Publications by authors named "Joscha Schmitz"

We have just started to understand the mechanisms underlying flexibility of motor programs among segmental neural networks that control each individual leg during walking in vertebrates and invertebrates. Here, we investigated the mechanisms underlying curve walking in the stick insect during optomotor-induced turning. We wanted to know, whether the previously reported body-side specific changes in a two-front leg turning animal are also observed in the other thoracic leg segments.

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Feedback from load and movement sensors can modify timing and magnitude of the motor output in the stepping stick insect. One source of feedback is stretch reception by the femoral chordotonal organ (fCO), which encodes such parameters as the femorotibial (FTi) joint angle, the angular velocity, and its acceleration. Stimulation of the fCO causes a postural resistance reflex, during quiescence, and can elicit the opposite, so-called active reaction (AR), which assists ongoing flexion during active movements.

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Much is known on how select sensory feedback contributes to the activation of different motoneuron pools in the locomotor control system of stick insects. However, even though activation of the stance phase muscles depressor trochanteris, retractor unguis, flexor tibiae and retractor coxae is correlated with the touchdown of the leg, the potential sensory basis of this correlation or its connection to burst intensity remains unknown. In our experiments, we are using a trap door setup to investigate how ground contact contributes to stance phase muscle activation and burst intensity in different stick insect species, and which afferent input is involved in the respective changes.

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We introduce a laser-supported setup to study the influence of afferent input on muscle activation during walking, using a movable ground platform. This approach allows investigating if and how the activity of stance phase muscles of an insect (e.g.

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Spider VS-3 mechanoreceptor neurons have a low-voltage-activated Ca2+ current that raises intracellular calcium concentration [Ca2+] when they are depolarized by agonists of GABAA receptors or fire action potentials. The Ca2+ rise produces negative feedback by modulating the mechanoreceptor current and regulates Ca2+- and voltage-activated K+ currents. However, nothing is known about Ca2+ buffering in VS-3 neurons.

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