Biomedical Engineering Reference
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after LTP induction demonstrated that the EPSP
amplitude enhancement resulted from a strong
increase (>2 fold) in the probability of neurotrans-
mitter release by the sensory terminal, without
any changes in the quantal size or total number
of quanta. This result and the lack of effect of
LTP on motoneuron properties (input resistance,
membrane time constant) strongly suggested
that this new form of LTP affects exclusively the
presynaptic site.
Whereas at resting potential (-65 mV) the decay
time of sensory-triggered unitary EPSPs is rapid
(5 ms), at a more depolarized potential (-55 mV),
it increases markedly (>15 ms), and consequently,
the summation of EPSPs is higher during a burst
of sensory spikes. By contrast, in the presence of
the muscarinic receptor antagonist scopolamine,
the unitary EPSP shape is no longer voltage-de-
pendent and is, thus, the same size and shape at
-65 and -55 mV. Our results therefore indicate
that the voltage-dependent enhancement of the
reflex response involves the muscarinic synaptic
component, and suggest that at higher depolarizing
potentials, this component would be responsible
for a strong reinforcing factor in the negative
feedback control.
What could be the functional role of such re-
inforcement of the feedback loop? Motoneurons
receive two types of inputs (Figure 4E): central
commands that organize the motor pattern, and
sensory cues that adapt the command to external
constraints. However, we can imagine that during
powerful central commands (or any source of
motoneuron activity increase) the proprioceptive
correction will be proportionally less effective.
Our results indicate that the sensory feedback is
indeed capable of maintaining a variable level of
control adapted to the ongoing activity, by alter-
ing the efficacy of the sensory-motor synapse in a
manner that is inversely proportional to the level
of motoneuronal activity.
Automatic Gain Adjustment of the
Sensory-Motor Synapse with
Increasing Central Activity
Applying repeated sinewave stimulation to the
CBCO evokes resistance reflex responses in an in-
tracellularly recorded Dep MN (Figure 4D) which
consists of a cyclic depolarization/repolarization
for each release/stretch of the strand. During this
time, if the motoneuron gradually depolarizes
(either spontaneously or by intracellular injection
of a ramp of depolarizing current), the amplitude
of the reflex response dramatically increases (up to
300%; compare (1) and (2) on Figure 4D), without
any change in the CBCO mean spike frequency.
In the range of membrane potentials studied
(-65 to -55 mV), the motoneuron input resistance
decreased, and no active slow depolarization oc-
curred (although spike bursts occurred when the
membrane potential reached spike threshold).
So, the voltage-dependent increase of the reflex
response was not due to intrinsic motoneuronal
electrical properties per se . On the other hand, the
response enhancement persisted in the presence
of a high divalent cation solution, indicating that
no polysynaptic pathways are involved. Rather,
the synapse between the sensory terminal and
the motoneuron is directly responsible for this
phenomenon.
The monosynaptic connections from CBCO
sensory neurons to Dep MNs are cholinergic
and include both nicotinic and muscarinic com-
ponents (Figure 4E; Le Bon-Jego et al. , 2006).
Overload Protection Mechanism
Exerted by MNs on their Sensory
Afferents
During intense motor activity (such as observed
in vitro when the walking CPG is activated by
oxotremorine, a muscarinic acetylcholine recep-
tor agonist, or when picrotoxin blocks central
inhibitory chloride-mediated synapses), intracel-
lular recordings from a CBCO terminal display
small amplitude, slowly developing primary
afferent depolarizations (sdPADs - Figure 4F;
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