MECHANISMS OF SU’PRASPINAL ACTIONS UPON

SPINAL CORD ACTIVITIES. RETICULAR INHIBITORY

MECHANISMS ON ALPHA-EXTENSOR MOTONEURONS
R. LLINAS2 AND C. A. TERZUOLO
Department of Physiology, Medical School, University of Minnesota,
Minneapolis, Minnesota
(Received for publication November 21, 1963)

DECEREBRATE RIGIDITY IS MELTED by an adequate electrical stimulation of

the bulbar inhibitory recticular formation (RF) (12). This inhibition of the
extensor hypertonus cannot be construed as being exclusively due to a
collapse of the myotatic reflex via a reticular action upon y-motoneurons
(10) since impulse activity in a-extensor motoneurons can still be sup-
pressed by a reticular stimulation after interruption of the spindle loop (15).
To investigate the mechanisms of this inhibitory reticular action upon
cr-motoneurons two requirements should be fulfilled: 1) the spindle loop in
muscles agonistic and antagonistic to the motor pool under study should be
interrupted, and 2) the effectiveness of the reticular stimulation should be
tested upon the extensor rigidity of the intact hind limbs. This second re-
quirement cannot be substituted by describing the location of the stimulat-
ing electrodes (obtained from histological controls or given in Horsley-Clarke
coordinates) and/or by specifying the parameters of the electrical stimuli.
Even testing the effect of the stimulation upon the monosynaptic reflex
alone is not adequate. A number of side effects can, in fact, be induced by
stimulations applied in the RF concomitantly with the suppression of the
monosynaptic reflex, with or without a decrease of the decerebrate rigidity.
These effects (such as tonic contractures of the neck, back and/or flexor
muscles of the forelimbs, forceful inspiratory arrest, etc.) are obviously
caused by inaccurate localization of the stimulating electrode within the
RF and/or by a spread of the stimulating current. Therefore, agents pro-
ducing muscle paralysis cannot be administered before the effects induced
by the stimulation have been assessed, since they preclude the possibility
of establishing the electrode placement and the stimulus parameters ade-
quate to suppress the myotatic reflex without producing undesired effects.
Indeed, only the observation that the decerebrate rigidity of the forelimbs
and the monosynaptic reflex recorded from lumbar ventral roots (after inter-
1 This work is part of a program supported by Grant B-2567 from the National Insti-
tute of Neurological Diseases and Blindness and by the University of Minnesota.
2 Postdoctoral Research Fellow of the National Institutes of Health. Present address:
Dept. of Physiology, John Curtin Medical School, Australian National University, Can-
berra, Australia.

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580 R. LLINAS AND C. A. TERZUOLO

ruption of the y-loop) are simultaneously inhibited can warrant the con-
tention that the results obtained by recording intracellularly from lumbar
cu-motoneurons refer to and account for the known reticular actions upon
these neurons.
The above requirements have been met in the studies on the mecha-
nisms of reticular actions upon a-extensor and flexor motoneurons to be
reported in this and in subsequent papers.
METHODS

The experiments were performed on cats decerebrated by pre- or intercollicular sec-

tions made after the lumbar segments of the cord had been exposed by laminectomy. The

FIG. 1. Effects induced on a-extensor motoneurons by “adequate” stimulation of the

bulbar inhibitory RF. A is a control record. Impulse activity in the impaled cell (second
trace at low gain and sweep speed, and third trace at higher gain and faster sweep speed)
was induced by stimulating the quadriceps nerve. The monosynaptic reflex was recorded
simultaneously from the ventral root (fourth trace; same sweep speed as for the second
trace). In B, during reticular stimulation, impulse activity in the impaled cell was pre-
vented and the monosynaptic reflex was inhibited. The sustained increase of membrane
potential caused by reticular inhibition can be seen in both low- and high-gain intracellular
recordings using the first trace as a reference line. Calibrations (0.5 msec.; 10 mV.) apply
only to the high-gain intracellular record. In subsequent figures the trace monitoring the
monosynaptic reflex has been omitted.

anesthetic (ether) was then discontinued; bilateral pneumothorax was performed and the
animals were maintained under artificial respiration (98 y0 0,; 2 y0 CO,).
Interruption of the spindle loop was produced by sections of peripheral nerves and of
the appropriate ventral roots. The biceps-semitendinosus and quadriceps nerves were pre-
pared for stimulation. The temperature of the animal and oil pools was maintained at
constant levels.
The RF was stimulated by means of stereotaxically oriented concentric electrodes.
The effectiveness of the stimulation was tested upon the rigidity of the forelimbs and upon
the monosynaptic extensor reflex recorded from the lumbar ventral roots. Flaxedil was
thereafter injected intravenously to permit intracellular recordings.
Square pulses of 0.5-l msec. duration were applied at frequencies between 60 and
lOO/sec. The voltage needed to produce inhibition of the decerebrate rigidity with the
electrodes used was usually between 0.5 and 1.2 V. No parameters of the electrical stimuli
will be given hereafter, the term “adequate” being used to indicate that the requirements
stated in the INTRODUCTION were fulfilled.
Micropipettes (resistance 75 megohms) filled with 3 M KC1 or 2 M K citrate were used.
They were mounted in a bridge to permit direct stimulation of the impaled cell and meas-
urements of membrane resistance. The resistance of the arm of the bridge opposing the
microelectrode was 200 megohms. A Tektronix 565 oscilloscope (two beams with inde-

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 RETICULAR INHIBITORY MECHANISMS 581
pendent time bases and delayed trigger) was used to display the potential changes after
suitable amplification.

RESULTS
Figure 1 illustrates the effects of an adequate stimulation of the bulbar
inhibitory RF upon the monosynaptic reflex (lower beam) and the activity
recorded simultaneously from a motoneuron participating in the reflex
(second beam at low gain, and third beam at higher gain and faster sweep
speed). In B, during reticular stimulation, impulse activity of the pene-
trated cell was prevented and the amplitude of the reflex recorded in the

FIG. 2. Time course of the sustained potential change caused by reticular inhibition.
Quadriceps motoneuron. A : control; B : during reticular stimulation; C: after the stimula-
tion had been discontinued; D: during a second reticular stimulation. Notice in B that
when the increase in membrane potential is not yet fully developed there is only a delay in
the origination of the action potential. Calibrations: IO mV. and 1 msec. E: time course of
the potential change caused by an “adequate” reticular stimulation applied at the time
indicated by the horizontal bar. Time: 50 msec. Voltage: 5 mV.

ventral root was greatly reduced, indicating that a large portion of the re-
sponsive population was similarly affec ted by the supraspinal stimulation.
Figure 1 also illustra tes that the steady level of ’ membrane polarization was
altered by the stimulation, the interior of the cell becoming more negative.
This point is further illustrated in records A through D of Fig. 2. The time
course of this increase in membrane potential is shown in E. Its maximum
amplitude (Fig. 3) was usually reached in 30-180 msec. High-speed record-
ings during its development failed to demonstrate individual steps of sub-
stantial amplitude bearing a constant time relation to each individual
stimulus.
At the end of the stimulation the membrane potential returned more or
less slowly (30-200 msec.) to its original level. In a few cells a rebound
phenomenon was observed when the stimulation was discontinued, the
membrane becoming transiently less polarized than it was prior to the
stimulation.
Excitability changes evoked by reticular inhibition. Present knowledge of
nerve cell physiology (cf. 5) suggests that the increase in membrane poten-
tial described above can be responsible for the suppression of the mono-

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582 R. LLINAS AND C. A. TERZUOLO
synaptic reflex by reticular action, the excitability of a-extensor moto-
neurons being reduced. Direct experimental evidence on this last point is
given in Fig. 4. In A, impulse activity was induced by stimulating the cell
directly through the impaling microelectrode. When a reticular stimulation
was simultaneously applied, the generation of the spike was either delayed
(B) or prevented (B, C, and 0). It can therefore be stated that the prob-
ability of initiating impulse activity in the axon by depolarizing the soma
membrane, either by synaptic activation (Fig. 1) or by a pulse of cathodal
current, is reduced by reticular inhibition.

Number
of Cells

20
I
FIG. 3. Amount of membrane poten-
tial change induced by reticular inhibition.
The histogram illustrates amount of sus-
I5 tained increase in membrane potential
measured in all cells. studied. Since the
values obtained from cells impaled with
KCl- or K citrate-filled microelectrodes
IO overlapped extensively, the two populations
of cells have not been separated. Although
no rigorous attempt was made to correlate
the amount of hyperpolarization induced by
reticular inhibition with the value of mem-
5 brane potential prior to stimulation, the
largest changes in membrane potential were
observed in motoneurons which were obvi-

0
r ously
reticular
depolarized
stimulation
at the moment
was applied.
that the

More subtle evidence of the excitability change of the soma-dendritic

membrane by reticular inhibition was obtained by stimulating the cells
antidromically. In this condition, the IS component of the intracellular
spike which is caused by the presence of impulse activity in the axon (1, 2,
3, 5, 14) would not be expected to be suppressed by reticular inhibition. In
fact, the moderate voltage changes occurring across the soma membrane
during reticular inhibition cannot be expected to overcome, after decrement
due to electrotonic spread, the large safety factor for impulse propagation
in the axon. In contrast, the SD component of the spike, currently attributed
to the invasion by impulse activity of the soma-dendrite complex (1, 2, 5, 9,
14) should be affected by reticular inhibition.
In agreement with these expectations, Fig. 5 shows that the SD com-
ponent of the second of two action potentials evoked by antidromic stimu-
lation at a short time interval, is blocked by reticular inhibition. As for the

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 RETICULAR INHIBITORY MECHANISMS 583
first action potential, the inflection present in the rising phase of the spike
between the IS and SD components, which denotes the time of invasion
of the soma membrane (2, 9)) becomes more prominent. This indicates that
the safety factor for invasion of the soma membrane is reduced, and there-
fore that the excitability of this region of membrane is decreased.
These data demonstrate that reticular inhibition affects the excitability

FIG. 4. Decrease in excitability during reticular inhibition as shown by direct stimula-

tion. Impulse activity was induced by stimulating directly the cell with a cathodal pulse of
constant amplitude (as shown by the upper trace of records A, B, and C). In A the spike
originated with a constant latency after the beginning of the cathodal pulse (five super-
imposed sweeps). In R and C, during reticular inhibition, the origin of the spike was either
delayed or prevented. Calibrations in C: IO mV. and 1 msec. Record D is taken from an-
other experiment in which the following arrangement was used. One beam (bottom trace)
recorded at high gain and low film speed the time course of the sustained potential change
caused by reticular inhibition. The second beam was synchronized with the current pulse
directly stimulating the cell and provided adequate time resolution for the events caused
by this stimulation. In order to orient these single frames in the conventional manner, the
record has to be read from right to left. In frame 1, taken before the reticular stimulation,
the applied pulse induced impulse activity. Reticular stimulation was then applied (approx.
at the time indicated by the arrow). During the ensuing increase of membrane potential
(which can also be seen in frame 2, taking the upper trace as a reference line), the applied
depolarization failed to induce impulse activity. Calibrating in frame 1: 10 mV., 1 msec.

of a-extensor motoneurons, in the absence of the y-loop. The nature of this

postsynaptic inhibitiory process or processes will now be analyzed.
Mechanisms producing the sustained membrane potential change. It has
already been stated that the sustained increase of membrane potential
caused by reticular inhibition might be largely responsible for the excit-
ability change demonstrated in the preceding section (a second factor which
might be involved will be considered later).
At least two mechanisms could induce the described potential change
during adequate reticular stimulations: 1) a sustained synaptic inhibitory
impingement, and/or 2) the suppression of a more or less steady background
excitatory impingement (cf. 13).
If the first mechanism were the predominant one, the membrane resistance

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584 R. LLINAS AND C. A. TERZUOLO

I !I
DqB i

2
4 ,I

FIG. 5. Decrease in excitability during reticular inhibition as shown by antidromic

activation. In A, B, and C two electrical stimuli were applied to the ventral root at a short
time interval. A is the control record (five superimposed sweeps). In B and C, during
reticular stimulation, the SD component of the second spike was either delayed (B) or.
prevented (C). Calibrations: 10 mV., 1 msec. Record D was obtained using the same ar-
rangement as described in the legend of Fig. 40. In this cell, the increase in membrane
potential produced by reticular action was quite large and the decrease in excitability of
the SD membrane during reticular inhibition (frame 2) quite obvious. Notice also that
amount of overshoot of the spike, the upper trace in the single frames indicating zero mem-
brane potential, was decreased. Further explanation in the text. Calibrations refer only to
the single frame; 20 mV. and 1 msec.

of a-extensor motoneurons would decrease during the sustained potential

change because of the increase in conductance due to the activation of
inhibitory synapses (cf. 4, 6). Moreover, on the assumption that the ions
responsible for this inhibitory process would be the same as those involved
in “direct inhibition” (4, 6), injection of Cl- inside the cell would affect the
amplitude and perhaps reverse the direction of the potential change caused
by reticular stimulation.
If, on the contrary, the second of the two above mechanisms was pre-
dominant, an increase in membrane resistance would be expected. More-
over, little or no change would occur in the amplitude of this potential
change by increasing the intracellular concentration of Cl- (cf. 5).
The data in Figs. 6, 7, and 8 will demonstrate that a sustained synaptic
inhibitory impingement produces the sustained potential change shown to
occur during reticular inhibition.
Figure 6 illustrates the decrease of membrane resistance during reticular
inhibition. The applied current pulse being constant, the voltage displace-
ment, with the bridge balanced, was less during reticular stimulation (B)

FIG. 6. Resistance change during re-

ticular inhibition. Cathodal and anodal
pulses of 20 msec. duration were applied
before (A) and during (B) reticular stimula-
tion. Full explanation in the text. Voltage
calibration: 5 mV.

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 RETICULAR INHIBITORY MECHANISMS 585
than at rest (A). Table 1 shows for 14 cells the percentage decrease of re-
sistance induced by RF stimulation. In each case the time constant of decay
of the voltage at the end of the pulse was also measured. With the bridge
balanced this time constant can be taken to approximate that of the mem-
brane of the impaled cell, the artifact produced by the current flowing
through the electrode being effectively compensated by the bridge. Even so,
no absolute values will be given. The measurements were used to compare
the amount by which the time constant was reduced with the amount by
which the resistance was decreased. In 80% of the cases the two values in
each cell were found to agree within 157& therefore increasing the reliability
of the resistance measurements.3 It would therefore seem that the mem-
brane conductance is increased by “adequate” reticular stimulations. If so,

Table 1. Per cent decrease of membrane resistance during reticular inhibition

-- -- ~-
Cell No. Per Cent Change Cell No. Per Cent Change

C-188 37 C-271 28
195 26 272 29
200 35 277 35
204 30 282 24
206 36 283 30
260 28 30
261 31 35

Average per cent change =31%.

the increase in membrane potential caused by reticular inhibition would be

due 9 either predominantly or exclusively, to a sustained synaptic inhibitory
impingement.
Conclusive evidence that this mechanism is indeed operating in cu-exten-
sor motoneurons was obtained: 1) by increasing the intracellular concentra-
tion of Cl- ions, and 2) by displacing the membrane potential with hyper-
polarizing currents. In the latter case the absolute level of membrane poten-
tial was not measured. The reversal of a hyperpolarizing IPSP, evoked by
stimulating the biceps-semitendinosus nerves, was used as a criterion ade-
quate and sufficient to establish that the voltage attained across the mem-
brane by the applied current had reversed the effective emf governing the
movemen t of the ions involved in the inhibitory process (cf. 4, 6). The same
3 A second set of data pertinent to this point was obtained by invading antidromically
the cells (ventral root stimulation) in the absence of and during reticular inhibition. The
total spike amplitude, the amount by which the spike overshot zero membrane potential,
and the amplitude of the IS and SD components were measured. Among the conclusions
reached by comparing the values obtained from these measurements is that of an increase
in conductance of the soma-dendritic membrane during reticular stimulations. In fact, the
amount of the overshoot and the amplitude of the SD component of the spike, known to be
due to impulse activity in the soma-dendrite complex, were found to be reduced during
reticular inhibition (see Fig. 50). These findings will be presented in a subsequent paper
since their discussion is more relevant to other problems than to the present one.

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586 R. LLINAS AND C. A. TERZUOLO
criterion, i.e., reversal of a “direct” IPSP, was also used in those experiments
in which the intracellular concentration of Cl- ions was increased by using
KCl-filled micropipettes and passing adequate currents.
As shown in Figs. 7 and 8, the polarity of the sustained change in poten-
tial caused by reticular inhibition was reversed by both the above proce-
dures. Such a reversal occurred at approximately the same level of mem-
brane potential and at the same Cl- concentration at which the direct IPSP
was reversed. It can be therefore concluded: 1) that a sustained synaptic

A B
-’

FIG. 7. Reversal of reticular hyperpolarization by displacing the membrane potential.

A and B : control records before the application of a hyperpolarizing current through the K
citrate-filled microelectrode. An IPSP, evoked by stimulating the biceps-semitendinosus
nerve, is shown in each record. In B, during reticular stimulation, the membrane potential
was increased. In C and D, during the application of the hyperpolarizing current both the
“direct” IPSP and the potential change caused by reticular inhibition were reversed in
polarity. The top beam in each record has to be taken only as reference line, and the dis-
placement of d.-c. potential between the upper and the lower pair of records is not a meas-
ure of the hyperpolarization of the membrane caused by the current. Further explanations
in the text. Calibrations: 5 mV.; 1 msec.

inhibitory impingement upon a-extensor motoneurons is produced by an ade-

quate reticular inhibitory stimulation, and 2) that the ionic mechanisms of
this postsynaptic inhibitory process are similar to those of direct inhibition.
Conductance changes as a part of the postsynaptic inhibitory process. From
the finding, presented above, that the membrane conductance is increased
during the sustained inhibitory synaptic impingement caused by reticular
stimulations, one would expect the postsynaptic efficacy of excitatory inputs
to a-extensor motoneurons to be reduced during reticular inhibition. The volt-
age drop caused across the motoneuron’s membrane by the flow of a given
synaptic excitatory current would, in fact, be reduced.
To investigate the above point as well as to exclude the possibility that a
mechanism of presynaptic inhibition (7, 8) is involved-together with the

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 RETICULAR INHIBITORY MECHANISMS 587
postsynaptic mechanism above demonstrated-in the suppression of the
monosynaptic reflex by reticular action, the following experiment was per-
formed. EPSPs subthreshold for impulse initiation were evoked by stimulat-
ing group Ia fibers in the absence of and during adequate reticular stimula-
tions. It was found that the peak amplitude and the time of decay of the
EPSP were reduced during reticular inhibition (Fig. 9). The measurements
from all cells studied are summarized in the plot of Fig. 10. The relevance of
these findings to the subject of this paper will be considered in the DIS-
CUSSION.

A B

C D

-L-4_

FIG. 8. Reversal of reticular hyperpolarization by the injection of Cl- ions. A and B

are the control records before the leakage of ions from the KCl-filled microelectrode was
intentionally increased by passing adequate currents. Reticular inhibition produces in B a
sustained increase in membrane potential. Records C and D were obtained following injec-
tion of Cl-. Notice that both “direct” inhibition and reticular inhibition do not induce at
this time any substantial potential change. In E and F, following further injection of Cl-,
the “direct” IPSP and the change in potential caused by reticular inhibition are reversed.
Further explanations in the text. Calibrations: 5 mV.; 1 msec.

DISCUSSION

Data have been presented which demonstrate that the excitability of a-

extensor motoneurons is decreased during electrical stimulation of the bulbar
reticular formation adequate to suppress the decerebrate rigidity and in-
hibit the monosynaptic extensor reflex in the absence of the r-loop. Reticu-
lar inhibition does, therefore, exercise a postsynaptic inhibitory influence
upon a-extensor motoneurons in the stated experimental conditions.

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588 R. LLINAS AND C. A. TERZUOLO

This inhibitory process has been shown to be due to a sustained synaptic

inhibitory impingement causing a hyperpolarization of the membrane. The
ionic mechanisms responsible for this voltage change were found to be simi-
lar to those of direct inhibition.
It should be noted, however, that the data reported here do not exclude
the possibility that the suppression by the reticular stimulation of a more or

FIG. 9. Changes in the amplitude and

time course of the EPSP during reticular
inhibition. Records A and B were obtained
before and during reticular stimulation (IO
superimposed sweeps in each record). In C
the EPSP obtained in another cell before
and during reticular inhibition have been
drawn superimposed. Full explanation in
the text. Calibrations in B and C: 5 mV., 1
msec.

less steady excitatory background impingement upon cu-extensor motoneu-

rons might contribute, to some extent at least, to the postsynaptic inhibitory
effect. Two considerations suggest, however, that the eventual contribution
by this mechanism, if present, is small. First, the membrane resistance de-
creases during reticular inhibition, indicating that the over-all synaptic im-
pingement is increased rather than decreased. However, one has to assume
equal distribution within the soma-dendritic membrane of the synapses in-
volved in the two processes. Second, no consistent and significantly large
difference was found in the equilibrium potential for reticular and direct in-
hibition. If the removal of a background excitatory impingement contributed
significantly to the sustained potential change produced by reticular stimu-
lation, one would expect a displacement of the equilibrium for reticular in-

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 RETICULAR INHIBITORY MECHANISMS 589

hibition to values of membrane potential more negative than that of the

equilibrium potential for direct inhibition. Such a difference was not appar-
ent in the experiments reported here.
The possibility of reticular influences upon the probability of firing of
spinal interneurons (cf. 11) is also to be considered in connection with the
changes of subthreshold EPSPs during reticular inhibition. Although these

0
/0

100

80

60 80

60
40

20
20

0 0
0 2 4 6 8 IO 12 msec
FIG. 10. Changes of the EPSP during reticular inhibition. The plot summarizes the
data obtained from measurement in 32 motoneurons and was obtained as follows: The
EPSPs recorded in each cell before and during each reticular stimulation (from 3 to 8 trials
in each cell) were normalized by taking the time of their peak as a reference point (because
of this procedure, data from several cells had to be discarded because of uncertainties about
the time at which the peak was attained). Thereafter the amplitude of the EPSP during
reticular inhibition at the times indicated in the plot was computed as a percentage of the
amplitude of the EPSP before reticular stimulation. Vertical bars in the plot represent
range of the values obtained. Ordinates on the left refer to the normalized EPSP before
reticular stimulation (upper trace). Ordinates on the right refer to the EPSP during reticular
inhibition as obtained by connecting the arithmetical means.

changes have been chiefly attributed to the decrease in membrane resistance,

shown to occur during reticular stimulations, it cannot be excluded that in
some of the cells included in Fig. 10 the drop in peak amplitude and/or the
faster decay of the EPSP might be due, in part at least, to the blocking of
activity in antecedent neurons. In the decerebrate cat it is frequently diffi-
cult, in fact, to obtain EPSPs with a time course superimposable on that ob-
tained after transection of the cord and/or the injection of Nembutal. Pos-
sibly the activity evoked in interneurons by the volley initiated by a stimu-

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590 R. LLINAS AND C. A. TERZUOLO
lus capable of activating a large percentage of group Ia fibers, might con-
tribute, in these instances, to the EPSPs recorded in extensor motoneurons.
If this possibility could be excluded, the shortening of the membrane time
constant during reticular inhibition, as measured by a current pulse applied
through the impaling microelectrode, could be compared to the decrease in
the time constant of decay of the EPSP in similar conditions. By this com-
parison some inference could perhaps be drawn about the location of the
synapses involved with respect to each other and to the region in which the
intracellular electrode is located. This will become possible after the findings
on reticular inhibitory actions upon a-flexor motoneurons have been pre-
sented. In these cells no resistance changes could be detected during ade-
quate reticular stimulation producing hyperpolarization of the membrane.
Because of this observation, a discussion of the role played in the integrative
processes of spinal motoneurons by the conductance changes consequent to
sustained synaptic activation can also not be initiated at this time, the da ta
on the effect of sustained facilitory actions of reflex activity, to be reported
soon, being another aspect to be taken into account in considering this
subject.
More relevant in the context of the present paper is the need to stress
that the described changes in time course of the EPSP during reticular inhi-
bition preclude the possibility of attributing the decrease in amplitude of the
EPSP to a phenomenon of presynaptic inhibition (7,s) affecting the activity
of group Ia fibers. In fact, presynaptic inhibition is said not to alter the time
course of the postsynaptic potentia change b iut only its amplitude (8). The
validity of our statement depends, however, on the exclusion of the possi-
bility that the block of interneuronal activity by the reticular stimulation is
not the cause of the reduced time of decay of the EPSP. Because of this
qualification, further experiments were specifically designed to ascertain
whether or not a presynaptic component contributes, in the present experi-
mental conditions, to the inhibition of the monosynaptic reflex by adequate
reticular stimulations. Although these findings will be reported separately,
it can be anticipated here that no such mechanism has been found.
The fact that no reference has been made throughout this paper to previ-
ous findings by other authors on the same subject requires a word of justifi-
cation. It will be realized that because of difference in the experimental de-
sign, the requirements of which have been stressed in the INTRODUCTION, in-
consistencies in the data available in the literature, as well as discrepancies
among some of these and those reported here, are difficult to resolve. If this
point is granted, then it also becomes difficult to decide whether the similari-
ties among data are fortuitous-similar effects being possibly attained by
more than one cause -or whether the data express the same finding.
SUMMARY
The mechanism by which an electrical stimulation of the bulbar reticular
formation capable of melting the decerebrate rigidity inhibits the mono-

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 RETICULAR INHIBITORY MECHANISMS 591

synaptic extensor reflex in the absence of the y-loop have been studied. It
has been demonstrated:
1. That the excitability of the a-extensor motoneurons, as tested by
direct and antidromic stimulations, is reduced.
2. That a sustained synaptic inhibitory impingement is induced by
“adequate” reticular stimulations, which causes a sustained hyperpolariza-
tion of the motoneuron membrane.
3. That the ionic mechanisms of this postsynaptic inhibitory process are
similar to those of direct inhibition.
No evidence for a presynaptic inhibitory mechanism has been found.
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