Jeffrey J. Wine - Neuroscience Publications

Wine, J.J.
"Escape reflex circuit in crayfish:  interganglionic interneurons activated by the giant command neurons." Biological Bulletin, 1971, 141, 408.

Wine, J.J. and Krasne, F.B. (1972).
"The Organization of Escape Behaviour in the crayfish."
Journal of Experimental Biology, 56, 1-18.

Mittenthal, J. E. and J. J. Wine (1973). [Full Text]
"Connectivity patterns of crayfish giant interneurons: visualization of synaptic regions with cobalt dye."
Science 179(69): 182-4.

Wine, J. J. (1973).
"Invertebrate synapse: long-term maintenance of postsynaptic morphology following denervation."
Exp Neurol 41(3): 649-60.

Wine, J. J. (1973).
"Invertebrate central neurons: orthograde degeneration and retrograde changes after axonotomy."
Exp Neurol 38(1): 157-69.

Kennedy, D., R. L. Calabrese and J. J. Wine (1974).
"Presynaptic inhibition: primary afferent depolarization in crayfish neurons."
Science 186(4162): 451-4.

Krasne, F. B. and J. J. Wine (1975).
"Extrinsic modulation of crayfish escape behaviour."
J Exp Biol 63(2): 433-50.

Extrinsic systems were shown to control the excitability of the neurones which mediate tail-flip escape in the crayfish. Restraint suppresses the escape mediated by giant fibres and some, but not all, categories of non-giant mediated escape; autotomy of claws increases the excitability of non-giant mediated escape without affecting the lateral giant reflex. The effects of restraint on the lateral giant reflex result from inhibition rather than reduced facilitation. The inhibition descends from thoracic and higher levels, and the lateral giant escape command neurone appears to be its primary target. Inhibition may serve to shift the control of escape behaviour from short latency 'reflex' systems to more flexible 'voluntary' ones which can produce responses at times most opportune for successful escape.

Wine, J. J. (1975).
"Crayfish neurons with electrogenic cell bodies: correlations with function and dendritic properties."
Brain Res 85(1): 92-8.

Wine, J. J., F. B. Krasne and L. Chen (1975).
"Habituation and inhibition of the crayfish lateral giant fibre escape response."
J Exp Biol 62(3): 771-82.

1. Decrement of the lateral giant fibre escape response was studied in intact, restrained, crayfish and in those with the ventral nerve cord transected at the thoracic-abdominal level. 2. Taps (delivered at rates of 1 per 5 min to the abdomen) depressed responsiveness to about 50% of its inital value in 10 trials, for both intact and operated animals. 3. With additional stimulation, responsiveness dropped to near zero for both groups. Recovery was negligible 2 h later, but nearly complete after an additional 24 h rest. 4. Protection against response decrement in this situation was obtained by directly activating the cord giant fibres 30 msec prior to the tactile stimulus. The directly-elicited giant fibre spikes which follow the tactile stimulus do not influence the course of response decrement. 5. The results establish the decrement as centrally mediated habituation, and minimize the role of receptor alterations or descending neuronal influences in the behavioural change. 6. A comparison is made between the properties of hibituation and the homosynaptic depression of afferent to interneurone synapses that is presumed to be the physiological mechanism of habituation in this situation.

Wine, J. J. (1977).
"Neuronal organization of crayfish escape behavior: inhibition of giant motoneuron via a disynaptic pathway from other motoneurons."
J Neurophysiol 40(5): 1078-97.

1. A circuit that produces a 70-100 ms IPSP in the crayfish giant motoneuron is described. The IPSP is produced by a disynaptic pathway from the nongiant fast flexor motoneurons to the motor giant. 2. An inhibitory interneuron in the pathway has been identified. Its axon runs at least the entire length of the abdominal nervous system. The inhibitory interneuron is excited bilaterally in all abdominal ganglia except the last and bilaterally inhibits the motor giants thoughout the abdominal CNS. 3. Evidence for a monosynaptic connection between the interneuron and the motor giant includes short latency, stability during repetitive stimulation, gradual decrement in high-Mg2+ solutions, and persistence in high-Ca2+ solutions. Similar but less complete evidence suggests a monosynaptic connection from the fast flexor motoneurons to the inhibitory interneuron. 4. A single impulse in the inhibitor can produce a prolonged IPSP in the motor giant. The inhibitor did not display trains of impulses and was not spontaneously active. 5. The inhibitory interneuron appears to be highly specific; no other outputs were observed. 6. Direct stimulation of axons in the connectives suggests that four pairs of inhibitory interneurons converge on the motor giants; at least two pairs are activated by the fast flexor motoneurons. 7. This circuit limits the burst duration of the motor giant and may function to protect the motor giant's depression-prone neuromuscular junction.

Wine, J. J. and D. C. Mistick (1977).
"Temporal organization of crayfish escape behavior: delayed recruitment of peripheral inhibition."
J Neurophysiol 40(4): 904-25.

Mittenthal, J. E. and J. J. Wine (1978).
"Segmental homology and variation in flexor motoneurons of the crayfish abdomen."
J Comp Neurol 177(2): 311-34.

Wine, J. and G. Hagiwara (1978). [Full Text]
"Durations of unitary synaptic potentials help time a behavioral sequence."
Science 199(4328): 557-9.

Recordings in identified neurons and muscles that mediate crayfish tailflips reveal inhibitory postsynaptic potentials of two distinct durations. Those of long duration are recorded in five classes of cells in the flexion circuit, while those of short duration are recorded in three classes of cells in the extension circuit. The durations of the inhibitory postsynaptic potentials are matched to the durations of inhibition required by the different phases of the behavior.

Kramer, A. P., F. B. Krasne and J. J. Wine (1981).
"Interneurons between giant axons and motoneurons in crayfish escape circuitry."
J Neurophysiol 45(3): 550-73.

1. Crayfish giant fibers are generally believed to generate tailflip movements by means of direct connections to two classes of phasic flexor muscle motoneurons, the motor giants (MoGs) and the nongiant fast flexor motoneurons (FFs). It is shown here that the giants also stimulate a network of interneurons that make connections with the FFs. 2. This network includes an intraganglionic neuron, the segmental giant (SG), in each abdominal hemisegment and a number of intersegmental neurons, two of which (I2 and I3) were studied in detail. 3. The SGs are driven reliably by the giant fibers and they in turn drive the FFs of their hemisegment about as effectively as do the giant fibers themselves; it is possible that the giant fibers excite the FFs mainly by way of the SGs. The SGs also have an efferent first root axon whose peripheral targets we have been unable to determine. 4. I2 and I3 originate in the second and third abdominal ganglia, respectively, and descend to the last ganglion. In their ganglia of origin they are reliably driven by the giant fibers and by the SGs. In addition, I2 weakly excites I3 and both receive weak, apparently direct, excitatory input from FFs as well as less direct excitatory and inhibitory input from unidentified afferent sources. Both weakly excite most FFs in ganglia behind the one in which they originate. This excitation adds to that produced directly by giant fibers and SGs and, we believe, is sometimes decisive in causing FF firing. Their firing also causes inhibition involved in suppressing effects of reafference, as do the giant fibers themselves. 5. I3 strongly excites the motoneurons of certain tail fan muscles (the ventral and posterior telson flexors). However, the contraction of these muscles would be maladaptive during some giant fiber-mediated tailflips. Accordingly, when the giant fibers, which always recruit I3, fire, they cause an inhibition of the motoneurons that nullifies the excitatory input from I3. At a formal level this means that the giants, viewed as command neurons, not only drive but also alter or modulate the subordinate motor pattern- generating network that they control. 6. Tailflips that are less stereotyped than those mediated by giant fibers are known to occur without participation of the giants. It is suggested that the presence of complex circuitry mediating between giant fibers and FFs may be related to the use of portions of this circuitry as well as the FFs themselves in production of nongiant tailflips.

Kuwada, J. Y. and J. J. Wine (1981).
"Transient, axotomy-induced changes in the membrane properties of crayfish central neurones."
J Physiol 317: 435-61.

1. In crayfish, the normally passive, non-spiking somata of certain unipolar, efferent neurones became spiking within 36 hr of axotomy. 2. The changes persisted for approximately 2 weeks and then waned. The decline in excitability occurred independently of regeneration, and excitability was not restored by recutting the axon stump. 3. The neuropilar processes also became capable of supporting spikes, but synaptic transmission onto the cells and the spike threshold for orthodromic activation were unchanged, as was the gross structure of the neurone. 4. In somata which normally spike, electrogenicity was nevertheless increased, as evidenced by soma spikes that were larger, faster rising, and easier to evoke. 5. We tested for post-axotomy excitability changes in a variety of identified neurones. Every type (n = 5) of phasically active efferent we tested responded as above, as did all three phasic interneurones. One class of spontaneously active interneurones and one spontaneously active efferent did not respond to axotomy. 6. Extensive damage to afferents did not initiate changes in efferents of the same ganglion, nor did it interfere with changes induced by axotomy of the efferents. 7. Transection of the larger of the two main branches of the phasic flexor inhibitor induced soma excitability, but cutting the smaller branch did not. However, after the excitability caused by cutting the larger branch waned, transection of the smaller branch then induced excitability. 8. Neurones with longer axon stumps took longer to develop soma excitability.

Reichert, H., M. R. Plummer and J. J. Wine (1982).
"Lateral inhibition mediated by a non-spiking interneuron: circuit properties and consequences for behavior."
J Physiol 78(8): 786-92.

The terminal abdominal ganglion of the crayfish contains about 650 cells, approximately 1/2 of which are local. In the mechanosensory system, an identified, non-spiking local interneuron mediates lateral inhibition (across the midline) of a highly restricted set of projecting sensory interneurons. Our evidence suggests that this neuron is the exclusive pathway for the form of lateral inhibition that we studied. The 'precurrent' mode of inhibition found in this system causes responses to stimuli that are common to both sides to be attenuated, and conversely will enhance the difference signal produced by partially lateralized input.

Reichert, H. and J. J. Wine (1982).
"Neural mechanisms for serial order in a stereotyped behaviour sequence."
Nature 296(5852): 86-7.

Roberts, A., F. B. Krasne, G. Hagiwara, J. J. Wine and A. P. Kramer (1982).
"Segmental giant: evidence for a driver neuron interposed between command and motor neurons in the crayfish escape system."
J Neurophysiol 47(5): 761-81.

1. The giant command neurons for tailflip escape behavior in crayfish have been thought to excite the nongiant fast flexor (tailflip producing) motor neurons (FFs) via monosynaptic connections. We show here that excitation of FFs instead occurs via a bilateral pair of segmental giant neurons (SGs) interposed between the command axons and FFs in each segment. 2. Anatomically, the SGs appear to make numerous contacts with ipsilateral command axons and FFs and fewer contacts contralaterally. In contrast, the command axons have only sparse direct connections to the FFs. An SG has an axon in the ipsilateral first ganglionic root and may be a modified swimmeret motor neuron. 3. Each SG is depolarized well beyond threshold by the firing of an ipsilateral command axon and is depolarized to near threshold by the firing of a contralateral command axon. The synapses between command axons and SGs are electrical and probably rectifying. 4. Each FF is excited to a level near firing threshold by the SG ipsilateral to its axon and is excited weakly by the contralateral SG. The synapses between SGs and FFs are electrical and nonrectifying. 5. Variations in excitatory postsynaptic potentials (EPSPs) recorded in FFs during prolonged, high- frequency firing of the command axons can be accounted for by refractoriness of SG spikes, as opposed to refractoriness of dendritic branch spikes as had previously been delivered. 6. These findings illustrate the limitations of conventional tests for monosynapticity. 7. The functional significance of having driver neurons interposed between command neurons and motor neurons is discussed.

Bishop, C. A., J. J. Wine and M. O'Shea (1984).
"Neuropeptide proctolin in postural motoneurons of the crayfish."
J Neurosci 4(8): 2001-9.

The neuropeptide transmitter candidate proctolin (H-Arg-Tyr-Leu-Pro-Thr- OH) was associated with three of the five excitatory motoneurons innervating the tonic flexor muscles of the crayfish abdomen. Proctolin immunohistochemical staining occurred in cell bodies and axons of these three identified neurons. Stained axon terminals were detected across the entire tonic flexor muscle. Bioassay of extracts of the tonic flexor muscles indicated the presence of 370 fmol of proctolin/muscle or 670 fmol/mg dry weight. Bioactivity was eliminated in muscles in which the tonic flexor motor root was cut 2 months prior to extraction and in muscle extracts pre-incubated with proctolin antiserum. High pressure liquid chromatography purification of tissue extract indicated that all bioactivity in the crude extract was due to authentic proctolin. Our findings suggest that these three cells function as peptidergic motoneurons. A precedent for this is the proctolin- containing postural motoneuron of the cockroach.

Kirk, M. D. and J. J. Wine (1984).
"Identified interneurons produce both primary afferent depolarization and presynaptic inhibition."
Science 225(4664): 854-6.

Crayfish interneurons were identified that appear to be directly responsible for presynaptic inhibition of primary afferent synapses during crayfish escape behavior. The interneurons are fired by a polysynaptic pathway triggered by the giant escape command axons. When directly stimulated, these interneurons produce short-latency, chloride- dependent primary afferent depolarizations and presynaptically inhibit primary afferent input to mechanosensory interneurons.

Lee, M. T. and J. J. Wine (1984).
"Plasticity of non-giant flexion circuitry in chronically cut abdominal nerve cords of the crayfish, Procambarus clarkii."
J Physiol 355: 661-75.

We have investigated the pattern of neuronal activity involved in the gradual return of sensory-evoked abdominal flexions in crayfish with chronically transected nerve cords. Recordings were made from eight types of identified neurone that mediate phasic abdominal movements, in a preparation consisting of the isolated abdominal nerve cord and tailfan. Responses of the cells to pinches and dorsiflexions of the tailfan were compared in two groups of animals: animals whose cords had been cut at the thoracic-abdominal junction 4-17 weeks earlier (chronic preparations), and animals whose cords had been cut at the same site either just before the experiment or up to 6 days earlier (acute preparations). Sensory stimuli produced bursts of spikes in 73% of the fast flexor motoneurones impaled in chronic preparations, but never fired these neurones in acute preparations. However, fast flexor motoneurones in both preparations were fired with approximately equal frequency by single impulses in the giant axons, suggesting that the firing thresholds of these motoneurones had not changed. Sensory stimuli also caused spiking in the extensor inhibitor and the flexor inhibitor in chronic preparations; in contrast, responses in the fast extensor motoneurones were always subthreshold and occasionally hyperpolarizing. None of these cells was fired by similar stimuli in acute preparations. Neurones restricted to the giant axon pathways (lateral, medial, segmental and motor giants) were silent during sensory-evoked flexor discharges in chronically transected cords. Flexor discharges were accompanied by intense activity in non-giant axons recorded from the dorsal cord. Two identified, non-giant interneurones with axons in the dorsal cord were substantially depolarized but never fired by sensory input in chronic preparations. Sensory-evoked firing in the fast flexor motoneurones was not abolished by removal of the posterior stump of the nerve cord at the transection site. About 20% of chronic preparations generated cyclic motor output in response to unpatterned sensory stimulation. The pattern of motor activity that develops in chronically transected cords resembles that seen in normal crayfish during non-giant tailflips. Because cord transection permanently isolates the abdomen from rostral neural centres normally required for the generation of such tailflips, the return of co-ordinated motor output in chronically cut cords may result from the sensory activation of non-giant circuitry within the abdominal nervous system.

Miller, L. A., G. Hagiwara and J. J. Wine (1985).
"Segmental differences in pathways between crayfish giant axons and fast flexor motoneurons."
J Neurophysiol 53(1): 252-65.

We have used electrophysiological techniques to document segmental differences in the pathways between the giant, escape command axons, lateral giants (LG) and medial giants (MG), and the nongiant, fast flexor (FF) motoneurons. We found no difference in the input from LG and MG axons to FF motoneurons in the posterior (4th and 5th) ganglia. Since flexor motor output in these segments would be inconsistent with the LG-evoked behavior pattern, this finding was puzzling. Electromyographic (EMG) recordings during escape responses by intact unrestrained animals confirm that the FF muscles innervated by the posterior ganglia are not excited during LG-mediated tailflips, but are excited during MG-mediated tailflips. In the 2nd and 3rd ganglia, the command axons fire the FF motoneurons with high probability, in part via electrical excitatory postsynaptic potentials (EPSPs) from premotor neurons, the segmental giants (SG). In the 4th and 5th ganglia, the equivalent pathway is much less effective. Single, directly elicited impulses in SGs in ganglia 2 and 3 fire their respective FF motoneurons with high probability, while those in ganglia 4 and 5 rarely fire FF motoneurons. The command axons fire the SGs reliably in all segments. The amplitude of the SG-evoked EPSP in FF motoneurons is significantly smaller in posterior vs. anterior ganglia. For technical reasons, we are unable to present conclusive evidence on ganglionic variations in FF-motoneuron thresholds. The FF motoneurons receive additional excitatory input from intersegmental interneurons recruited by the command neurons. Motoneurons in ganglia 4 and 5 are excited by large interneurons that do not synapse on motoneurons in ganglia 2 and 3, but this additional input is not sufficient to compensate for the weaker effect of SG input. Unlike the all-or-none segmental differences demonstrated previously for the LG-to-motor giant pathway (24), the SG- to-FF pathway changes gradually, retains significant though subthreshold strength in posterior ganglia, and is common to both LGs and MGs. These features provide opportunities for variation in the spatial patterning of flexion and in the resulting escape trajectories.

Kirk, M. D., J. P. Dumont and J. J. Wine (1986).
"Local inhibitor of the crayfish telson-flexor motor giant neurons: morphology and physiology."
J Comp Physiol [A] 158(1): 69-79.

The motor circuits that control telson flexion in the crayfish (Procambarus clarkii) include a curiously arranged sub-circuit: a premotor 'command' neuron excites a motor neuron via a trisynaptic pathway, but also inhibits (and prevents firing of) the motor neuron via a shorter latency pathway (Kramer et al. 1981 a). The premotor and motor neurons in this circuit have been previously identified (Kramer et al. 1981 a; Dumont and Wine 1985a, b; see Fig. 1). We have now identified a local interneuron that inhibits the motor neurons. The cell we studied is called the 'C' cell because of its distinctive structure (Figs. 2, 3). A single pair of bilaterally homologous C-cells was found in the last (6th) abdominal ganglion. The C-cells are invariably dye coupled to one another following injections of lucifer yellow into either one of them, and are frequently dye coupled to smaller axons in the 2nd, 3rd, and 6th nerves. In addition, some of the extensive branches of the C-cell extend out into the 6th nerve, where they are in close proximity to the axons of the motor neurons they inhibit (Fig. 3). Two kinds of evidence established that the C-cell directly inhibits the motor neurons. First, when simultaneous recordings were made from the C-cell and the motor neurons, spikes in the C-cell, no matter how evoked, were invariably followed, within 1.5 ms, by depolarizing IPSPs in the motor neuron (Fig. 6). Second, when the C-cell was hyperpolarized so that it could not fire, that same IPSP in the motor neuron was abolished (Fig. 6). The inhibitory pathway to the motor neurons must be fired at short latency in order to prevent firing caused by the trisynaptic excitatory input (Fig. 1). The C-cells were fired at short latency (less than 3 ms) by impulses in either of the escape command cells (Fig. 4), and at even shorter latency by impulses in the Segmental Giant of the 6th ganglion (SG6) (Fig. 5). It has been established elsewhere that the SGs are a major output pathway of the escape command cells; our results suggest that they may be the pathway for command-evoked firing of the C-cell. The C-cells are also excited by two descending, non-giant, flexion premotor neurons, called I2 and I3 (Fig. 5). The EPSPs from a single I2 or I3 impulse were subthreshold, but temporal and spatial summation of EPSPs from the non- giant pathway sometimes fired the C-cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Plummer, M. R., J. Tautz and J. J. Wine (1986).
"Frequency coding of waterborne vibrations by abdominal mechanosensory interneurons in the crayfish, Procambarus clarkii."
J Comp Physiol [A] 158(6): 751-64.

Nine identified interneurons that originate in the 6th abdominal ganglion were studied with intracellular techniques while activating the receptors presynaptic to them with coherent water vibrations of precisely controlled amplitude and frequency. Each of the interneurons showed a characteristic response to different stimulus frequencies that was consistent from animal to animal. As a first approximation, the cells were categorized as low pass, broad band, and high pass interneurons. Two interneurons classified as low pass interneurons (LPIs) have low thresholds to waterborne vibrations below 100 Hz, are inhibited by stimuli above 100 Hz, and respond maximally to 30 Hz stimuli. Three interneurons classified as broad band interneurons (BBIs) respond maximally to stimuli from 30-60 Hz, but also respond well to oscillations as low as 1 Hz and as high as 80 Hz. This class is heterogeneous, spanning the range between low pass and high pass interneurons. Two interneurons classified as high pass interneurons (HPIs) have very high thresholds to water oscillations below 6 Hz. They respond best to 60 Hz oscillations, above which their responsiveness sharply declines, although they continue to respond weakly up to 400 Hz. Two other neurons, also classified as HPIs, responded with relatively few spikes to the stimuli we used. As a result, they do not show a clear peak responsiveness to a particular stimulus frequency.

Bishop, C. A., J. J. Wine, F. Nagy and M. R. O'Shea (1987).
"Physiological consequences of a peptide cotransmitter in a crayfish nerve-muscle preparation."
J Neurosci 7(6): 1769-79.

The pentapeptide proctolin is colocalized with a conventional, conductance-increasing neurotransmitter in 3 of 5 excitatory motoneurons that innervate a posture-related tonic flexor muscle of the crayfish. It is released from these neurons in response to nerve impulses. Nanomolar concentrations of proctolin superfused on the tonic flexor muscle act postsynaptically to potentiate tension generated by a given level of depolarization. Proctolin alone has no detectable effect on muscle tension, nor does it alter the resting membrane potential of the muscle. Proctolin produces no detectable effect on the EPSPs of the 1 proctolinergic motoneuron that was examined. Neurally released proctolin can be selectively depleted from severed motor axons following prolonged, low-frequency stimulation; EPSPs reflecting conventional transmitter release are unaltered by this procedure. After proctolin depletion, tension generated by the motoneuron is greatly reduced. Taken together, these results indicate that the peptide secondary transmitter in this neuromuscular preparation is an important contributor to the magnitude of tension generated by the motoneuron, but since its effect is dependent on the depolarizing EPSPs of the conventional neurotransmitter, it does not contribute to the temporal aspects of tension generation. These aspects are controlled exclusively by the conventional neurotransmitter.

Takahata, M. and J. J. Wine (1987).
"Feedforward afferent excitation of peripheral inhibitors in the crayfish escape system."
J Neurophysiol 58(6): 1452-67.

1. Each abdominal ganglion of the crayfish contains peripheral inhibitors of the fast flexor muscles. These flexor inhibitors (FIs), which can effectively inhibit tension development in the tailflip powerstroke muscles, are excited by a delayed central pathway from the same giant axons which trigger escape (33). The FIs also received sensory input, which increases in efficacy in the more posterior segments (4), but until now neither the origin of the input nor its central pathways had been well described. We have used intracellular recording and staining techniques to investigate the afferent input onto the two telson flexor inhibitors (F16 and F17), which receive more powerful sensory input than any of their anterior homologs (4). 2. Both F16 and F17 showed a delayed (3.7 ms) compound postsynaptic potential (PSP), which peaked at long latency when any afferent nerve in the abdomen was stimulated. The amplitude of these slow PSPs waned rapidly with repeated stimulation at 1 Hz and was increased by hyperpolarization and decreased by depolarization of the FI. The PSPs are most likely to be mediated chemically, via polysynaptic pathways. 3. When any afferent nerve from the telson was stimulated, both telson FIs showed an additional fast-rising, short-latency (1.4 ms) PSP, which preceded the slow component. This fast component was not produced by afferent nerves innervating any region other than the telson. The fast PSPs of the two FIs were similar, but in F16 the fast component was always subthreshold, whereas in F17 it often elicited an impulse at short latency. 4. The amplitude of the fast component was not affected by changing the membrane potential of the FIs, suggesting electrical transmission. In spite of its short latency, the fast component is unlikely to be mediated monosynaptically, since it was variably present even in the same animal, and occlusion was observed when any two of the four telson nerves that evoked the response were stimulated simultaneously. 5. Although occlusion was seen among responses produced by stimulating afferents from any source, the responses summated linearly with the compound excitatory postsynaptic potential evoked in FI by the lateral giant escape command axons. Thus at least two separate suprathreshold pathways converge onto the telson FIs.

Takahata, M. and J. J. Wine (1987).
"A local interneurone which receives differential input from the medial and lateral giant axons."
J Exp Biol 129: 385-9.

Bishop, C. A., M. E. Krouse and J. J. Wine (1991).
"Peptide potentiation of calcium channel activity can be seasonally variable."
J Exp Biol 156: 607-10.

Bishop, C. A., M. E. Krouse and J. J. Wine (1991).
"Peptide cotransmitter potentiates calcium channel activity in crayfish skeletal muscle."
J Neurosci 11(1): 269-76.

The activity of 2 types of Ca2+ channels (38 and 14 pS in 137 mM Ba2+) in the plasma membrane of the crayfish tonic flexor muscle is modulated by the peptide proctolin. This peptide serves as a cotransmitter in 3 of the 5 excitatory tonic flexor motoneurons and greatly enhances tension after depolarization by the conventional neurotransmitter. Proctolin alone has no effect on these channels, but renders them capable of sustained activity following depolarization. After depolarization induces activity, 5 x 10-9 M proctolin increases the open probability of the larger channel up to 50-fold due to a marked decrease in the mean channel closed time. There is also at least a 4- fold increase in the percentage of patches with active channels for the large channel and a 2-fold increase for the small channel. Proctolin modulation appears to occur via an intracellular messenger, possibly cAMP. The peptide's effect on channel activity is dose dependent in a manner that parallels its effect on tension. These results indicate that the activation of these channels and the resulting influx of Ca2+ into the muscle fiber play a role in the potentiation of tension in this muscle.

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