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W J Heitler

Publications and source records attributed to W J Heitler.

29 records · Page 2Linked to original sources

Post-embryonic development of rectifying electrical synapses in the crayfish: ultrastructure.

The post-embryonic development of the rectifying Giant Fibre-Motor Giant (GF-MoG) synapse and the Giant Fibre-Segmental Giant (GF-SG) synapse has been investigated using electron-microscopy. In adults, the MoG and SG neurons make contact with the GFs by sending narrow 'finger-like' processes through the glial and connective tissue sheath surrounding each GF. The junctional region is characterized by closely apposed membranes (approximately 4 nm separation) traversed by regularly spaced connections, and large (60-80 nm) spherical vesicles in the presynaptic fibre. In newly hatched crayfish junctional contact is made over extensive areas of flat membrane apposition, due to the absence of a thick connective sheath around the giant fibres. Initially the junctional region is dominated by contacts which are morphologically indistinguishable from chemical synapses, i.e. 1. The apposed membranes are separated by a cleft of approximately 20-30 nm (an order of magnitude larger than the cleft distance at electrotonic synapses). 2. There is pre- and post-synaptic thickening of the junctional membranes with a dense cytoplasmic material. 3. Small (25-40 nm) pleomorphic vesicles are found on the presynaptic side of the junction, commonly in association with a dense presynaptic bar. Regions of junctional contact displaying the adult electronic-type morphology first appear at approximately one week post-hatching. At this age they are limited in distribution and occupy a central position in the area of contact surrounded by a broad 'chemical-like' annulus. During subsequent development these sites with electrotonic-type morphology grow in relative size, so that the 'chemical-like' sites become compressed towards the edges of the regions of contact. The adult type of morphology, in which the 'chemical-like' regions are vestigial, is achieved approximately two months after hatching.

Animals↗

Ultrastructure of the phasic stretch receptor in the crayfish abdominal nerve cord.

The ultrastructure of the abdominal ganglionic cord stretch receptor of the crayfish Pacifastacus leniusculus is described. This bilaterally-paired, segmentally-repeating phasic receptor monitors stretch applied to the central nervous system itself. It consists of a connective tissue mass closely applied to the medial margin of each medial giant fibre, into which ramifies a collection of specialized terminal dendrites originating from branches (primary dendrites) of a single axon. The connective tissue consists of an electron-opaque matrix in which are embedded many short, electron-lucent, tubular structures whose lumens are continuous with the matrix. Some filamentous material penetrates the connective tissue from its boundaries, and glial cells are present. The primary dendrites are irregular in size and orientation, and contain many microtubules and much filamentous material. The terminal dendrites are of consistent diameter and longitudinal orientation, containing very regularly-spaced microtubules with no microfilaments. The terminal dendrites contain a well-defined cytoskeletal 'tube' or lamina 6 nm thick, evenly spaced about 25 nm below the plasma membrane and connected to it by filamentous material 5 nm in diameter, which is deposited in rings or helices. This lamina arises just at the point where the primary dendrites gave rise to the terminal dendrites. Its function is not known, but it shows some similarities to the subaxolemmal lamina found in some regions of spike initiation.

Abdomen↗

Ultrastructure of the segmental giant neuron of crayfish.

The ultrastructure of the crayfish segmental giant (SG) neuron is described, and compared to other identified and unidentified crayfish neurons. The SG was specifically stained by intracellular injection of horseradish peroxidase and is divided into four regions of interest. In the dorsal region, finger-like dendrites of the SG make contact with the through-conducting giant fibres (GF). These contacts are physiologically defined rectifying electrical synapses. They are characterized by the presence of 30-95 nm agranular vesicles in the presynaptic GFs, some postsynaptic density in the SG, and a narrowing of the intermembrane cleft to approximately 5 nm. There is little evidence for connecting cytoplasmic bridges. Unidentified neurons make chemical input with either round or elliptical vesicle types onto SG bottlenecks close to the electrical synapses. Ventral to the GFs, dendritic profiles of the SG make three sorts of contact with unidentified neurons. (a) Regions of close membrane apposition (approximately 5 nm) are presumed to be electrical output synapses, but there are no vesicles such as at the input synapses, and, again, little sign of connecting bridges. (b) Chemical input is received from unidentified presynaptic neurons containing either round or elliptical vesicles. These synapses are characterized by 30-75 nm presynaptic agranular vesicles, widened cleft (approximately 20 nm), granular cleft material and postsynaptic density. There is no sign of any presynaptic density. (c) Very occasional SG profiles containing vesicles and making output synapses to unidentified neurons occur. In the lateral neuropil at the edge of the ganglion the SG gives rise to a small tuft of very fine dendrites. These are nearly all laden with vesicles and ramify in a complex region of neuropil containing many small profiles which are also vesicle-laden. The SG axon diminishes in diameter as it progresses along its peripheral nerve root, and finally terminates at a blind ending near the base of the swimmerets. It is sheathed along its entire length, and there is no sign of vesicles within it. We conclude that the SG axon makes no peripheral output.

Abdomen↗

Motor programme switching in the crayfish swimmeret system.

Intracellular and extracellular recordings have been made from neurones of the swimmeret system in the semi-isolated abdominal ganglion of the crayfish during rhythmic activity. Extracellular recordings commonly reveal a motor programme (MP1) consisting of low-amplitude symmetrical power and return stroke activity with phase-constant posterior-to-anterior intersegmental coordination. Occasionally a different motor programme (MP2) is expressed. MP2 has higher amplitude episodic activity, with return stroke duration greater than power stroke, and with latency-constant anterior-to-posterior or near synchronous intersegmental coordination. Preparations may switch spontaneously between the two motor programmes. Intracellular recordings show that interneurones whose membrane potentials oscillate during MP1 and which can reset its rhythm usually cease to oscillate during MP2. During production of MP1, current injected into any one of a small number of interneurones can induce MP2. The polarity of current required is usually such as to drive the membrane potential towards the level normally associated with return stroke during MP1. During MP1 many motor neurones receive synaptic input with approximately sinusoidal waveform. During MP2 they may receive an episodic input with approximately sawtooth waveform, and/or input consisting of large, unitary EPSPs. The unitary EPSPs drive a 'bursty' mode of MP2 activity that is sometimes seen. The bursts of unitary EPSPs in MP2 appear to derive from a different source to that of the sinusoidal input in MP1. These sources are probably caudally-conducting through-interneurones and non-spiking local interneurones respectively. Thus experimental perturbation of a single neurone can induce a motor programme switch such as to change the activity of some hundreds of neurones in at least three ganglia. Neurones with this property would be convenient targets for controlling influences in the intact animal.

Animals↗

Triggering of locust jump by multimodal inhibitory interneurons.

1. The locust jump is triggered by a sudden inhibition of activity in hindleg flexor tibiae motoneurons following cocontraction of the hindleg flexor and extensor tibiae muscles. The main result of this investigation was the identification of two interneurons (one for each hindleg) that monosynaptically inhibit flexor tibiae motoneurons and whose properties are all consistent with them being the trigger interneurons for initiating a jump. 2. These interneurons receive strong excitatory input from many sensory modalities (visual, auditory, tactile, and proprioceptive). Because of their multimodal response characteristics, we designated them M-neurons. A particularly strong excitatory input to each M-neuron is from both descending contralateral movement detector (DCMD) interneurons. 3. The threshold for spike initiation in the M-neurons is high (approximately 14 mV). As a consequence, input from any one sensory modality alone rarely initiates action potentials. 4. Each M-neuron is depolarized by sensory input from leg proprioceptors. We propose that proprioceptive feedback during the cocontraction phase depolarizes the M-neurons to decrease their threshold, thus enabling extrinsic sensory stimuli to generate action potentials in both M-neurons and in so doing trigger a jump. The function of the proprioceptive gating of inhibitory transmission from the various sensory systems to the flexor motoneurons (via the M-neurons) is to ensure the development of a strong isometric contraction of the extensor tibiae muscle, and thus a powerful jump in response to external stimuli. 5. Insofar as the initiation of the locust jump depends on sensory convergence onto large identified interneurons, this behavior is similar to ballistic movements in some other animals such as the crayfish tail flip and the startle response in fish. The unique feature of the locust jump is that the trigger interneurons initiate the jump only after a preceding phase (cocontraction) has been accomplished.

Animals↗

The locust jump. I. The motor programme.

A motor programme is described for defensive kicking in the locust which is also probably the programme for jumping. The method of analysis has been to make intracellular recordings from the somata of identified motornuerones which control the metathoracic tibiae while defensive kicks are made in response to tactile stimuli. Three stages are recognized in the programme. (1) Initial flexion of the tibiae results from the low spike threshold of tibial flexor motorneurones to tactile stimulation of the body. (2) Co-contraction of flexor and extensor muscles followa in which flexor and extensor excitor motoneurones spike at high frequency for 300-600 ms. the tibia flexed while the extensor muscle develops tension isometrically to the level required for a kick or jump. (3) Trigger activity terminates the co-contraction by inhibiting the flexor excitor motorneurones and simultaneously exciting the flexor inhibitors. This causes relaxation of the flexor muscle and allows the tibiae to extend. If the trigger activity does not occur, the jump or kick is aborted, and the tibiae remain flexed.

Action Potentials↗

The locust jump. II. Neural circuits of the motor programme.

1. Neural circuits which co-ordinate the motorneurones of the meta-thoracic tibiae of the locust in jumping and kicking have been investigated. 2. The fast extensor motorneurone is reflexly excited by the subgenual organ, by a network of cuticle strain receptors, and by Brunner's organ. The subgenual organ and the cuticle strain receptors are excited by tension in the extensor muscle and mediate a positive feedback which could help to produce the burst of fast extensor spikes which precedes a jump or kick. Brunner's organ is stimulated by pressure from the flexed tibia, and will be excited by the initial flexion and throughout the co-contraction phase of a kick. 3. A central excitatory connexion from the fast extensor to the slow extensor ensures that extensor muscle tension is as great as possible early in the co-contraction phase of a kick. 4. A central excitatory connexion from the fast extensor to flexor motorneurones is confirmed. This ensures that flexor muscle tension is great enough to keep the tibia flexed when the extensor muscle tension starts to develop before a jump or kick. 5. Reflex excitation of flexor motorneurones occurs in response to an extensor muscle twitch when the tibia is flexed. This helps to maintain the flexor connexion. 6. A receptor, the 'lump receptor', which is stimulated by flexor muscle tension only when the tibia is flexed, can inhibit the flexor motorneurones and may activate the trigger system which allows the extension of the tibia in a jump or kick. 7. Recptors in the suspensory ligaments of the joint inhibit the fast extensor when the tibia extends.

Action Potentials↗