Neural Mechanisms of Leg Motor Control in Crayfish - Advancing Artificial Intelligence Through Biological Process Applications - page 35

exerting a continuous and gradual shunting
effect on passive spike propagation (Cattaert
et al. , 1992): the higher the PAD frequency,
the greater shunting of spike conduction.
During fictive locomotion (Figure 5B) bursts
of larger amplitude (20 mV) PADs occur,
which also exert an inhibitory shunting ef-
fect on spike amplitude and, consequently,
on EPSP amplitude (Figure 5C). To ensure
that this shunting mechanism is functionally
inhibitory, GABA synapses are present at
a special location on the CBCO terminal
where active spike propagation ceases and
is replaced by electrotonic propagation (Cat-
taert & El Manira, 1999).

in a single CBCO unit may reach 100 Hz
during active locomotion (Figure 5F) and
totally suppress any orthodromic sensory
activity for 200-400 ms. This mechanism
therefore exerts the strongest blockade of
sensory activity and allows active movement
to be achieved without reflex co-contraction
of the antagonistic muscle. Moreover, we
demonstrated that antidromic discharges
are also present during joint immobilization,
suggesting that this inhibitory mechanism
may allow the central network effectively to
prevent disturbing signals from the blocked
joint.

behavioral Plasticity

• Although our results indicate that most of

the presynaptic inhibition is achieved via a
shunting mechanism, inactivation of sodium
channels involved in spike conduction may
also occur during very large PADs.

Can such plasticity be placed in a behavioral
context? Predators like crayfish live in a commu-
nity and are known to be very aggressive. Thus,
fighting, which could cause damage to either the
sensory or motor apparatus, is extremely frequent
and establishes a social dominance hierarchy (Issa
et al. , 1999). We have studied how the sensory-
motor system controlling postural adjustments is
modified in two different experimental situations:
(1) when the integrity of the sensory system is af-
fected, and (2) when serotonin, a neuromodulator
known for its role in the establishment of social
dominance is superfused on the CNS.

• The third mechanism of presynaptic inhibi-

tion occurs when PAD amplitude reaches
spiking threshold. Indeed, because of the
high reversal potential of Cl - ions in CBCO
terminals (-30 mV), GABAergic PADs can
generate bursts of antidromic spikes that are
conveyed to the peripheral proprioceptor
(Cattaert et al. , 1994c; Cattaert et al. , 2001).
In contrast, picrotoxin-sensitive spikes
(Figure 5D) are never conducted toward
the central sensory-motor synapse (Cattaert
et al. , 2001), and no EPSP is ever evoked
in postsynaptic motoneurons (Figure 5E).
Moreover, the antidromic discharges exert
a long-lasting (several hundred millisec-
onds) inhibition on the sensory activity of
the CBCO (Cattaert & Bévengut, 2002).
Recently we demonstrated that these
mechanisms described in vitro also operate
in vivo (Le Ray et al. , 2005). In the freely
behaving crayfish, a pair of wire electrodes
was used to discriminate orthodromic and
antidromic spikes from the CBCO neuro-
gram (Figure 2C1, C2). Antidromic bursts

Functional Plasticity Caused by the
Absence of Sensory Information

What happens to a motor network deprived of
its sensory inflow? We addressed this issue in
the crayfish CBCO sensory-motor system after
cutting the sensory nerve in vivo. In crustaceans,
sectioned sensory axons do not degenerate (even
though axons are devoid of cell bodies), probably
due to the proliferation of glial cells that allow
axon survival (Parnas et al. , 1998). At various
post-lesion time intervals, CNS were dissected
out for testing intracellularly the Dep MN re-