Insects Memory Essay, Research Paper 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
Insects Memory Essay, Research Paper
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
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.
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