Insects Have Sensors
Insects have sensors (force-sensitive organs) concentrated in areas near
joints, tips of the
legs, and near exoskeletal sites attached to muscle
tendons. These sensors act as strain gauges to
detect compression of the
exoskeleton. Using this information, insects recognize environments,
regulate
walking movements, and astonishingly "remember" stepping patterns and
location.
Through memory experiments, scientists see that a spider
memorizes its own previous
walking movements to backtrack to a fly. After
presenting the fly to the spider on a petri dish,
scientists chased the
spider some distance away from the capture site. The spider then returns
to
the original spot, even though the fly has been placed elsewhere. If
guided along a curved detour
path, the spider cuts corners, indicating that
it remembered the fly's position.
Limitations in this memory experiment
include odor and magnetic sense to backtrack to the
capture site. To test the
latter hypothesis we can place magnets inside the petri dish and run
the
experiment during cloudy weather to disorient the spider's navigational
magnetic sense.
Parkinson's is a neurodegenerative disease that causes
involuntary movement, muscle
rigidity, slowing of movement, and loss of
spontaneous motion. As excessive amounts of
dopamine-producing neurons of the
brain die, the resulting decline in dopamine signaling disrupts
smooth
functioning of the overall motor network. Damage to the substantia nigra
accounts for
most symptoms.
L-dopa, which readily crosses the
blood-brain barrier, was developed to compensate for
the decline of dopamine.
It is then converted to dopamine by dopamine-making neurons that
survive in
the substantia nigra and nonneuronal cells in the striatum.
Patients
experience a desensitization phenomenon, gradually losing sensitivity to
L-dopa,
which works for shorter and shorter increments. This may be
attributed to dopamine's ability to
promote free radical synthesis, which may
help explain why dopamine-making neurons are
particularly susceptible to
dying from oxidation. L-dopa increases dopamine levels, eases
symptoms, and
may ironically damage nigral neurons. With more L-dopa usage, more
nigral
neurons die, leading to gradual ineffectiveness of the compound. Total
desensitization occurs when
nigral neuron levels are extremely
low.
L-dopa's wearing-off effect is similar to that of protease-inhibitor
drugs used to help treat
HIV. After many years, the drugs lose effect;
HIV persists and leads to full-blown
AIDS.