The basal ganglia communicate with the cerebellum.
The basal ganglia and cerebellum are major subcortical structures that influence not only movement, but putatively also cognition and affect. Both structures receive input from and send output to the cerebral cortex. Thus, the basal ganglia and cerebellum form multisynaptic loops with the cerebral cortex. Basal ganglia and cerebellar loops have been assumed to be anatomically separate and to perform distinct functional operations. We investigated whether there is any direct route for basal ganglia output to influence cerebellar function that is independent of the cerebral cortex. We injected rabies virus (RV) into selected regions of the cerebellar cortex in cebus monkeys and used retrograde transneuronal transport of the virus to determine the origin of multisynaptic inputs to the injection sites. We found that the subthalamic nucleus of the basal ganglia has a substantial disynaptic projection to the cerebellar cortex. This pathway provides a means for both normal and abnormal signals from the basal ganglia to influence cerebellar function. We previously showed that the dentate nucleus of the cerebellum has a disynaptic projection to an input stage of basal ganglia processing, the striatum. Taken together these results provide the anatomical substrate for substantial two-way communication between the basal ganglia and cerebellum. Thus, the two subcortical structures may be linked together to form an integrated functional network.
Bostan
Andreea C
AC
Department of Neurobiology, University of Pittsburgh School of Medicine, Center for the Neural Basis of Cognition, Systems Neuroscience Institute, Pittsburgh, PA 15261, USA.
Dum
Richard P
RP
Strick
Peter L
PL
D000818:Animals; D001479:Basal Ganglia / Q000503:physiopathology* / Q000821:virology; D002428:Cebus / Q000502:physiology* / Q000821:virology; D002531:Cerebellum / Q000503:physiopathology* / Q000821:virology; D005260:Female; D008297:Male; D011818:Rabies / Q000503:physiopathology / Q000821:virology; D011820:Rabies virus / Q000502:physiology
Lancet. 1991 Feb 16;337(8738):403-6
1671433
J Comp Neurol. 1988 May 22;271(4):473-92
2454970
J Comp Neurol. 1995 Jun 5;356(3):457-80
7642806
J Neurosci Methods. 2000 Nov 15;103(1):63-71
11074096
J Comp Neurol. 1985 May 15;235(3):343-59
3998215
Prog Brain Res. 2004;143:449-59
14653187
Arch Neurol. 2004 Aug;61(8):1307-13
15313852
Brain Res Brain Res Rev. 1997 Feb;23(1-2):62-78
9063587
J Neurosci. 2003 Sep 10;23(23):8432-44
12968006
Neuron. 2003 Apr 24;38(2):329-37
12718865
Neuroscience. 1979;4(2):193-208
106327
J Neurophysiol. 2009 Dec;102(6):3740-52
19846625
Brain Res Brain Res Rev. 1996 Aug;22(2):93-181
8883918
Nat Rev Neurosci. 2008 Mar;9(3):222-34
18285800
Vis Neurosci. 2001 Sep-Oct;18(5):725-40
11925008
Brain. 2004 Jan;127(Pt 1):4-20
14607789
J Comp Neurol. 1979 Jan 1;183(1):33-45
102667
Curr Opin Neurobiol. 2000 Dec;10(6):732-9
11240282
Brain. 1994 Aug;117 ( Pt 4):859-76
7922471
Exp Brain Res. 1980;38(1):29-36
6766109
Neurosci Lett. 1997 Dec 12;239(1):13-6
9547160
J Neurosci. 2002 Sep 1;22(17):7825-33
12196606
Brain Res Brain Res Rev. 1995 Jan;20(1):128-54
7711765
Exp Brain Res. 1978 Nov 15;33(3-4):395-403
83239
Neurology. 2006 Apr 25;66(8):1192-9
16636237
Curr Opin Neurol. 1998 Aug;11(4):319-26
9725077
Brain Res. 1999 Jul 3;833(2):191-201
10375694
J Comp Neurol. 1981 Sep 20;201(3):375-93
7276256
J Neurosci. 1996 Apr 15;16(8):2671-83
8786443
Cereb Cortex. 2010 Jan;20(1):214-28
19465740
Annu Rev Neurosci. 1986;9:357-81
3085570
Nat Neurosci. 2005 Nov;8(11):1491-3
16205719
Nature. 2004 Jun 10;429(6992):664-7
15190354
Annu Rev Neurosci. 2009;32:413-34
19555291
Biol Cybern. 2005 Jun;92(6):427-37
15915357