OCTOPAMINE INDUCES STEADY STATE REFLEX REVERSAL IN CRAYFISH THORACIC
GANGLIA.
Skorupski, Peter.
Department of Physiology, University of Bristol, School of Veterinary
Science, Southwell Street, Bristol BS8 2EJ, UK, Tel. (+44) 117 928 7822, Fax.
(+44) 117 925 4794
APStracts 2:0363N, 1995.
SUMMARY AND CONCLUSIONS
1. This paper investigates the effect of octopamine on spontaneous and reflex
motor output of crayfish leg motor neurons. Octopamine modulated spontaneous
activity, both rhythmic and tonic, and dramatically modulated the pattern of
reflex motor output elicited by stimulating identified proprioceptors of the
basal limb. 2. Spontaneous reciprocal motor patterns, involving alternating
bursts of promotor and remotor motor neuron activity, were reversibly
abolished by octopamine. The threshold concentration for this effect was about
1 M. 3. At concentrations greater than about 10µM octopamine inhibited
spontaneous promotor nerve activity in both bursting and nonbursting
preparations. In some experiments promotor inhibition was correlated with the
induction of tonic remotor nerve activity. The EC50 for complete inhibition of
promotor nerve activity by octopamine was 20-30 M. 4. Reflexes mediated by two
basal limb proprioceptors, the TCMRO (which signals leg promotion) and the
TCCO (which signals leg remotion) were analysed in a number of promotor and
remotor motor neurons. In both cases assistance reflexes (excitation of
promotors by the TCCO and remotors by the TCMRO) were restricted to subgroups
of the motor pool. Among remotor motor neurons the first two units recruited
during bursts of spontaneous activity were members of the assistance reflex
group (group 1). A third unit, sometimes recruited during more intense
spontaneous bursts, was excited by TCCO stimulation and was therefore a member
of the resistance reflex group (group 2). Other resistance group remotors were
also excited by the TCCO, but this input normally remained subthreshold. 5.
Stimulation of the TCCO afferent nerve elicited EPSPs in group 2 (resistance
group) remotor motor neurons at a latency compatible with a monosynaptic
connection. The same stimulation excited group 1 (assistance group) promotor
motor neurons, but at a greater and more variable latency. Thus the remotor
resistance reflex from the TCCO is probably monosynaptic, but the promotor
assistance reflex, also elicited by TCCO stimulation, is likely to be di- or
polysynaptic. Assistance group (group 1) remotor motor neurons are inhibited
by mechanical stimulation of the TCCO, or electrical stimulation of its nerve.
6. Octopamine had selective effects on individual remotor units. First,
assistance group remotor motor neurons were affected in two ways. One unit was
inhibited, so that reflex spiking in response to TCMRO stimulation was
abolished. A second unit was not inhibited, but its reflex response mode
changed, so that instead of responding to TCMRO input with an assistance
reflex, it responded to TCCO input with a resistance reflex. Second, among
motor neurons that normally respond to TCCO input with resistance reflexes,
these responses were enhanced by octopamine. 7. Promotor motor neurons were
inhibited by octopamine and reflex responses were also affected selectively.
Responses to TCCO input (assistance reflexes) were abolished, whereas
responses to TCMRO input (assistance reflexes) were relatively less affected.
8. Intracellular recordings revealed that the majority of remotor motor
neurons depolarized in the presence of octopamine. In preparations where these
could be classified on the basis of TCMRO/TCCO inputs, all were identified as
group 2 (resistance group). A minority of remotor motor neurons were
hyperpolarized by octopamine. All of these were identified as group 1
(assistance group), with strong TCMRO input. 9. The majority of promotor motor
neurons were depolarized by octopamine. This depolarization was nevertheless
inhibitory since it reversed slightly positive to rest and was associcated
with a substantial fall in input resistance.
Received 21 February 1995; accepted in final form 30 November 1995.
APS Manuscript Number J120-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 December 95