 |
|||||
|
|||||
|
|||||
|
|||||
|
|||||
Previous Article | Next Article
The Journal of Neuroscience, September 15, 2002, 22(18):8034-8041
The Role of Interleukin-1, Interleukin-6, and Glia in Inducing Growth of Neuronal Terminal Arbors in Mice
Clare L. Parish*, David I. Finkelstein*, Wanida Tripanichkul, Abhay R. Satoskar, John Drago, and Malcolm K. Horne Neurosciences Group, Department of Medicine, Monash University, Monash Medical Centre, Clayton 3168, Australia
After injury to the substantia nigra pars compacta (SNpc), remaining neurons sprout to ensure normal dopamine delivery to the striatum. The consequent striatal reinnervation is highly regulated, with remaining cells sprouting so that density of dopamine terminals returns to normal. Sprouting as a result of injury is accompanied by a strong glial response; however, it is difficult to know whether this response is as a result of the injury or whether it is aiding in the sprouting. The two cytokines interleukin-1 (IL-1) and interleukin-6 (IL-6) are important modulators of the glia response. This study demonstrates their role in regulating the sprouting of dopaminergic neurons and the associated glia response as a means to examine the role of glia in sprouting. Sprouting was induced by 6-hydroxydopamine lesions of the SNpc and by haloperidol treatment (in the absence of injury). In wild-type animals, sprouting in association with microglial and astrocyte proliferation followed partial lesions of the SNpc and haloperidol treatment. Neither treatment evoked sprouting or glia proliferation in the type I IL-1 receptor-deficient mice, whereas in IL-6-deficient mice, both treatments resulted in glial proliferation but not sprouting. We conclude that IL-1 plays a role in modulating glia proliferation and thereby guidance and trophic factors for new fibers, whereas IL-6 may be important in triggering the outgrowth of new fibers. This study demonstrates that these cytokines play an important role in plasticity and regeneration that is separate from the inflammatory response associated with brain injury.
Key words: interleukin-1; interleukin-6; regeneration; sprouting; haloperidol; lesioning; glia
* C.L.P. and D.I.F. contributed equally to this work.
Copyright © 2002 Society for Neuroscience 0270-6474/02/22188034-08$05.00/0
This article has been cited by other articles:
B Resch, A Radinger, C Mannhalter, A Binder, J Haas, and W D Muller
Interleukin-6 G(-174)C polymorphism is associated with mental retardation in cystic periventricular leucomalacia in preterm infants
Arch. Dis. Child. Fetal Neonatal Ed., July 1, 2009; 94(4): F304 - F306.
[Abstract] [Full Text] [PDF]
I. Gantois, K. Fang, L. Jiang, D. Babovic, A. J. Lawrence, V. Ferreri, Y. Teper, B. Jupp, J. Ziebell, C. M. Morganti-Kossmann, et al.
Ablation of D1 dopamine receptor-expressing cells generates mice with seizures, dystonia, hyperactivity, and impaired oral behavior
PNAS, March 6, 2007; 104(10): 4182 - 4187.
[Abstract] [Full Text] [PDF]
C. L. Parish, J. Nunan, D. I. Finkelstein, F. N. McNamara, J. Y. Wong, J. L. Waddington, R. M. Brown, A. J. Lawrence, M. K. Horne, and J. Drago
Mice Lacking the {alpha}4 Nicotinic Receptor Subunit Fail to Modulate Dopaminergic Neuronal Arbors and Possess Impaired Dopamine Transporter Function
Mol. Pharmacol., November 1, 2005; 68(5): 1376 - 1386.
[Abstract] [Full Text] [PDF]
E. K. de Jong, I. M. Dijkstra, M. Hensens, N. Brouwer, M. van Amerongen, R. S. B. Liem, H. W. G. M. Boddeke, and K. Biber
Vesicle-Mediated Transport and Release of CCL21 in Endangered Neurons: A Possible Explanation for Microglia Activation Remote from a Primary Lesion
J. Neurosci., August 17, 2005; 25(33): 7548 - 7557.
[Abstract] [Full Text] [PDF]
A. Navarro, E. del Valle, and J. Tolivia
Differential Expression of Apolipoprotein D in Human Astroglial and Oligodendroglial Cells
J. Histochem. Cytochem., August 1, 2004; 52(8): 1031 - 1036.
[Abstract] [Full Text] [PDF]
|
|
|
|
 |
|