolateral, the ventromedial, and, in some rats, the reticular thalamic nucleus. The remote microglial reaction started in the first-order projection areas at Day 1 (GP) or Day 3 (EP, SN) and was found in the second-order projection areas (thalamic nuclei) by Day 5. Areas projecting to the striatum such as the amygdala and intralaminar thalamic nuclei remained free of activated microglia. It is concluded that a microglial response in striatal projection areas accompanies excitotoxic striatal injury. Anterograde degeneration of striatal projection neurons can explain the microglial activation in first-order projection areas but other mechanisms such as neuronal hyperexcitation following removal of inhibitory striatal input must be responsible for the rapid transsynaptic microglial activation seen in the thalamus. SN - 0014-4886 UR - https://www.unboundmedicine.com/medline/citation/8405289/Remote_microglial_activation_in_the_quinolinic_acid_model_of_Huntington's_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4886(83)71159-3 DB - PRIME DP - Unbound Medicine ER -