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K G Pearson

Publications and source records attributed to K G Pearson.

87 records · Page 5Linked to original sources
PubMed1975

Nonspiking interneurons in walking system of the cockroach.

Intracellular recordings were made from the neurites of interneurons and motoneurons in the metathoracic ganglion of the cockroach, Periplaneta americana. Many neurons were penetrated which failed to produce action potentials on the application of large depolarizing currents. Nevertheless, some of them strongly excited and/or inhibited slow motoneurons innervating leg musculature, even with weak depolariziing musculature, even with weak depolarizing currents. Cobalt-sulfide-straining of these nonspiking neurons showed them to be interneurons with their neurites contained entirely within the metathoracic ganglion. Two further characteristics of these interneurons were rapid spontaneous fluctuations in membrane potential and a low resting membrane potential. One nonspiking neuron, interneuron I, when depolarized caused a strong excitation of the set of slow levator motoneurons which discharge in bursts during stepping movements of the metathoracic leg. During rhythmic leg movements the membrane potential of interneuron I oscillated with the depolarizing phases occurring at the same time as bursts of activity in the levator motorneurons. No spiking or any other nonspiking neuron was penetrated which could excite these levator motoneurons. From all these observations we conclude that oscillations in the membrane potential of interneuron I are entirely responsible for producing the levator bursts, and thus for producing stepping movements in a walking animal. During rhythmic leg movements, bursts of activity in levator and depressor motoneurons are initiated by slow graded depolarizations. The similarity of the synaptic activity in these two types of motoneurons suggests that burst activity in the depressor motoneurons is also produced by rhythmic activity in nonspiking interneurons. The fact that no spiking neuron was found to excite the depressor motoneurons supports this conclusion. Interneuron I is also an element of the rhythm-generating system, since short depolarizing pulses applied to it during rhythmic activity could reset the thythm. Long-duration current pulses applied to interneuron I in a quiescent animal did not produce rhythmic activity. This observation, together with the finding that during rhythmic activity the slow depolarizations in interneuron I are usually terminated by IPSPs, suggests that interneuron I alone does not generate the rhythm. No spiking interneurons have yet been enccountered which influence the activity in levator motoneurons. Thus, we conclude that the rhythm is generated in a network of nonspiking interneurons. The cellular mechanisms for generating the oscillations in this network are unknown. Continued.

Action Potentials↗
PubMedDate not supplied

Neural circuits for jumping in the locust.

The locust jump consists of three distinct phases: Cocking: a rapid flexion of both hindleg tibia and locking of both tibia in full flexion. Co-contraction: simultaneous contractions in hindleg flexor and extensor muscles lasting about 0.5 s resulting in the storage of energy for the jump in elastic elements of the legs and muscles. Triggering: a sudden inhibition of flexor activity to allow the shortening of the contracted extensors and the release of the energy stored during the co-contraction phase. The neural circuitry controlling these three phases is now reasonably well understood. Some of its major features are: (1) pairs of large identifiable interneurons in the thoracic ganglia for evoking the cocking response (C-neurons) and for triggering the jump (M-neurons), (2) a central excitatory pathway from extensor to flexor tibiae motoneurons to ensure simultaneous activation of extensor and flexor motoneurons during the initial part of the co-contraction phase, (3) a positive feedback pathway from cuticular receptors to extensor motoneurons for maintaining extensor activity during the co-contraction phase, (4) proprioceptive feedback to the trigger interneurons for increasing their excitability during the co-contraction phase and thereby allowing a variety of external stimuli to activate the trigger neurons and evoke a jump, (5) presynaptic inhibition of visual pathways to the trigger neurons to ensure that the trigger neurons are not activated by the simultaneous occurrence of visual and auditory stimuli in the absence of proprioceptive input, and (6) a pair of multifunctional visual movement detecting neurons which can initiate cocking or trigger the jump depending on the animal's state.

Animals↗