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Eye position and eye velocity integrators reside in separate brainstem nuclei.

Abstract

Two types of central nervous system integrators are critical for oculomotor performance. The first integrates velocity commands to create position signals that hold fixation of the eye. The second stores relative velocity of the head and visual surround to stabilize gaze both during and after the occurrence of continuous self and world motion. We have used recordings from single neurons to establish that the 'position' and 'velocity' integrators for horizontal eye movement occupy adjacent, but nonoverlapping, locations in the goldfish medulla. Lidocaine inactivation of each integrator results in the eye movement deficits expected if horizontal eye position and velocity signals are processed separately. These observations also indicate that each brainstem compartment generates and stores these signals. Consequently, each integrator exhibits functional autonomy. Therefore, we propose that the intrinsic electrophysiological properties of the constituent neurons in each brainstem subnucleus may be sufficient for producing integrator rhythmicity.

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Eye position and eye velocity integrators reside in separate brainstem nuclei.

Author: Pastor Loro, Ángel Manuel; Rodríguez de la Cruz, Rosa María; Baker, Robert
Publisher: National Academy of Sciences
Year: 1994
DOI: 10.1073/pnas.91.2.807
Source: https://idus.us.es/bitstreams/638987bb-dda7-4360-a6d9-70164ab7b030/download
P oc.
Na l.
Acad.
Sci.
USA
Vol.
91,
pp.
807-811,
Janua y
1994
Neu obiology
Eye
posi ion
and
eye
eloci y
in eg a o s
eside
in
sepa a e
b ains em
nuclei
(gaze
s abiliza ion/mo o
pe o mance/in eg a o
hy hmici y/p eposi us
nudeus/lidocaine
inac i a ion)
ANGEL
M.
PASTOR*,
ROSA
R.
DE
LA
CRUZ*,
AND
ROBERT
BAKER
*Labo a o y
o
Neu oscience,
Depa men
o
Physiology
and
Biology,
Uni e si y
o
Se ille,
41012
Se ille,
Spain;
and
Depa men
o
Physiology
and
Biophysics,
New
Yo k
Uni e si y
Medical
Cen e ,
New
Yo k,
NY
10016
Communica ed
by
R.
Llinds,
Augus
25,
1993
ABSTRACT
Two
ypes
o
cen al
ne ous
sys em
in eg a-
o s
a e
c i ical
o
oculomo o
pe o mance.
The
is
in e-
g a es
eloci y
commands
o
c ea e
posi ion
signals
ha
hold
ixa ion
o
he
eye.
The
second
s o es
ela i e
eloci y
o
he
head
and
isual
su ound
o
s abilize
gaze
bo h
du ing
and
a e
he
occu ence
o
con inuous
sel
and
wo ld
mo ion.
We
ha e
used
eco dings
om
single
neu ons
o
es ablish
ha
he
"posi ion"
and
" eloci y"
in eg a o s
o
ho izon al
eye
mo e-
men
occupy
adjacen ,
bu
nono e lapping,
loca ions
in
he
gold ish
medulla.
Lidocaine
inac i a ion
o
each
in eg a o
esul s
in
he
eye
mo emen
de ici s
expec ed
i
ho izon al
eye
posi ion
and
eloci y
signals
a e
p ocessed
sepa a ely.
These
obse a ions
also
indica e
ha
each
b ains em
compa men
gene a es
and
s o es
hese
signals.
Consequen ly,
each
in eg a-
o
exhibi s
unc ional
au onomy.
The e o e,
we
p opose
ha
he
in insic
elec ophysiological
p ope ies
o
he
cons i uen
neu ons
in
each
b ains em
subnucleus
may
be
su icien
o
p oducing
in eg a o
hy hmici y.
Main aining
gaze
on
a ge s
ha
mo e
ela i e
o
he
ob-
se e
equi es
ha
es ibula
and
isual
e lexes
de ec ing
bo h
sel
and
wo ld
mo ion
espond
wi h
app op ia e
eye
and/o
head
mo emen s.
Neu al
in eg a o s
ac ing
as
com-
pu a ional
elemen s
a e
essen ial
building
blocks
wi hin
his
senso y-mo o
ans o ma ion
(1-3).
The
concep
o
a
"neu-
onal"
in eg a o
whose
inpu -ou pu
cha ac e is ics
could
be
desc ibed
by
a
ma hema ical
in eg al
was
i s
en isioned
a e
obse ing
he
ac i i y
o
abducens
mo oneu ons
du ing
changes
in
ho izon al
eye
posi ion
(4).
Cu en
hypo heses
equi e
neu al
ne wo ks
o
cascading,
e e be a ing
colla -
e als
wi h
posi i e
and/o
nega i e
eedback;
howe e ,
pu-
a i e
neu onal
mechanisms,
le
alone
causal
chains
o
syn-
ap ic
connec ions,
a e
s ill
no ional
in
he
ope a ion
o
in eg a o s
o
ei he
spinal
o
b ains em
ci cui s
(5-7).
He e
we
desc ibe
he
p ecise
loca ion
o
hindb ain
neu ons
ha
a e
necessa y
and
su icien
o
accomplishing
wo
dis inc
ypes
o
in eg a ion
in
he
oculomo o
sys em.
In
mammals,
he
p eposi us
hypoglossi
nucleus
was
ini-
ially
p oposed
o
ul ill
he
c i e ia
pos ula ed
as
necessa y
o
he
" eloci y
o
posi ion"
ans o ma ion
(8-11).
Recen
pha macological
and
lesion
s udies
implica e
bo h
he
es i-
bula
and
p eposi us
egions
o
he
b ains em
(12-14).
Join ly
hese
da a
sugges
ha
all
ho izon al
eye
mo emen - ela ed
subsys ems
(e.g.,
saccadic,
es ibula ,
and
isual)
p obably
sha e
a
common
posi ion
in eg a o
(15,
16).
Un o una ely,
i
has
no
been
possible
o
causally
place
any
iden i ied
es ibula
o
p eposi us
neu on
wi hin
his
ci cui
(5).
The
obse a ions
ha
es ibula
and
isual
senso y
signals
ela ed
o
sel
o
ex e nally
gene a ed
mo emen
a e
la gely
encoded
in
a
eloci y
domain
(17,
18)
led
o
iden i ica ion
o
a
second
ype
o
in eg a o
ha
could
accumula e
eye
eloc-
The
publica ion
cos s
o
his
a icle
we e
de ayed
in
pa
by
page
cha ge
paymen .
This
a icle
mus
he e o e
be
he eby
ma ked
"ad e isemen "
in
acco dance
wi h
18
U.S.C.
§1734
solely
o
indica e
his
ac .
i y
in
he
ho izon al
plane
(19,
20).
In
his
case,
neu al
in o ma ion
p opo ional
o
he
eloci y
o
he
head
and/o
isual
su ound
is
compiled
and
p ese ed
cen ally
(i.e.,
s o ed
up).
By
discha ging
he
s o ed
eloci y
a e
cessa ion
o
he
ini ia ing
senso y
s imulus,
his
in eg a o
ex ends
he
ime
o
oculomo o
compensa ion
o
ei he
head
o
isual
wo ld
mo ion.
The
loca ion
o
his
in eg a o ,
le
alone
i s
ope a ion,
has
emained
qui e
elusi e,
al hough
mos
e i-
dence
sugges s
a
c ucial
ole
o
he
es ibula
nuclei
(14,
21).
In
his
pape ,
he
posi ion
and
eloci y
in eg a o s
will
be
shown
o
occupy
spa ially
sepa a e,
non es ibula ,
loci
in
he
gold ish
medulla
ha
can
be
accu a ely
iden i ied,
eco ded
om,
and
e e sibly
inac i a ed.
MATERIALS
AND
METHODS
Gold ish
(Ca assius
au a us)
we e
p epa ed
unde
gene al
anes hesia
( icaine
me hanesul ona e;
1:20,000,
w / ol)
o
eye
mo emen
and
neu onal
eco ding.
Su ge y
consis ed
o
implan ing
an
ac ylic
pedes al
o
head
s abiliza ion
and
ephining
a
hole
in
he
occipi al
bone
o
eco ding
b ains em
neu al
ac i i y
(22).
Eye
posi ion
was
moni o ed
wi h
scle al
sea ch
coils.
A e
a
eco e y
pe iod
o
se e al
days,
ully
ale
animals
we e
es ed
in
a
e ical-axis
op okine ic
and
es ibula
s imula o .
This
sys em
consis ed
o
a
se o-
con olled
plane a ium
and
o a ing
able
in e aced
by
a
wa e o m
gene a o
ha
p oduced
any
desi ed
in e ac ion
in
phase
and/o
ela i e
eloci y
be ween
he
wo
s imuli
(23).
Compensa o y
eye
eloci y
is
nea ly
o
equal
ampli ude,
bu
opposi ely
di ec ed,
o
head
eloci y
and
exhibi s
nea ly
1800
phase
shi
wi h
espec
o
he
s imulus
[e.g.,
es ibuloocula
e lex
(VOR)
gain
o
1.0
in
Fig.
2
B
and
D].
Neu onal
ac i i y
was
eco ded
du ing
spon aneous
and/o
isual- es ibula -induced
e lex
eye
mo emen s
(see
Fig.
2).
Ins an aneous
i ing
a e
his og ams
we e
con-
s uc ed
as
he
ecip ocal
o
he
in e spike
in e al
( e .
22;
see
Fig.
2
A
and
B,
FR).
To
p oduce
local
anes hesia,
mic opipe es
illed
wi h
4%
lidocaine
and
be eled
o
a
ip
size
o
10
,Am
we e
si ua ed
a
he
physiological
cen e
o
each
iden i ied
a ea
by
eco ding
he
su ounding
ex acellula
ac i i y.
On
a e age,
1
nl
o
lidocaine
was
injec ed
wi h
5-
o
10-ms,
200-kPa
ai
p essu e
pulses
o e
30
s
(see
Figs.
3
and
4).
Fo
bila e al
inac i a ion,
wo
sepa a e
injec ions
we e
comple ed
wi hin
2
min.
Biocy in
dissol ed
in
0.1
M
phospha e
bu e
was
ei he
p essu e
injec ed
o
ion opho esed
in o
he
caudal
lobe
o
he
ce ebellum
o
label
b ains em
nuclei
(see
Fig.
1
B-E).
A e
pe usion
wi h
eleos
saline
and
aldehyde
ixa i e,
50-,um
sec ions
we e
eac ed
wi h
a idin-bio in-pe oxidase
com-
plex
(Vec o
Labo a o ies)
ollowed
by
diaminobenzidine
his ochemical
analysis
( e .
22;
see
Fig.
1
C-F).
Abb e ia ion:
VOR,
es ibuloocula
e lex.
807
P oc.
Na l.
Acad.
Sci.
USA
91
(1994)
RESULTS
Fou
hindb ain
nuclei
dis ibu ed
pe iodically
a
-500-,um
in e als
be ween
he
obex
and
he
abducens
nucleus
we e
designa ed
om
caudal
o
os al
as
a eas
I-IV
(Fig.
1
A
and
B).
Each
subg oup
con ained
a
o al
o
25-40
neu ons
ha
we e
in ol ed
in
ei he
posi ion
(a eas
I
and
III)
o
eloci y
(a eas
II
and
IV)
in eg a ion
o
oculomo o
(a eas
I
and
II)
and
pos u al
(a eas
III
and
IV)
con ol.
Biocy in
injec ions
in
he
es ibuloce ebella
lobe
selec i i y
labeled
neu ons
in
he
in e io
oli e
and
a ea
II
(Fig.
1
C-F).
Elec ical
s imula ion
o
he
ce ebellum
(Fig.
1B,
CL)
p oduced
an id omic
ac i-
a ion
o
a ea
II
eye
eloci y-only
neu ons
desc ibed
in
Fig.
2
(32).
A eas
I
and
II
we e
si ua ed
di ec ly
abo e
he
in e io
oli e
as
shown
in
bo h
sagi al
(Fig.
1
C
and
F)
and
co onal
(Fig.
1
D
and
E)
iews
o
he
b ains em.
The
longi udinal
dis ibu ion
o
he
ou
hindb ain
nuclei
could
be
ecognized
in
ela ionship
o
a
se
o
epea ing
ascula
b anches
ha
was
con i med
by
neu ophysiological
co ela es
in
e e y
animal.
Neu ons
we e
iden i ied
in
each
o
he
ho izon al
eye
mo emen - ela ed
a eas
I-IV
wi h
ex acellula
single
uni
eco dings
(Fig.
2).
Discha ge
p ope ies
we e
highly
co e-
la ed
in
he
wo
pos e io
a eas
(I
and
II)
wi h
eye
mo emen
pa ame e s,
while
ela ionships
we e
less
ob ious
in
he
wo
os al
a eas
(III
and
IV).
In
he
mos
caudal
subnucleus
(a ea
I),
neu onal
i ing
a e
du ing
spon aneous
eye
mo emen s
inc eased
in
p opo ion
o
he
angle
o
eye
de ia ion
owa d
he
ipsila e al
side
o
eco ding.
Du ing
di e gen
saccades,
_
F
P...
o
p.X_S
.. .. w. .. s
C
IV ..
..............
a ea
I
neu ons
encoded
he
posi ion
o
he
ipsila e al
eye
(Fig.
2A;
dashed
lines).
The
majo i y
o
a ea
I
neu ons
(70%)
demons a ed
a
sensi i i y
p opo ional
o
he
eloci y
o
he
eyes
du ing
saccades
(Fig.
2A,
a ow).
Some
o
hese
neu-
ons
we e
pu ely
posi ion ela ed
(30%)
since
he
eloci y
sensi i i y
du ing
apid
eye
mo emen s
was
negligible
(Fig.
2B,
a ows).
Du ing
he
slow
phase
o
ei he
es ibula
(Fig.
2B)
o
op okine ic
nys agmus,
i ing
a e
o
neu ons
in
a ea
I
was
p opo ional
o
eye
posi ion,
exhibi ing
li le
eye
eloci y
sensi i i y.
A ea
II
was
loca ed
immedia ely
os al
o
a ea
I.
Neu ons
in
his
a ea
ei he
emained
silen
o
showed
a
s eady
i ing
a e
du ing
spon aneous
saccadic
eye
mo emen
(Fig.
2C).
A ea
II
neu ons
modula ed
in
phase
wi h
eye
eloci y
di-
ec ed
owa d
he
ipsila e al
side
o
eco ding
du ing
he
slow
componen
o
ei he
op okine ic
(Fig.
2D)
o
es ibula
nys agmus.
The
wo
main
ypes
o
neu onal
esponses
de-
ec ed
in
a ea
II
we e
eye
eloci y
only
(51%)
and
eye
combined
wi h
a
head
eloci y
sensi i i y
measu ed
du ing
isual
supp ession
o
he
VOR
(49%).
Some
o
hese
neu ons
also
paused
o
all
as
phases
(eye
eloci y
pause,
25%).
Du ing
ei he
sinusoidal
op okine ic
o
es ibula
s imula-
ion,
he
i ing
a e
o
neu ons
in
a ea
I
peaked
in
phase
wi h
eye
posi ion
(Fig.
2B,
do ed
line),
while
neu ons
in
a ea
II
modula ed
in
phase
wi h
eye
eloci y
(Fig.
2D,
do ed
line).
Thus,
he
main
physiological
di e ence
be ween
a eas
I
and
II
was
an
exquisi e
seg ega ion
o
eye
posi ion
and
eye
eloci y
signals.
Ne e heless,
neu ons
in
bo h
a eas
we e
conside ed
p emo o
since
hey
i ed
15-20
ms
p io
o
he
FIG.
1.
O ganiza ion
o
hind-
::
:b ain
nuclei
in
he
gold ish.
Whole
+
b ain
(A)
and
sagi al
Nissl
sec-
ions
(B)
showing
he
os ocaudal
and
en al
loca ion
o
he
majo
$-
FL
V:
j
es ibula
subdi isions
(24)
and
'.
'
.i3-..a eas
I-IV.
(C-F)
Neu ons,
ax-
ons,
and
p ocesses
labeled
a e
biocy in
injec ion
in o
he
es ib-
uloce ebellum
(CL).
(C)
Pa asag-
i al
sec ion
300
Pm
om
he
mid-
line
showing
he
os al
in e io
oli e
(TO)
decussa ion
and
neu-
*g
_
s
ons
in
a ea
II.
Mossy
ibe
pa h-
ways
(a)
and
g anule
cell
(g)
clus-
e s
a e
ma ked.
(F)
High
magni-
S
#
::
ica ion
o
a ea
II
(s a
in
C)
illus a ing
soma
and
dend i es
o
pu a i e
eye
eloci y
in eg a o
neu ons.
(D)
Co onal
sec ion
showing
axons
(a)
o
labeled
con-
ala e al
IO
neu ons
c ossing
he
midline
and
he
ipsila e al
en o-
medial
loca ion
o
pu a i e
a ea
IT
eye
eloci y
neu ons.
(E)
Clus-
e ed
somas
(s)
and
dend i es
(d)
o
a ea
II
neu ons
a e
shown
a
highe
magni ica ion
(s a
in
D).
A,
D,
P,
M,
and
T,
an e io ,
de-
scending,
pos e io ,
magnoceliu-
la ,
and
angen ial
subdi isions
o
es ibula
nuclei;
VC,
CL,
CC,
and
CB,
al ula,
caudal
lobe,
ce -
-4i*
d
s
¢
¢ *
<
ebella
c es ,
and
co pus
o
he
ce ebellum;
ABD,
abducens;
OC
and
T,
oculomo o
and
ochlea
nuclei;
FL,
acial
lobe;
I-IV,
a eas
I-IV
o
he
hindb ain;
OT,
op ic
ec um;
SC,
spinal
co d;
TE,
elencephalon;
VIIIn,
oc a ola -
e alis
ne e;
Xn,
agal
ne e;
VL,
agal
lobe.
808
Neu obiology:
Pas o
e
al.
P oc.
Na l.
Acad.
Sci.
USA
91
(1994)
809
C
I
D
3000ms
#
~~~~~~~~~~~~~
L
Z
.
*.
100~~~~~~~~~~~~~~~~~oSp/s.
.~0
FIG.
2.
Discha ge
cha ac e is-
ics
o
a ea
I
(A
and
B)
and
a ea
II
(C
and
D)
neu ons.
(A)
Fi ing
a e
(FR)
o
an
a ea
I
neu on
du ing
spon aneous
eye
mo emen s.
Dis-
cha ge
was
co ela ed
o
le
eye
posi ion
(LE)
du ing
ixa ion
(dashed
lines)
and
some
neu ons
also
exhibi ed
saccade
sensi i i y
(a ow).
(B)
FR
o
a
pu ely
posi-
ion- ela ed
a ea
I
neu on
(a ows)
du ing
sinusoidal
head
o a ion
( i)
in
he
da k.
Head
eloci y
is
in e ed
in
B
and
D
o
acili a e
compa ison
o
eye
eloci y.
FR
was
associa ed
wi h
ho izon al
eye
posi ion
(LE)
bu
no
eye
e-
loci y
(do ed
line).
(C)
A ea
II
neu ons
we e
no
modula ed
du -
ing
spon aneous
eye
mo emen s.
(D)
Du ing
head
o a ion
a ea
II
neu ons
modula ed
in
phase
wi h
eye
eloci y
(1:E,
do ed
line)
bu
no
eye
posi ion
(LE).
Calib a-
ions
a e
indica ed.
occu ence
o
saccades,
as
phases,
o
eye
esponses
o
sudden
s ep
o a ions
o
he
head
(da a
no
shown).
Du ing
spon aneous
eye
mo emen s,
mos
neu ons
in
a ea
III
(75%)
exhibi ed
an
i egula
i ing
a e
poo ly
co ela ed
(
<
0.7)
wi h
ipsila e al
eye
posi ion.
A
weak
eye
eloci y
sensi i i y
was
de ec ed
du ing
es ibula
and
op okine ic
e lexes.
The
second
ype
(25%)
exhibi ed
a
simila
p o ile
bu
paused
o
saccades
and
as
phases
in
all
di ec ions.
A ea
IV
(100%)
was
composed
o
eye
eloci y-like
neu ons
ha
inc eased
i ing
du ing
con ala e al
eye
mo emen .
Th ee
sepa a e
clus e s
o
medially
loca ed
bu s ing
neu ons
we e
si ua ed
be ween
a eas
I
and
IV.
E e y
bu s
neu on
be ween
a ea
I
and
II
i ed
30-40
ms
be o e
he
occu ence
o
all
ipsila e ally
di ec ed
as
phases
and
saccades.
Bu s
neu ons
loca ed
be ween
a eas
II
and
III
exhibi ed
a
a iable
la ency
and
co ela ion
wi h
saccades
while
hose
be ween
a eas
III
and
IV
we e
bidi ec ional.
Selec i e
lidocaine
inac i a ion
o
he
ou
medulla y
a eas
was
used
o
assess
he
po en ial
con ibu ion
o
cons i uen
neu ons
o
he
in eg a ion
p ocess.
The
inac i a ion
o
ei he
a ea
I
o
II,
bu
no
a ea
III
o
IV,
p oduced
quali a i ely
dis inc
changes
in
eye
mo emen
pa ame e s
(Figs.
3
and
4).
Bila e al
lidocaine
injec ion
o
a ea
I
p oduced
se e e
gaze-
holding
de ici s
o
ho izon al
eye
mo emen s.
By
2
min
a e
he
injec ion,
and
du ing
he
20
min
o
e ec i e
inac i a ion,
ho izon al
saccades
o
bo h
eyes
and
in
bo h
di ec ions
we e
ollowed
by
an
exponen ial
d i
di ec ed
asymp o ically
owa d
a
null
poin
(Fig.
3A).
The
exponen ial
ime
cou se
o
he
d i
can
be
in e p e ed
as
he
passi e
ecen e ing
o
he
eye
due
o
o bi al
iscoelas ic
issue
o ces.
The
ime
con-
s an
o
he
exponen ial
d i
was
p og essi ely
sho ened
owa d
a
minimum
o
0.3
s
o e
he
i s
10
min
(Fig.
3B,
10
min).
Then
he
ime
cons an
p og essi ely
eco e ed
o
con ol
o e
he
nex
20
min
(Fig.
3B,
30
min).
Thus,
inac i a ion
o
he
in eg a o
appea s
o
emo e
he
posi ion
signals
a ailable
o
he
mo oneu ons
o
main aining
he
ho izon al
angle
o
gaze.
Bila e al
inac i a ion
o
a ea
I
also
p oduced
de as a ing
e ec s
on
bo h
he
VOR
and
op okine ic
e lex.
Sinusoidal
s imula ion
a
low
equency
(s0.25
Hz)
g ea ly
educed
VOR
gain
om
1.0
o
an
a e age
o
0.2
and
eye
eloci y
led
able
eloci y
by
70°
(Fig.
3C,
do ed
lines).
A
highe
o a ional
equencies,
gain
and
phase
p og essi ely
ap-
p oached
ypical
alues
(Fig.
3D,
do ed
line).
Consequen ly,
VOR
measu emen s
a
w1
Hz
exhibi ed
a
no mal
senso y
o
mo o
ans o ma ion
in
he
absence
o
any
cen al
neu onal
p ocessing
o
eloci y
o
posi ion
signals.
Eye
mo emen
de ici s
induced
a e
unila e al
lidocaine
inac i a ion
o
a ea
I
we e
ne e
as
ma ked
as
hose
ollowing
bila e al
injec ion
and
he
ime
cons an
o
he
pos saccadic
d i
was
ne e
lowe ed
o
<1.0
s.
Compa ison
o
da a
a e
many
e e sible
uni-
and/o
bila e al
inac i a ions
demon-
s a ed
ha
a
single
in ac
a ea
I
could
p ocess
posi ion
signals
capable
o
d i ing
bo h
eyes.
Independen
in eg i y
o
he
bila e ally
loca ed
posi ion
in eg a o s
implies
ha
he
in e connec ions
be ween
he
wo
a e
no
c i ical
o
he
eloci y
o
posi ion
ans o ma ion.
By
con as ,
unila e al
es ibula
and/o
p eposi us
lesions
in
mammals
we e
e-
po ed
as
su icien
o
p oduce
a
o al
gaze-holding
ailu e
(21,
25).
Lidocaine
inac i a ion
o
a ea
II
also
p oduced
dis inc
oculomo o
abno mali ies.
A
single
unila e al
lidocaine
in-
jec ion
in
a ea
II
caused
a
nys agmus
o
he
wo
eyes
wi h
as
phases
always
di ec ed
owa d
he
side
o
he
inac i a ion
(Fig.
4A).
The
saw oo h
mo emen
o
he
eyes
likely
o igi-
na ed
om
imbalancing
he
eloci y
ou pu
om
he
bila e al
a ea
II
nuclei
(Fig.
2).
The
esul ing
eye
eloci y
bias
was
maximal
in
he
da k,
16-22°/s du ing
he
slow
phase
o
nys agmus;
howe e ,
in
he
p esence
o
an
illumina ed
s a-
iona y
backg ound,
he
bias
was
educed
o
:4°/s,
indica -
ing
isual
supp ession
h ough
he
in ac
a ea
II
(Fig.
4A,
dashed
line).
This
amp-like
eye
mo emen
(Fig.
4B)
was
clea ly
dis inguishable
om
he
exponen ial
d i
in
eye
posi ion
ollowing
inac i a ion
o
a ea
I
(Fig.
3B).
Du ing
sinusoidal
head
o a ion
in
he
da k,
he
eloci y
bias
shi ed
he
eye
eloci y
by
a
cons an
alue
o
=20O/s
(Fig.
4C,
a ows).
All
he
as
phases
o
nys agmus
occu ed
in
he
di ec ion
opposi e
he
eloci y
bias
because
eye
eloci y
could
no
c oss
ze o
alue
(Fig.
4C,
LE).
A e
bila e al
lidocaine
inac i a ion
o
a ea
II,
saccades
and
ixa ions
exhibi ed
li le
sign
o
ei he
bias
o
gaze-
holding
ailu e
(Fig.
4D).
Ne e heless,
bila e al
anes hesia
o
a ea
II
maximally
comp omised
bo h
he
VOR
and
he
op okine ic
e lex.
Eye
eloci y
p ocessing
was
o ally
abol-
ished
du ing
ei he
sinusoidal
o
s ep
o a ion
o
he
head.
The
no mal
ime
cons an
o
he
eloci y
s o age
in eg a o
was
educed
om
10-12
s
(Fig.
4E,
a ow)
o
0.3
s
(Fig.
4F,
a ows).
By
con as ,
he
posi ion
in eg a o
con inued
o
pe o m
one-s ep
in eg a ion
o
he
eloci y- ela ed
signals
because
bo h
eyes
ollowed
wi h
an
eye
posi ion
s ep
esem-
bling
he
s imulus
eloci y
p o ile
(Fig.
4F,
RE
and
LE).
B
Neu obiology:
Pas o
e
al.
50SP/
W%l
i
P oc.
Na l.
Acad.
Sci.
USA
91
(1994)
B
1oo.
0-
100-
50
50
50]
16~
O-
w
~~~~.
500ms,
6E
FIG.
3.
E ec s
o
bila e al
lidocaine
injec ion
in
a ea
I.
(A)
Ho izon al
posi ion
o
he
le
(LE)
and
igh
(RE)
eyes
12
min
a e
a ea
I
inac i a ion.
A e
saccades
in
bo h
di ec ions
he
eyes
d i ed
cen ipe ally
wi h
an
exponen ial
p o ile
exhibi ing
a
ime
cons an
o
0.3
s.
(B)
Time
cou se
in
minu es
illus a ing
inac i a ion
and
eco e y
a e
bila e al
a ea
I
lidocaine
injec ion.
Saccades
o
simila
size
di ec ed
le wa d
we e
supe imposed
a
he
poin
o
peak
ampli ude
o
illus a e
sho ening
o
he
eloci y
o
posi ion
in eg a-
o
ime
cons an .
(C
and
D)
E ec s
o
a ea
I
inac i a ion
on
he
VOR
a
low
(0.125
Hz;
C)
and
high
(1
Hz;
D)
equency.
Lidocaine
injec ions
o
1
nl
in o
ei he
a ea
III
o
a ea
IV
did
no
in luence
eye
mo emen s.
La ge
amoun s
(10
nl)
p oduced
some
d i
and
eloci y
bias,
likely
due
o
sp ead
in o
adjacen
nuclei
and/o
ibe
ac s.
Lidocaine
injec ions
o
1
nl
in o
he
medial
bu s
neu ons
be ween
a ea
I
and
II
nea ly
abolished
saccades
and
as
phases
bu
did
no
a ec
in eg a o
ope a ion.
Inac i a ion
o
a ea
II
did
no
in e up
he
es ibula
con-
nec ion
o
he
posi ion
in eg a o .
These
esul s
a e
no
consis en
wi h
models
(26)
o
lesion
s udies
(21)
ha
place
he
si e
o
eloci y
s o age
in
a
sys em
o
ecip ocal
com-
missu al
connec ions
be ween
he
es ibula
complex.
DISCUSSION
Ou
da a
demons a e
ha
he
neu al
mechanisms
equi ed
o
bo h
eloci y
o
posi ion
and
eloci y
s o age
in eg a ion
eside
in
adjacen
medulla y
nuclei
clea ly
isola ed
om,
bu
likely
in ima ely
connec ed
o,
he
es ibula
nuclei.
The
spa ial
disc e eness
o
hese
in eg a o s
co esponds
o
con-
s an
mo phological
landma ks
in
he
gold ish
medulla
ha
e lec
he
adul
e en ion
o
a
segmen al
bluep in
desc ibed
in
la al
zeb a ish
(27).
We
p opose
ha
hese
hindb ain
nuclei
in
gold ish
a e
analogous
in
unc ion
o
he
mammalian
p eposi us
nuclei
and
ha
homologous
neu onal
ypes
can
be
e en ually
ecognized.
The e o e,
he
hindb ain
opog aphy
in
eleos s
(Fig.
1
A
and
B)
is
mo e
ad an ageous
o
esol ing
neu ophysiological
co ela es
as
well
as
in es iga ing
he
de elopmen al
and
gene ic
plans
unde lying
assembly
o
hindb ain
ho izon al
eye
mo emen
pa hways
(28).
In
each
disc e e
nono e lapping
compa men ,
he
quan-
i a i e
analysis
o
discha ge
cha ac e is ics
and
oculomo o
de ici s
a e
lidocaine
injec ions
we e
complemen a y.
A ea
I
and
a ea
II
neu ons
we e
co ela ed
wi h
eye
posi ion
and
eloci y,
espec i ely.
Signal
p ocessing
appea ed
o
be
au onomous
o
each
nucleus.
Since
a ea
I
esponses
we e
co ela ed
o
saccades,
VOR,
and
isually
induced
e lexes,
he
posi ion
in eg a o
is
indeed
common
o
all
eye
mo e-
men s
(15).
Ne e heless,
a ea
I
p obably
ep esen s
he
summing
junc ion
o
wo
qui e
di e en
modali ies
o
eye
eloci y
signal
because
as
phases
and
spon aneous
saccadic
eye
mo emen s
we e
spa ed
a e
bila e al
lidocaine
inac i-
a ion
o
a ea
II
(Fig.
4D).
Thus,
es ibula
and
op okine ic
eye
eloci y
signals
p ocessed
in
a ea
II
each
a ea
I
by
a
pa hway
dis inc
om
ha
o
bu s
neu ons
p oducing
sac-
cades.
An
equally
likely
supposi ion
is
ha
a ea
II
also
ep esen s
a
summing
junc ion
o
es ibula
and
isual
eye
eloci y,
because
hese
neu ons
do
no
i e
o
ei he
sac-
cades
o
as
phases
(Fig.
2
C
and
D).
Homogenei y
o
discha ge
pa e n
and
inac i a ion
wi h
lidocaine
a gues
ha
a ea
II
plays
wo
sequen ial
oles
in
eye
mo emen .
We
sugges
ha
he
neu ons
i s
gene a e
and
hen
s o e
eye
eloci y
since
lidocaine
inac i a ion
no
only
abolished
eloci y
s o age
bu
also
educed
he
VOR
ime
cons an
o
alues
less
han
he
a e age
es ibula
a e en
ime
cons an
(0.3
s
s.
3-4
s,
espec i ely).
Inac i a ion
o
a ea
II
g ea ly
impai s
bo h
es ibula
and
op okine ic
e-
lexes
because
all
neu ons
in
a ea
II
exhibi
a
con inuous
le el
o
onic
ac i i y
(Fig.
2C).
Hence,
he
VOR
ime
cons an s
a e
lowe
han
ha
expec ed
om
p edic ions
based
on
a e aged
p ima y
a e en
discha ges
(29),
and,
in
ac ,
many
species
o
eleos
exhibi
ypical
VOR
ime
cons an s
a
less
han
mean
a e en
alues
(30).
This
lowe ed
VOR
ime
cons an
was
accompanied
by
a
ma ked
comp omise
in
he
VOR
when
es ed
wi h
lowe
equency
sinusoidal
s imuli.
By
con as ,
he
di ec ,
p esumed
h ee-neu on,
VOR
pa h-
way
emained
in ac
as
indica ed
by
he
la ency
and
ampli-
ude
o
he
eye
posi ion
s ep
( e .
23;
Fig.
4F).
We
sugges
ha
a ea
II
eloci y
neu ons
comp ise
a
b ains em
loop
ha
suppo s
he
di ec
VOR
pa hway
loca ed
in
he
descending
oc a al
nucleus
(Fig.
1
A-C).
O e all,
he
mos
s aigh o wa d
a gumen
is
ha
a ea
I
and
a ea
II
a e
independen
eye
posi ion
and
eloci y
gen-
e a o s.
Assu edly,
a ea
I
is
he
equisi e
posi ion
in eg a o .
P incipally,
a ea
II
con e s
senso y
signal
eloci y
( es ib-
ula
and
isual)
o
mo o
(eye)
commands
as
well
as
assuming
he
impo an
ole
o
eye
eloci y
s o age.
The e o e,
he
pa e ns
o
neu al
ac i i y
wi hin
each
in eg a o
can
be
p oposed
o
a ise
om
in insic
p ope ies
o
hei
cons i uen
neu ons
as
opposed
o
in e ac ions
wi h
ex insic
synap ic
ci cui y.
One-s ep
signal
gene a ion
and
s o age
is
an
a ac i e
idea
because
he
same
neu ons
used
o
c ea e
can
also
s o e
he
neu al
ac i i y
co ela ed
wi h
ei he
posi ion
o
eloci y.
Such
neu onal
beha io
is
p edic ed
based
on
he
s uc u al
uniqueness,
homogenei y,
and
clea
sepa a ion
o
he
indi-
idual
a eas
om each
o he
and
he
es ibula
nuclei
(Fig.
810
Neu obiology:
Pas o
e
al.
P oc.
Na l.
Acad.
Sci.
USA
91
(1994)
811
100]
0
D
LE
l
A,
80
I
RE
ls
1).
Midline
sagi al
lesions
be ween
hese
a eas
do
no
block
ei he
posi ion
o
eloci y
s o age
(da a
no
shown);
howe e ,
es ibula
pa hways
a e
highly
p obable
h ough
mo e
os al
commissu es
(Fig.
1B).
The
medio en al
loca ion
o
hese
hindb ain
nuclei
and
hei
sepa a e
inac i a ion
clea ly
dem-
ons a e
ha
nei he
axonal
pa hways
no
neu ons
wi hin
he
es ibula
complex
we e
a ec ed
by
lidocaine
(Figs.
3
and
4).
We
belie e,
he e o e,
ha
all
o
he
s uc u al
and
unc ional
cha ac e is ics
expec ed
o
each
in eg a o
a e
embodied
by
neu ons
cen alized
wi hin
a
single
nucleus.
Since
hese
unusual
compa men s
a e
necessa y
and
p e-
sumed
su icien
o
p ocess
he
neu onal
ope a ions
elemen-
a y
o
in eg a ion,
we
hypo hesize
ha
ans o ma ions
wi hin
each
compa men
con e
au o hy hmic
cha ac e is-
ics
ha
a e
la gely
modula ed,
no
commanded,
by
ex e nal
synap ic
ci cui y.
In
p inciple,
he
inhe en
elec o espon-
si e
p ope ies
o
he
neu ons
alone
may
be
su icien
o
p oduce
in eg a ion
(31).
The e o e,
we
p opose
ha
signal
ans o ma ions
may
la gely
a ise
om
he
in insic
elec o-
physiological
p ope ies
o
cons i uen
neu ons
(32).
The
di e si y
o
eye
mo emen s
and
he
a ied
in eg a o
ime
cons an s
ha
exis
be ween
eleos ean
species
should
pe mi
hese
s uc u al
and
neu ophysiological
hypo heses
o
be
sa is ac o ily
se led.
We
hank
D s.
M.
U.
L.
Benne ,
B.
Cohen,
and
T.
Raphan
o
discussion
and
commen s
on
his
manusc ip .
1.
Robinson,
D.
A.
(1%8)
Science
161,
1219-1224.
2.
Raphan,
T.,
Ma suo,
V.
&
Cohen,
B.
(1979)
Exp.
B ain
Res.
35,
229-248.
3.
Raphan,
T.
&
Cohen,
B.
(1981)
in
Models
o
Oculomo o
Beha io
and
Con ol,
ed.
Zube ,
B.
L.
(CRC,
Boca
Ra on,
FL),
pp.
91-109.
4.
Ska enski,
A.
A.
&
Robinson,
D. A.
(1973)
J.
Neu ophysiol.
36,
724-738.
5.
Robinson,
D.
A.
(1989)
Annu.
Re .
Neu osci.
12,
33-45.
6.
Cannon,
S.
C.,
Robinson,
D. A.
&
Shamma,
S.
(1983)
Biol.
Cybe n.
49,
127-136.
7.
Anas asio,
T.
J.
&
Robinson,
D.
A.
(1989)
Biol.
Cybe n.
61,
79-89.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
10°-
O-
4s
.
J
FIG.
4.
E ec s
o
unila e al
(A-C)
I
and
bila e al
(D-F)
lidocaine
inac i-
a ion
o
a ea
II.
(A)
Unila e al
inac-
i a ion
o
he
le
a ea
II
p oduced
nys agmus
o
he
le
in
he
da k,
bu
slow
phases
we e
a enua ed
in
he
ligh
(dashed
line).
(B)
Supe imposi-
ion
o
as
phases
demons a es
J
amp-like
eye
mo emen s
a e
inac-
1
11
I
i a ion.
(C)
Du ing
head
o a ion
in
4s
.
he
da k
eloci y
bias
added
o
he
sinusoidal
nys agmus
in
bo h
eyes.
l
(D)
Bila e al
lidocaine
injec ion
p o-
8
duced
nei he
d i
no
eloci y
bias
du ing
spon aneous
eye
mo emen s.
(E)
Pe - o a o y
nys agmus
(a ow)
du ing
cons an
head
eloci y
exhib-
1
i ed
a
no mal
ime
cons an
o
10-12
s.
H
320/s
(F)
Bila e al
lesion
o
a ea
II
i ually
]
elimina ed
eloci y
s o age
in
bo h
di ec ions
(VOR
ime
cons an
shown
l /;
by
a ows)
bu
eloci y
o
posi ion
in eg a ion
was
una ec ed
[le
eye
(LE)
and
igh
eye
(RE)].
L6pez-Ba neo,
J.,
Da lo ,
C.,
Be hoz,
A.
&
Bake ,
R.
(1982)
J.
Neu ophysiol.
47,
329-352.
Bake ,
R.
&
Be hoz,
A.
(1975)
B ain
Res.
86,
121-127.
Delgado-Ga c a,
J.
M.,
Vidal,
P.
P.,
G6mez,
C.
&
Be hoz,
A.
(1989)
Neu oscience
29,
291-307.
Bake ,
R.
(1977)
in
Eye
Mo emen s,
eds.
B ooks,
B.
A.
&
Bajandas,
F.
J.
(Plenum,
New
Yo k),
pp.
145-178.
Che on,
G.,
Godaux,
E.,
Laune,
J.
M.
&
Vande kelen,
B.
(1986)
J.
Physiol.
(London)
372,
75-94.
Cannon,
S.
C.
&
Robinson,
D.
A.
(1987)
J.
Neu ophysiol.
57,
1383-1409.
Kaneko,
C.
R.
S.
(1992)
Ann.
N.
Y.
Acad.
Sci.
656,
408-427.
Robinson,
D.
A.
(1975)
in
Basic
Mechanisms
o
Ocula Mo ili y
and
Thei
Clinical
Implica ions,
eds.
Lenne s and,
G.
&
Bach-y-Ri a,
P.
(Pe gamon,
New
Yo k),
pp.
337-374.
Tomlinson,
R.
D.
&
Robinson,
D. A.
(1984)
J.
Neu ophysiol.
51,
1121-1136.
Simpson,
J.
I.
(1984)
Annu.
Re .
Neu osci.
7,
13-41.
Goldbe g,
J.
M.
&
Fe nandez,
C.
(1975)
Annu.
Re .
Physiol.
37,
129-162.
Collewijn,
H.
(1972)
B ain
Res.
36,
71-88.
Cohen,
B.,
Ma suo,
V.
&
Raphan,
T.
(1977)
J.
Physiol.
(Lon-
don)
270,
321-344.
S aube,
A.,
Ku zan,
R.
&
Bu ne ,
U.
(1991)
Exp.
B ain
Res.
86,
347-358.
Pas o ,
A.
M.,
To es,
B.,
Delgado-Ga c a,
J.
M.
&
Bake ,
R.
(1991)
J.
Neu ophysiol.
66,
2125-2140.
Pas o ,
A.
M.,
de
la
C uz,
R.
R.
&
Bake ,
R.
(1992)
J.
Neu-
ophysiol.
68,
2003-2015.
Highs ein,
S.
M.,
Ki ch,
R.,
Ca ey,
J.
&
Bake ,
R.
(1992)
J.
Comp.
Neu ol.
319,
501-518.
Che on,
G.
&
Godaux,
E.
(1987)
J.
Physiol.
(London)
394,
267-290.
Galiana,
H.
L.
&
Ou e b idge,
J.
S.
(1984)
J.
Neu ophysiol.
51,
210-241.
Kimmel,
C.
B.,
Me cal e,
W.
K.
&
Schab ach,
E.
(1985)
J.
Comp.
Neu ol.
233,
365-376.
T e a ow,
B.,
Ma ks,
D.
L.
&
Kimmel,
C.
B.
(1990)
Neu on
4,
669-679.
Boyle,
R.
&
Highs ein,
S.
M.
(1990)
J.
Neu osci.
10,
1570-
1582.
Die inge ,
N.,
Reichenbe ge ,
I.
&
G a ,
W.
(1992)
B ain
Beha .
E ol.
39,
289-304.
Llinis,
R.
R.
(1988)
Science
242,
1654-1664.
De
la
C uz,
R.
R.,
Pas o ,
A.
M.
&
Bake ,
R.
(1993)
Soc.
Neu osci.
Abs .
19,
858.
Neu obiology:
Pas o
e
al.
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