Two papers about cellular mechanisms for prepulse inhibition studied in Tritonia

 

A cellular mechanism for prepulse inhibition (2003)

by William N. Frost, Li-Ming Tian, Travis A. Hoppe, Donna L. Mongeluzi, and Jean Wang

This paper shows the first cellular-level evidence for prepulse inhibition in Tritonia. A weak sensory stimulus has both excitatory and inhibitory effects on S-cells. The inhibitory effects shunt the synaptic output of some S-cells.

Prepulse inhibition (PPI):

Strong, unexpected stimuli elicit startle responses in all animals, but it can be markedly attenuated if closely preceded by a weak stimulus. 

Schizophrenics show abnormally low level of PPI.

Tritonia PPI

A prepulse stimulus was given by vibrated stick before an electric shock to elicit the swim

The prepulse acts to hyperpolarize two cell types in the swim circuit

Tactile stimuli hyperpolarized DSI and S-cells, but it also cause a lot of excitatory responses in other neurons.

The prepulse shortens and narrows the S cell action potential

Spike narrowing seen in the S cell AP.

Identification of a neuron, Pl 9, mediating the prepulse-elicited S cell inhibition

Pl 9 appears to receive direct EPSPs from most or all ipsilateral S cells and inturn produces direct IPSPs bilaterally onto the entire S cell population, as well as onto the Tr1, DRI, and VSI-B interneurons.

Pl 9 mediates prepulse-elicited hyperpolarizing inhibition of the S cells.

Evidence that Pl 9 mediates PPI

Intracellular stimulation of a single Pl 9 blocked the swim motor program.

Killing a single Pl 9 reduced PPI

Pl 9 inhibits S cell synaptic efficacy

S cell-evoked EPSPs in the swim network neurons were reduced in size when S cells were activated. 

Pl 9 reduces S cell synaptic efficacy via presynaptic inhibition of S cell transmitter release

Pl 9-evoked IPSPs are mediated by Chloride ion, blocked by d-tubocurarine

Pl 9 caused reduction of presynaptic action potentials of S cells in duration and amplitude

The S cell synaptic efficacy depended on its membrane potential

Identification of a neuron, Pl 10, involved in prespulse-elicite postsynaptic inhibition of the DSIs

PI 9 had no direct contact onto DSI, but Pl 10 does.

Pl 10 can block the swim

This study above looking at change in synaptic efficacy of S cells

The next study then looked at change in spike propagation

Axonal conduction block as a novel mechanism of prepulse inhibition

by Anne H. Lee, Evgenia V. Megalou, Jean Wang, and William N. Frost

Prepulse nerve stimuli produce PPI of the swim motor program, and conduction block of S-cell action potential trains

PdN3 alone (swim) vs PdN3 preceded by CN1,4,5 (prepulse) - in all cases CN1,4,5 stim prevented the swim.

Stim of CN1,4,5 caused conduction failure of S-cells evoked by PdN3 stim

Sometimes saw incomplete blockade

Prepulse-elicited conduction block has the temporal features of behavioral PPI in Tritonia

Conduction failure seen when stim was given with 250-500 ms latency (stim, 400 ms)

Conduction block also occurs in response to skin prepulse

Evidence that interneuron Pl-9 mediates PPI of S-cell conduction block

Peak Pl firing was 43 and 59 Hz in response to the tactile stimulation

photoinnactivation of Pl-9 blocked PPI

Variability, compensation and homeostasis in neuron and network function

Eve Marder and Jean-Marc Goaillard

Hebbian learning can be appropriately balanced by stability mechanisms that allow neurons and synaptic connections to be maintained in appropriate operating ranges (by Turrigiano and Nelson, various mechanisms including synaptic scaling and changes in individual ionic currents).

omeostatic tuning rules that maintain a constant activity pattern could, in principle, operate to tune conductances so that an individual neuron remains within a given region of parameter space, although its values for one or more conductances may be substantially
altered.

Variability in channel densities
How can we reconcile the apparent sensitivity of many neurons to rapid pharmacological treatments with new data indicating that individual neurons within a class can differ by as much as two- to fourfold in the densities of many of their currents?
Computational models show that a number of different compensating combinations of conductances can result in similar activity patterns38,51.

In contrast to pharmacological manipulations, slow mechanisms that function during development and over days and weeks can result in a set of compensating conductances that give rise to a target activity pattern.

Figure 2 | Neurons with similar intrinsic properties have different ratios of conductances.

Figure 3 | Comparison of short-term pharmacological manipulations and long-term genetic deletions.

Slow developmental and homeostatic mechanisms can ‘find’ multiple solutions of correlated
and compensating values of membrane conductances consistent with a given activity pattern, even while rapid pharmacological treatments that vary the value of one current at a time result in altered activity57.

Recovery of Locomotion After Spinal Cord Injury: Some Facts and Mechanisms

Serge Rossignol and Alain Frigon

The model provide...The model has...This model produces...How this model can be approached...What can we learn from it.
This study focuses on...by first describing...Specifically we here show...We propose that...
First figure explains the system we study...How the system functions...We first describe the effects of a procedure...We then discuss the effects of...to establish new interactions for the generation of hindlimb locomotion.

LOCOMOTOR RECOVERY AFTER COMPLETE SPINAL TRANSECTION

Cats with a complete SCI (i.e., spinalization) at the last thoracic segment (T13) gradually recover hindlimb locomotion on a treadmill following a few weeks of locomotor training.

The Inescapable Central Spinal Pattern Generator

In acutely spinalized and paralyzed cats, fictive locomotion can be recorded with pharmacological stimulation (L-DOPA) in the complete absence of overt movement (Grillner & Zangger 1979).
In chronic spinal cats, fictive locomotion can occur spontaneously without drugs, indicating that functional changes have occurred within the spinal locomotor circuitry enabling the spontaneous expression of this endogenous pattern (Pearson & Rossignol 1991).

Functional organization of locomotorgenerating circuits.
The mammalian locomotor CPG is thought to be composed of interconnected modules that coordinate activity around specific joints (Grillner 1981). A multilayered spinal locomotor CPG, in which rhythm-generation and pattern formation are functionally separated, has been proposed to account for some experimental findings (reviewed in McCrea & Rybak 2008).

Spinal localization of locomotor-generating circuits.
For instance, although rhythmogenic properties within the lumbosacral spinal cord are somewhat distributed over several segments, the L3-L4 segments in cats (Marcoux & Rossignol 2000, Langlet et al. 2005, Delivet-Mongrain et al. 2008) and L1-L2 segments in rodents (Cazalets et al. 1995, Kiehn 2006) are critical for rhythm generation. This segmental
heterogeneity has important implications for the recovery of walking after SCI.

A balance between excitation and inhibition.
Function within the spinal locomotor network is governed by excitatory and inhibitory connections. During locomotion, motoneurons receive rhythmic alternating pushpull patterns of glutamatergic excitation and glycinergic inhibition during the active and inactive phases, respectively (Shefchyk & Jordan 1985, Cazalets et al. 1996, Grillner 2003). Excitatory connections are sufficient to drive rhythmic bursting because blocking inhibitory transmission, through GABAA (i.e., bicuculline) and glycine (i.e., strychnine) receptor antagonists, does not abolish oscillatory activity (Kjaerulff & Kiehn 1997, Grillner & Jessell 2009). However, inhibition is necessary to produce appropriate flexion/extension (Cowley & Schmidt 1995) and left-right (Cowley & Schmidt 1995, Kremer & Lev-Tov 1997, Hinckley et al. 2005) alternations (Grillner &Jessell 2009).

Intrinsic properties of central pattern generator neurons.
voltage-dependent persistent inward currents (PICs) that amplify excitatory synaptic inputs and sustain neuronal firing are thought to facilitate rhythmogenesis by timing and shaping locomotor output (Brownstone et al. 1994, Kiehn et al. 1996, Tazerart et al. 2008).

Cellular changes in spinal locomotorgenerating circuits.
Immediately after SCI, the excitability of spinal interneurons and motoneurons is depressed because of the loss of excitatory neuromodulatory inputs from brainstem-derived pathways. The return of neuronal excitability is required for functional recovery and can be mediated by several factors.
Some 5-HT receptors became constitutively active following SCI in adult rats, indicating that intracellular signaling occurred without normal ligand binding. Some receptors can also become supersensitive to remaining endogenous sources of neurotransmitters.
Changes in inhibitory circuits could also play a part in modifying neuronal excitability following SCI; increased levels of inhibitory neurotransmitters (i.e., more inhibition) could depress neuronal excitability and impair specific spinal circuits.
The switch from inhibition to facilitation in adult rats was partly attributed to downregulation of potassiumchloride cotransporter 2 (KCC2) in lumbar neurons (Boulenguez et al. 2010, Boulenguez & Vinay 2009). KCC2 expression progressively decreased within the ventral horn following complete or incomplete SCI, and increased levels of intracellular Cl− diminished the efficacy of synaptic inhibition.

The Key Role Played by Sensory Inputs

Sensory inputs play a key role in the regulation of normal locomotion, which can be altered after SCI. After complete SCI, intrinsic changes at the cellular level of the CPG promote the return of hindlimb locomotion through interactions with peripheral sensory inputs.

Spinal reflexes during locomotion.
Reflex responses are　state- and phase-dependent, indicating that sensory processing is regulated by context or, in other words, the current configuration of the spinal circuitry.
Changes at the cellular level following SCI will directly impact the regulation of peripheral sensory inputs and their interaction with the spinal locomotor CPG.

Changes in spinal reflexes after spinal lesion.
If a small portion of sensory feedback is reduced by lesioning specific peripheral nerves before a complete SCI in adult cats, the recovery of hindlimb locomotion is severely impaired.

LOCOMOTOR RECOVERY AFTER PARTIAL SPINAL LESIONS

After incomplete SCI, spared pathways originating from supraspinal and propriospinal structures can play an active role in the recovery process, and also in restoring some voluntary
control. However, intrinsic spinal circuits and peripheral afferents still remain to initiate and
organize hindlimb locomotion.

Accessing the Locomotor Circuitry by Descending Inputs

Ventral and ventrolateral lesions (reticulospinal and vestibulospinal pathways).

Dorsal/dorsolateral lesions (corticospinal and rubrospinal pathways).

Other pathways.Propriospinal pathways. Propriospinal pathways appear to be of considerable importance for volitional aspects of locomotor recovery.Noradrenergic and serotonergic pathways. The loss of neurotransmitters will in turn
have important consequences on themembran properties of target neurons.

Multiple pathways severed by contusions or hemisections.Contusions. Locomotor recovery did not depend on the sparing of corticospinal or long propriospinal pathways (Basso et al. 1996), indicating a role for short intraspinal circuits.
Hemisections.

Mechanisms of Locomotor Recovery After Partial Spinal Cord Injury

Intrinsic spinal mechanisms and afferent mechanisms are still critical in locomotor recovery after an incomplete SCI. In turn, new interactions can modify spared structures throughout the CNS, not just the spinal cord.
Functional recovery is often thought to result from a combination of regeneration, sprouting, or other ill-defined plastic changes in descending pathways (Cafferty et al. 2008).

Compensation by sensory afferents.
Sprouting of sensory afferents on the lesioned side is prominent and could partly account for the functional recovery of various motor patterns (Goldberger 1977, Helgren & Goldberger 1993).
Sensory feedback is of crucial importance in the recovery process.

Compensation by descending pathways.
New circuits could result from new anatomical connections (new circuits) or from enhanced connectivity(enhancing existing circuits).

Regeneration and sprouting. There is a lack of hard evidence that regenerated lesioned axons induce significant functional improvements because of the small number of regenerating axons.
A critical question is whether regenerated fibers are even functional.
Experiments using staggered spinal hemisections show that the regeneration of long descending pathways is not necessary (Kato 1989).
Locomotor recovery depends more on intrinsic spinal mechanisms and contributions from sensory afferents.

New/old circuits. There is no doubt that the propriospinal systems (long and short) can reach the CPG.
The recovery of hindlimb locomotion after a complete SCI in cats, rats, and mice absolutely requires a spinal circuitry capable of generating the basic locomotor pattern independently of descending commands (Grillner 1981; Rossignol 1996, 2006; Rossignol et al. 2006).

Compensation by the Intrinsic Spinal Circuitry. Recent work on the escape swim of a mollusc (Tritonia diomedea) showed near immediate changes within the functional connectivity of the swim CPG following a lesion within the intrinsic circuitry that compensated for the loss of long projections and reinstated function in the absence of regeneration (Sakurai&Katz 2009). A considerable portion of the recovery could be mediated within spinal circuits rather than by a functional takeover by descending pathways.
We propose that the recovery of function by descending or afferent inputs after SCI essentially depends on how the circuitry has adapted to the total or partial absence of descending inputs.

IMPLICATIONS FOR HUMANS WITH SPINAL CORD INJURY

Varieties of behavioral natural variation

by Patrick T. McGrath

Current Opinion in Neurobiology 2012, 23: 1-5

- Behavioral variation in different time scales: 

1) learning or experience driven changes

2) evolutionary change

- The genetic basis of heritable behavioral differences is complex with multiple genetic variants of small effects.

- How genetic differences between individuals cause behavioral difference?

- Many trait differences are caused by a complex combination of genetic changes distributed throughout the genome.

- Coding changes, duplications, small noncoding RNA changes, cis -regulatory changes, neural specific alternative splicing changes

- How do the underlying genetic networks impact the types of genetic variants?

Comparison and contrast between evolution of behavior and development

- Development of body - largely controlled by gene

- Development of Behavior - genetic, acquired information, environment, internal state

Evolution of sensory systems

Three drivers for sensory evolution

1) Change of environment - heterogenetic, changing both spatially and temporally

2) Animals only sense a subset of their environment or stimuli that are also changing 

3) Animals obtain information through proxies that can be sensed

1) Evolution of sensory genes reproducible upon an environmental shift

- Strains of C. elegans grown at high density for long periods of time have become resistant to dauer-inducing pheromones

- This is caused by deletions of pheromon receptor genes

2) Evolution of a metabotropic bioamine receptor 

- Changes in connection between behavior state and sensory systems

- Changes nearby tyra-3 gene (G-protein-coupled receptor for norephinephrine) 

- Increased expression of tyra-3 in a pair of sensory neurons correlated with and sufficient to cause a decreased frequency of leaving a depleting food source.

- The genetic change seems to modify how an internal state of the animal affects behavior. 

- Changes are not only in genes themselves but changes in regulation of these genes at cis-regulatory regions.

Neuromodulator-evoked synaptic metaplasticity in a CPG

Mark D. Kvarta, Ronald M. Harris-Warrick and Bruce R. Johnson

Metaplasticity (Philpot et al. 1999): Characteristics of activity-dependent changes in synaptic strength altered by neuromodulation (Fischer et al. 1997; Kreitzer and Regehr 2000; Parker 2001; Parker and Grillner 1999; Qian and Delaney 1997).

In this study, the authors showed amines (5-HT, DA, and OA) change the properties of homosynaptic plasticity of a specific graded synapse in STG. The synapse used in this study was PD-to-LP synapse. This is apparently due to modification of vesicle traffic dynamics but the authors did not further dig experimentally into the vesicle release dynamics referring to the readily releasable pool sizes and replenishment rates. Recovery rate of homosynaptic depression was also dependent on the presynaptic activity. The authors discussed that maintained presynaptic depolarization would cause more calcium influx, which consequently increases mobilization of the recovery process.

Dopamine had reliable, significant and independent effects to accelerate the time course of synaptic depression onset and recovery from synaptic depression. It consistently accelerated both the onset of, and the recovery from, synaptic depression. This acceleration of onset and recovery from depression did not depend on the sign of the rather variable DA effect on gIPSP amplitudes described above.

DA had weak and highly variable effects on the LP gIPSPs in different preparations. It increased the rate of synaptic depression and of recovery from it. The variability to DA responses cane be caused by the known opposing effects of DA to decrease pre-synaptic PD transmitter release and increase post-synaptic LP input resistance (Harris-Warrick and Johnson 2010), but to differing amounts in different preparations.

DA may be acting postsynaptically to accelerate the kinetics of transmitter receptor desensitization and recovery from desensitization (Papke et al. 2011).

Octopamine - Increased both initial and steady amplitude, slowed the onset of synaptic depression, while speeding up the recovery rate from depression.

- What about contribution of post-synaptic receptors?

Serotonin - Serotonin depresses the synapse and accelerated the time course of synaptic depression measured with square pulse PD stimulation, but not reach statistical significance for oscillation.

The authors stated in the discussion that individual parameters of synaptic strength can be independently modulated by each amine. I disagree. The synaptic strengh should be determined by the fraction of readily releasable pool activated by depolarization, which must be under a strong influence of the vesicle replenishment rates. I don't think they are independent.

Fixing a power hub for micromanipulators

   There was overnight leakage of the cooling water for the chilling stage under dissection microscope in one of our student's electrophysiology rig. The dripped water soaked the the entire power hub for micromanipulators under the anti-vibration table. It stopped working, of course. It is Siskiyou MC1000e. It would cost $$$ if you buy a new one.

   By checking around with an electrical tester, I found a disconnected path on the printed circuit board. I had to create a new path with a hook-up wire (red arrow).

    There was another bad news. One of the pins in the male D-SUB connector was also broken. I don't know how it could happen but it was one of the critical one that feeds current to the manipulator. I created a fake pin from a piece of hook-up wire and attached into the connector. It worked well.

    Now the manipulator is moving fine.
    You know, I can be the author of "Zen and the art of electrophyiology rig maintenance" some day.

Organization of spinal circuitry for rodent locomotion

Neuronal activity in the isolated mouse spinal cord during spontaneous deletions in fictive locomotion: Insights into locomotor CPG organization

by Guisheng Zhong, Natalia A Shevtsova, Ilya A Rybak, Ronald M Harris-Warrick

Journal of Physiology (2012)

Deletions are spontaneous errors in the rhythmic locomotor pattern when a set of synergist motoneurons (for example, flexor motoneurons on one side) loses rhythmic firing or falls silent during a time period when they are normally active. 

In the non-resetting deletions, the phase of the rhythm after the deletion did not change. The resetting deletions show rhythm resetting which was recognized by a shift in the phase of the motor bursts after the deletion. This study follows Rybak-McCrea model of the locomotor CPG, which has two functional levels: a half-center rhythm-generator and pattern formation networks. 

Deletions occur simultaneously in motor activity across more than one spinal segment. Spontaneous non-resetting deletions on one side are independent of the other side. The CPG can be functional within an isolated hemisegment. The reduction in locomotor frequency after simulated hemisection results mainly from the elimination of excitatory input to the rhythm-generating ipsilateral RG-F population from the contralateral RG-E population. The resumption of activity an integer number of cyces later does not require input from other parts of the spinal cord. Each hemicord contains an independent rhythmogenic network that can function in the absence of the other hemicord, although the left and right networks are normally coupled via commissural interneurons.

Among V2a interneurons, there are deletion-sensitive types and insensitive type (type I and II V2a interneurons). Type I V2a does not respond to non-locomotory firing in iL2, whereas type II V2a does. Both neurons were depolarized by synaptic drive. The type I V2a interneurons are involved in rhythm generation and/or coordination between left and right networks via the CINs. In contrast, the type II V2a interneurons do not belong to rhythm generator networks, but can be components of the pattern gormation network and/or last-order interneurons that directly project to motoneurons. Commissural interneurons (CINs) send their axons to the opposite side of the cord and coordinate left-right alternation. CINs were not affected by motoneuronal deletion. There was asymmetry in deletion: During all of the flexor deletions, the ipsilateral extensor root showed sustained activity with no interruptions at the times of the missing flexor bursts. In contrast, during all extensor deletions, the ipsilateral flexor root continued unperturbed bursting.

Their computational model combines the Rybak-McCrea concept of the two-level locomotor CPG (Rybak et al., 2006a,b; McCrea and Rybak, 2007,2008) with the Duysens-Pearson concept of an asymmetric rhythm generator with a dominant flexor half-centre (Pearson and Duysens, 1976).

3 talks in 2 weeks

   I did 3 different talks in 3 symposiums in 2 weeks.
   First two were in workshops in the Computational Neuroscience: "Dynamics of rhythm generation" and "Principles of motor pattern generation: experiments and modeling." Gennady and Andrey kindly invited me as a speake. The 3rd talk was a symposium talk in the 10th International Congress of Neuroethology.

   For "Dynamics of...," I talked about potential mechanism of termination of an episodic behavior. This was a difficult talk for me because I have not worked on this aspect of the CPG. Some of the data I presented were not my own; those were not conclusive results. Very hard to interpret. I did some additional experiments in last moments only for figures. I was very nervous, because I was not so confident of what I was going to talk. 

   In the second workshop I talked about swim CPGs of Melibe and Dendronotus.It was fun and I enjoyed it. Andrey always admires my work.

   For the Neuroethology symposium, I was very grateful that Dr. Ron Calabrese kindly invited me to give a talk in his symposium. This is such a great honor. I gave a talk in the same symposium with Dr. Eve Marder. She even used my own laser pointer!
   About 17 years ago, my friend took me to Univ of Maryland when I visited Washington DC. It was after visiting Birmingham, England to attend the International Congress of Comparative Biochemistry and Physiology. In those days I was reading papers written by Ron Calabrese and Eve Marder like textbooks. I admire them so much. And now, they have invited me to give a talk. So happy.
   I talked about individual variability in the effect of injury to the nervous system. Many people gave me good feedbacks. Some told me they got inspired by my story, which also made me very happy.

Gap Junctions Compensate for Sublinear Dendritic Integration in an Inhibitory Network

 By Koen Vervaeke, Andrea Lorincz, Zoltan Nusser, R. Angus Silver


This intense study show an example of how dendritic synaptic signals are integrated into action potentials in the electrically-coupled Golgi cells.
Major punch line results were drawn from a computer model.

Background:
1) A Golgi cell has big dendrites in one side and axon on the other side of the soma.
2) Parallel fibers make excitatory synapses on distal dendrites, whereas mossy fibers make excitatory synapses near the cell body.
3) Golgi cells are electrically coupled by gap junctions.

I. Local application of Glu to see how the synaptic signals were integrated and conducted to the soma.
This gave an imprecation of active conductance somewhere along the path (axon).

II. Indeed, proximal region from the soma has V-dependent potassium (outward) conductance.

III. Sponteneous EPSPs get bigger when recorded at more distal dendrite. The same EPSPs appear smaller in the soma, but the action potentials were always evoked near the soma.

IV. Because of the locational difference, MF and PF have different effects: MF can evoke spikes more efficiently whereas PF depolarized the dendrites more.

V. How gap-junction play a role in MF/PF-evoked excitation (model study)
 - Gap-junctions reduced overall Rinput - on average it reduces the responsiveness (Fig. 4D) by reduction of responsiveness in directly-innervated GoCs.
 - However, there is remarkable increase in coupled-firing in GoCs that are not innervated but coupled to the innervated ones. More in PF-generated firing.

VI. Discussion:
 - GJ-mediated lateral excitation counteracts the effects of sublinear dendritic behavior by enabling distal inputs to drive network activity more effectively.
 - The combination of passive dendrites and gap junctions facilitates wide-spread excitation among the interneurons whether or not each of them are innervated.
 - No need to boost synaptic potentials with active dendritic conductance.
 - How gap junction contribute spatial averaging and gain control of inhibitory interneurons.
 - The coupled interneurons exhibit features of a syncitium.
 - Similar mechanisms must be going on in other cortex inhibitory neurons, granule cells, retina and other sensory systems.



 -

A slug on focus

One of our collaborator trying to do motion capture of swimming slugs.

The white beads glued on the skin fell off because this shy slug sweated a lot of slime.







It did perform an excellent swim, though.

Interesting SfN posters

It is a bit late but this is about the SfN meeting. During cleaning up my desk near the end of year I rescued a bunch of notes I took during the meeting. Most of them were hard to read. Here are some.


497.06 Presentation Title: Endogenous neuropeptide facilitates INap pacemakers and acts on low respiratory frequency
*A. DOI, J. M. RAMIREZ

I often heard of Dr. Doi's work in Dr. Ramirez's talks. This was actually my first time visiting his poster. He explained to me in very clear logic in English and then we chatted in Japanese. He studied the role of endogenous substance P (SP) and toic activation of neurokinin1 (NK1) receptors in the generation of eupneic respiratory rhythm in pre-Bötzinger complex (pre-BötC) by blocking of NK1 receptors.
Both Cd²⁺-sensitive (CS) and Cd²⁺-insensitive (CI) pacemakers received endogenous SP release, but CI pacemaker activities were only tonically facilitated by activation of NK1 receptors. This seems to be due to the difference in voltage-sensitivity between CS pacemakers and CI pacemakers. The former mediated by non-selective cation channel (ICaN) whereas the latter by persistent Na⁺ channel (INaP).


585.09 Presentation Title: Electrical coupling in Aplysia bag cell neurons: Biophysical characterization and role in synchronous firing.
P. L. W. COLMERS, *N. S. MAGOSKI
The role of gap-junctions among the Aplysia bag cell neurons were examined. Meclofenamic acid is an electrical coupling blocker.


699.20 Presentation Title: Developmental reconfiguration of gaze control commands from spinal locomotor circuitry during Xenopus metamorphosis.
*D. COMBES, G. VON UCKERMANN, D. LE RAY, F. LAMBERT, H. STRAKA, J. SIMMERS
Dr. Denis Combes' poster is always one of my favorite in this meeting. This is a true NEUROBIOLOGY work. He studied the developmental changes in the neural control of eye movement in tadpole. During metamorphosis, Xenopus switches its mode of locomotion from tail-based undulatory movements to bilaterally-synchronous hindlimb kick propulsion, with intervening stages where these two modes co-exist.
There is a developmental transition in spinal efference copy control of extraocular motor output during Xenopus metamorphosis that corresponds to the change in locomotor strategy.


818.15 Evolution of a behavior mediated by the lateral line system adapts Astyanax to life in darkness.
*M. YOSHIZAWA, W. R. JEFFERY
This is also a very interesting work that grasped the moment of evolution of cavefish traits during the adaptation processes. Showing physiological and genetic basis of an adaptive behavior, vibration attraction behavior (VAB) inAstyanax mexicanus, which has an eyed surface (surface fish) and a blind cave (cavefish) dwelling forms.
Quantitative laboratory assays indicate that VAB is common in cavefish but rarely observed and much less robust in surface fish. VAB is beneficial for feeding in the dark. Increase in superficial neuromast (SN) during development is important forVAB.