Reciprocal excitation between identified flight motor neurons inDrosophila and its effect on pattern generation

1983 ◽  
Vol 150 (3) ◽  
pp. 305-317 ◽  
Author(s):  
J. H. Koenig ◽  
Kazuo Ikeda
1999 ◽  
Vol 82 (5) ◽  
pp. 2579-2589 ◽  
Author(s):  
Tatsumi Nagahama ◽  
Kenji Narusuye ◽  
Hidekazu Arai

Japanese species, Aplysia kurodai, feeds well on Ulva but rejects Gelidium ( Geli.) or Pachydictyon ( Pach.) with different rhythmic patterned movements of the jaws and radula. During ingestion the jaws open at the radula-protraction phase and remain half open at the initial phase of the radula-retraction, whereas during rejection the jaws open similarly but start to close immediately after the onset of the radula-retraction. These can be induced not only by the natural seaweed but by the extract solutions. We previously showed that the change of the patterned jaw movements from the ingestion to the rejection may result from the decrease in the delay of the firing onset of the jaw-closing (JC) motor neurons during their depolarization. This diminished delay produces a phase advance relative to the radula-retraction phase. In that study, we showed that during ingestion the buccal multiaction (MA) neurons may generate the delay of firing onset of the JC motor neurons by producing monosynaptic inhibitory postsynaptic potentials (IPSPs) during the initial portion of their depolarization. In the present experiments, the firing patterns in the MA neurons induced by application of the Geli. or Pach. extract to the lips were explored in the semi-intact preparations. During the Pach. response the duration and the firing frequency of the MA firing at each depolarizing phase were decreased in comparison with the Ulvaresponse. No decreases in the MA firing were observed during the Geli. response, suggesting that the similar patterned jaw movements during rejection of Geli. and Pach. may be generated by different neural mechanisms. Moreover, the size of the MA-induced IPSP in the JC motor neurons was largely decreased by application of the Geli. or Pach. extract to the lips in the reduced preparations consisting of the tentacle-lips and the cerebral-buccal ganglia. Voltage-clamp experiments on the JC motor neurons showed that the size of synaptic current induced by the MA spikes was decreased by application of these solutions to the lips. The decrease was induced when the buccal ganglia were bathed in a solution to block polysynaptic pathways. These results suggest that the advance of the onset of the JC firing at each depolarizing phase during the Geli. or Pach. response may be mainly or partly caused by the decrease in the size of the MA-induced IPSP in the motor neurons. Modulatory action of cerebral neurons or peripheral afferent neurons in the lip region may contribute to this synaptic plasticity.


1989 ◽  
Vol 279 (2) ◽  
pp. 272-280 ◽  
Author(s):  
S. Wang ◽  
R. M. Robertson

1985 ◽  
Vol 53 (2) ◽  
pp. 466-480 ◽  
Author(s):  
P. A. Getting ◽  
M. S. Dekin

Swimming behavior in the marine mollusc Tritonia diomedea is episodic, consisting of a series of alternating dorsal and ventral flexions initiated by a brief sensory stimulus. The swim motor pattern is generated by a network formed of four groups of premotor interneurons: cerebral cell 2 (C2), dorsal swim interneurons (DSIs), and two types of ventral swim interneurons (VSI-A and VSI-B). The initiation and maintenance of swimming depends on the establishment of a long-lasting ramp depolarization in both the premotor, pattern-generating interneurons, and the motor neurons (i.e., flexion neurons). Voltage clamp was used to measure the membrane current responsible for the ramp depolarization. In all cell classes the current had two components: a tonic inward current, which decayed as the swim progressed, and phasic inward current waves, which provided the synaptic drive during each swim burst. The ramp current in the flexion neurons and in C2 was generated largely by activity within the interneuronal pattern-generating network (PGN). The ramp current could be mimicked by driving activity in the pattern-generating interneurons. In VSI-B, the tonic component of the ramp current was independent of activity within the PGN and appeared to be derived from the long-lasting effect of an extrinsic input. The phasic components of the ramp, however, were dependent on PGN activity. The phasic inward current waves were blocked when pattern generation was prevented. In addition, phasic inward currents similar to those occurring during swimming could be produced by driving the C2. The tonic component of the ramp current in a DSI was dependent both on extrinsic inputs and PGN activity. Extrinsic inputs appeared to control the first 10-15 s of the tonic current. At longer times, activity within the DSI population itself maintained the ramp current. When one DSI was driven in a quiescent preparation, all other DSIs were inhibited, yet the DSIs are known to be coupled by monosynaptic, reciprocal excitatory synapses. This effect could be explained by the action of an unidentified inhibitory interneuron (I-neuron), which was excited by DSIs and in turn inhibited all other DSIs. The DSIs were therefore coupled reciprocally by both monosynaptic excitation and polysynaptic inhibition. Activity in C2 switched the DSI-DSI interaction from inhibition to excitation by inhibiting the I-neuron.(ABSTRACT TRUNCATED AT 400 WORDS)


2012 ◽  
Vol 108 (1) ◽  
pp. 148-159 ◽  
Author(s):  
Sean E. Low ◽  
Ian G. Woods ◽  
Mathieu Lachance ◽  
Joel Ryan ◽  
Alexander F. Schier ◽  
...  

The molecular and physiological basis of the touch-unresponsive zebrafish mutant fakir has remained elusive. Here we report that the fakir phenotype is caused by a missense mutation in the gene encoding voltage-gated calcium channel 2.1b ( CACNA1Ab). Injection of RNA encoding wild-type CaV2.1 restores touch responsiveness in fakir mutants, whereas knockdown of CACNA1Ab via morpholino oligonucleotides recapitulates the fakir mutant phenotype. Fakir mutants display normal current-evoked synaptic communication at the neuromuscular junction but have attenuated touch-evoked activation of motor neurons. NMDA-evoked fictive swimming is not affected by the loss of CaV2.1b, suggesting that this channel is not required for motor pattern generation. These results, coupled with the expression of CACNA1Ab by sensory neurons, suggest that CaV2.1b channel activity is necessary for touch-evoked activation of the locomotor network in zebrafish.


1976 ◽  
Vol 112 (2) ◽  
pp. 143-158 ◽  
Author(s):  
George B. Casaday ◽  
Jeffrey M. Camhi
Keyword(s):  

1982 ◽  
Vol 48 (6) ◽  
pp. 1392-1415 ◽  
Author(s):  
J. S. Eisen ◽  
E. Marder

1. The pyloric dilator (PD) and anterior burster (AB) neurons in the pyloric system of the lobster stomatogastric ganglion are electrically coupled and synchronously active. We have used the lucifer yellow photoinactivation technique to separate the connections made by the PD motor neurons from those made by the AB interneuron. 2. Photoinactivation of either the two PD neurons or the single AB neuron allowed us to separate the compound inhibitory postsynaptic potentials (IPSPs) in the lateral pyloric (LP) and pyloric (PY) motor neurons resulting from synchronous PD and AB activity into AB-evoked and PD-evoked components. These IPSPs have different time courses, reversal potentials, ion selectivities, and pharmacological properties. 3. Photoinactivation and membrane-potential manipulations indicated that a readily observable IPSP recorded in the AB neuron and correlated with action potentials in the LP neuron is actually an electrotonic potential due to an LP-evoked IPSP in the PD neurons. 4. Selective inactivation of either the two PD neurons or the AB neuron revealed that the IPSP recorded in the ventricular dilator (VD) motor neuron is due solely to AB-released transmitter. 5. The electrical coupling potentials measurable between the AB, PD, and VD neuron somata are due to direct electrical coupling between all of these neurons. 6. Circuit analysis and transmitter identification may be complicated by electrical coupling. We suggest that the presence of electrical coupling between nonidentical neurons may provide a new mechanism that allows changes in synaptic characteristics among neurons within a "hard-wired" circuit.


1969 ◽  
Vol 170 (3) ◽  
pp. 293-300 ◽  
Author(s):  
Ingrid Waldron ◽  
Donald M. Wilson

Sign in / Sign up

Export Citation Format

Share Document