VSI-B

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VSI-B is a Neuron in Tritonia. See also VSI.

Basic information

There is one VSI-B in each pleural ganglion. VSI-B projects the primary axon ipsilaterally to the pedal ganglion through the posterior path of the cerebro-pedal connective, and then to the contralateral pedal ganglion through the pedal-pedal connective (Pedal nerve 6) (Getting, 1983; Sakurai and Katz, 2004).

Drawing of a VSI-B dye-fill

The VSI-Bs play an important role in the swim central pattern generator by making reciprocal inhibitory connections with the C2 and DSI neurons (Getting 1983). VSI-B makes excitatory synaptic contact with premotor neurons including the Ventral Flexion Neurons (VFNs) in the pedal ganglia to produce ventral body flexion.

Initially, it was thought that another neuron, VSI-A, is responsible for the ventral phase of the motor pattern, but a modeling study suggested that its properties were not sufficient to account for the behavior.

Simultaneous intracellular recordings of C2, DSI, VSI-B and VFN, exhibiting the swim motor pattern. Notice that VSI-B fires in alteration with DSI and C2. 5 Hz, 3 sec stimulation was given to PdN3 as indicated by arrows.

Identification

Anatomy:

  • The soma is spindle shaped and located below the ventral surface of the pleural ganglion anterior to the base of PlN3.
  • In the dissection microscope, with some reflected illumination, the VSI-B soma appears translucent with a small pigment spot.
  • Sends axon to the pedal-pedal connective (PdN6).

Electrophysiology:

  • Produces fast and large discrete EPSPs (~10 mV) in the ventral flexion neurons in both pedal ganglia.
  • Exhibits solid bursts with flat tops due to relatively constant spike amplitude during the swim motor pattern.
  • Excites Large Unit neuron in the Pedal Ganglion.
  • Sends axonal impulses to PdN6.
  • Delayed excitation due to A-current (Getting, 1983; Sakurai et al., 2006)
  • Mostly silent.
  • VSI-B is the only neuron that can phase-shift the swim motor pattern.
  • A DSI burst produces the spike timing-dependent neuromodulation (STDN) at VSI-B-to-VFN synapse (Sakurai and Katz, 2003).
  • Produces large discrete IPSPs in DSI with a relatively long latency (~0.2 sec).
  • High-frequency stimulation of VSI-B induces the post-tetanic potentiation at VSI-B-to-VFN synapse(Sakurai, unpublished).
  • C2 excites the VSI-B (Getting, 1983). The C2-evoked VSI-B action potential propagate antidromically from the pedal ganglion contralateral to the VSI-B soma (Sakurai, unpublished).

References

  1. Getting PA (1983). Mechanisms of pattern generation underlying swimming in Tritonia. III. Intrinsic and synaptic mechanisms for delayed excitation. J. Neurophysiol 49: 1036-1050.
  2. Katz PS (2009) Tritonia swim network. Scholarpedia 4 (5):3638. [1]
  3. Sakurai A and Katz PS (2003). Spike timing-dependent serotonergic neuromodulation of synaptic strength intrinsic to a central pattern generator circuit. J Neurosci 23: 10745-10755.
  4. Sakurai A and Katz PS (2004). Serotonergic enhancement of a 4-AP sensitive current causes spike propagation failure in a Tritonia swim CPG neuron with multiple spike initiation zones. Soc Neurosci Abstr 30. 537.1.
  5. Sakurai A, Darghouth NR., Butera RJ., and Katz PS (2006). Serotonergic enhancement of a 4-AP-sensitive current mediates the synaptic depression phase of spike timing-dependent neuromodulation. J Neurosci 26: 2010-2021.