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Despite their successes, the VITE and FLETE models have several limita-
tions. First, in an attempt to simulate the joint movement and joint stiffness,
Bullock and Grossberg speculated the presence of the two partly independent
cortical processes [30], a reciprocal signal of antagonist muscles responsible for
the joint rotation, and a co-contraction signal of antagonist muscle responsible
for joint stiffness. However, neither the VITE-FLETE model studies [9] nor the
Humphrey and Reed [30] experimental study has identified the exact neural corre-
lates (i.e., cell types) for the reciprocal activation and co-contraction of antagonist
muscles.
Second, they failed to provide functional roles of experimentally identified neu-
rons in primary motor cortex (area 4) and parietal cortex (area 5), such as the phasic
A
Extended-VITE
T
1
GO
T
2
V
1
V
2
GV
1
GV
2
P
A
1
A
2
Extended-FLETE
I
1
I
2
M
2
S
2
D
2
D
1
S
1
M
1
R
1
R
2
X
1
X
2
Z
1
Z
2
Y
1
Y
2
spindle response
spindle response
Fig. 10.1: Extended VITE-FLETE models without dopamine (DA). (A and B)
Top
:
Extended-VITE model for variable-speed trajectory generation.
Bottom
: Extended-
FLETE model of the opponent processing spinomuscular system.
Arrow lines
:ex-
citatory projections;
solid dot lines
: inhibitory projections;
dotted arrow lines
: feed-
back pathways from sensors embedded in muscles.
GO
: basal ganglia output signal;
P
: bidirectional co-contractive signal;
T
: target position command;
V
: DV activity;
GV
: DVV activity;
A
: current position command;
M
: alpha motoneuronal (MN) ac-
tivity;
R
: renshaw cell activity;
X, Y, Z
: spinal inhibitory interneuron (IN) activities;
I
a
: spinal type a inhibitory IN activity;
S
: static gamma MN activity;
D
: dynamic
gamma MN activity;
1,2
: antagonist cell pair.
