Quantitative Reflection Imaging of Fixed Aplysia californica Pedal Ganglion Neurons on Nanostructured Plasmonic Crystals

2013 ◽  
Vol 117 (42) ◽  
pp. 13069-13081 ◽  
Author(s):  
An-Phong Le ◽  
Somi Kang ◽  
Lucas B. Thompson ◽  
Stanislav S. Rubakhin ◽  
Jonathan V. Sweedler ◽  
...  
Keyword(s):  
Aplysia Californica ◽  
Pedal Ganglion ◽  
Plasmonic Crystals ◽  
Reflection Imaging ◽  
Ganglion Neurons

scholarly journals Quantitative Reflection Imaging for the Morphology and Dynamics of LiveAplysia californicaPedal Ganglion Neurons Cultured on Nanostructured Plasmonic Crystals

Langmuir ◽  
2017 ◽  
Vol 33 (35) ◽  
pp. 8640-8650 ◽  
Author(s):  
Somi Kang ◽  
Adina Badea ◽  
Stanislav S. Rubakhin ◽  
Jonathan V. Sweedler ◽  
John A. Rogers ◽  
...  
Keyword(s):  
Plasmonic Crystals ◽  
Reflection Imaging ◽  
Ganglion Neurons

Motor controls of opaline secretion in Aplysia californica

1980 ◽  
Vol 43 (3) ◽  
pp. 581-594 ◽  
Author(s):  
S. H. Tritt ◽  
J. H. Byrne
Keyword(s):  
Motor Neurons ◽  
Synaptic Input ◽  
Spike Activity ◽  
Aplysia Californica ◽  
Low Frequency ◽  
Synaptic Activity ◽  
Biophysical Properties ◽  
Ganglion Neurons ◽  
Pleural Ganglion

1. Using combined morphological and electrophysiological techniques, we have identified motor neurons in the right pleural ganglion of Aplysia californica that contribute to the release of opaline from the opaline gland. 2. Three pleural ganglion neurons were found to meet the requirements for identification as opaline gland motor neurons by a) sending processes in nerve P5, which innervates the gland; b) producing contractions of the gland in the absence of central synaptic activity; and c) producing excitatory junctional potentials (EJPs) in cells making up the opaline gland itself. The neurons can be reliably located and have been designated PLR1, PLR2, and PLR3. 3. When gland contraction is measured by the change in luminal pressure, the gland response is a graded function of low-frequency spike activity in the motor neurons. 4. Presumptive EJPs recorded from opaline gland cells are reversibly decreased in size by high extracellular Mg2+ and reversibly increased in size by raising the concentration of extracellular Ca2+. These results suggest that the presumptive EJPs are chemically mediated. The presumptive EJPs show facilitation and posttetanic potentiation. 5. The identified opaline motor neurons may constitute a significant portion of the motor input to the opaline gland via nerve P5 since hyperpolarization of the cells prevents the opaline gland response elicited by right connective stimulation in vitro. 6. We have compared the properties of the opaline motor neurons with the previously identified properties of the ink motor neurons (6--9, 19). Like the ink motor neurons, the opaline motor neurons have high resting potentials, are electrically coupled, and have no spontaneous spike activity. They also receive a slow and long-lasting evoked depolarizing synaptic input, which appears to be mediated by a decreased conductance mechanism. The firing pattern of the opaline motor neurons produced by synaptic input shows the same delayed bursting pattern previously described for the ink motor neurons. 7. The biophysical properties and synaptic input to the ink motor neurons have been shown to affect the features of inking behavior (4, 6--9, 19). The opaline motor neurons share some of these biophysical characteristics and mediate a defensive behavior similar to ink release. Further comparisons of these behaviors and their underlying neural circuits may provide a better understanding of the extent to which cellular biophysical properties and patterns of synaptic input influence the features of the behaviors that individual neurons mediate.

Identification and characterization of cerebral ganglion neurons that induce swimming and modulate swim-related pedal ganglion neurons in Aplysia brasiliana

1995 ◽  
Vol 74 (4) ◽  
pp. 1444-1462 ◽  
Author(s):  
G. N. Gamkrelidze ◽  
P. J. Laurienti ◽  
J. E. Blankenship
Keyword(s):  
Central Pattern Generator ◽  
Motor Neurons ◽  
Cerebral Ganglion ◽  
Motor Program ◽  
Pattern Generator ◽  
Pedal Ganglion ◽  
Cell Type ◽  
Command Neurons ◽  
Sensory Stimuli ◽  
Ganglion Neurons

1. We have identified and characterized a family of several pairs of neurons in the cerebral ganglion of Aplysia brasiliana that are capable of inducing, maintaining, or modulating a motor program that underlies swim locomotion in this marine mollusk. We have operationally defined these cells as command neurons (CNs) for swimming. 2. The command cells occur in bilateral pairs in the cerebral ganglion and make direct and indirect outputs to neurons in the pedal ganglia, including motor neurons, a central pattern generator circuit, and modulatory neurons that enhance muscle contractions during swimming. Several of the CNs are sufficient individually to induce the swim motor program (SMP), all receive sensory feedback from the periphery, and several interconnect with other swim-related CNs. 3. Tonic discharges of approximately 10 Hz in CN types 1-3 (CN1-CN3) are capable of eliciting the oscillatory, phasic SMP as recorded in peripheral nerves that innervate the swim appendages, the parapodia. CN1, CN2, and CN3 make monosynaptic excitatory connections onto ipsilateral, contralateral, and bilateral pedal swim-modulatory neurons [parapodial opener-phase (POP) cells], respectively; and each command cell type activates the pedal central pattern generator (CPG), leading to sustained phasic output of motor neurons and POP cells. 4. Tonic firing of CN4 causes weak activation of the SMP contralaterally. These neurons occur as two pairs of neurons in each cerebral hemiganglion, with mutual electrical and chemical synaptic interconnections. CN4 cells also excite CN1 and CN2 cells. Thus CN4 is classified as a higher-order swim command cell type. 5. Command cells classified as types 5-8 (CN5-CN8), although not capable of inducing the SMP individually, nonetheless have strong synaptic connections with pedal POP cells and/or with other command neurons. These command cells may excite or inhibit follower cells on the same or opposite sides of the preparation and modulate the swim output. 6. All the command cells tested received strong input from mechanical stimulation, either stretch or pinching, of either parapodium. Mechanosensory input from the parapodia was shown to depend on the presence of the pedal ganglion, but not the pleural. Sensory stimulation activated command cells and motor neurons, but POP cells received input from sensory stimuli only through the cerebral ganglion, probably via command cells. The effects of applied mechanosensory stimuli could be entirely mimicked by motor neuron-induced contractions of the parapodia.

Neuronal modulation of foot and body-wall contractions in Aplysia californica

1992 ◽  
Vol 67 (1) ◽  
pp. 23-28 ◽  
Author(s):  
D. R. McPherson ◽  
J. E. Blankenship
Keyword(s):  
Relaxation Rate ◽  
Action Potentials ◽  
Body Wall ◽  
Aplysia Californica ◽  
Body Wall Muscle ◽  
Pedal Ganglion ◽  
Medial Border ◽  
Evoked Contractions ◽  
Large Neurons

1. Large neurons in the pedal ganglia of Aplysia californica were examined for their potential to modulate motoneuron-evoked contractions in foot and body-wall muscle. These neurons lie near the medial border of each pedal ganglion and have peripheral axons but no detectable motor effect. 2. Neurons in this region fire in rhythmic bursts during fictive escape crawling, and their action potentials resemble those recorded from parapodial opener-phase (POP) neurons in the swimming species, A. brasiliana. 3. Firing these neurons in conjunction with pedal motoneurons potentiates the force of contractions and increases their relaxation rate. Similar effects are produced by the serotonin (5-HT) analogue, bufotenine. 4. The modulatory neurons can be stained in vivo by 5,7-dihydroxytryptamine (5,7-DHT), suggesting they are serotonergic. 5-HT immunoreactivity is present in axons associated with foot and body-wall muscle. 5. Bath-applied 5-HT causes rhythmic bursting in the modulatory neurons. It appears likely that they are homologous to the POP cells of A. brasiliana.

Regeneration of pedal ganglion neurons in the sea butterfly Clione limacina

1986 ◽  
Vol 17 (4) ◽  
pp. 317-322
Author(s):  
Yu. I. Arshavskii ◽  
I. M. Gel'fand ◽  
G. N. Orlovskii ◽  
G. A. Pavlova ◽  
Yu. V. Panchin ◽  
...  
Keyword(s):  
Pedal Ganglion ◽  
Clione Limacina ◽  
Ganglion Neurons

Registered Report: Transcriptional Analysis of Savings Memory Suggests Forgetting Is Due to Retrieval Failure

2020 ◽  
Author(s):  
Robert Calin-Jageman ◽  
Irina Calin-Jageman ◽  
Tania Rosiles ◽  
Melissa Nguyen ◽  
Annette Garcia ◽  
...  
Keyword(s):  
Memory Trace ◽  
Aplysia Californica ◽  
Transcriptional Response ◽  
Transcriptional Analysis ◽  
Retrieval Failure ◽  
Initial Learning ◽  
Rigorous Test ◽  
Stage 1 ◽  
Induced Changes

[[This is a Stage 2 Registered Report manuscript now accepted for publication at eNeuro. The accepted Stage 1 manuscript is posted here: https://psyarxiv.com/s7dft, and the pre-registration for the project is available here (https://osf.io/fqh8j, 9/11/2019). A link to the final Stage 2 manuscript will be posted after peer review and publication.]] There is fundamental debate about the nature of forgetting: some have argued that it represents the decay of the memory trace, others that the memory trace persists but becomes inaccessible due to retrieval failure. These different accounts of forgetting lead to different predictions about savings memory, the rapid re-learning of seemingly forgotten information. If forgetting is due to decay, then savings requires re-encoding and should thus involve the same mechanisms as initial learning. If forgetting is due to retrieval failure, then savings should be mechanistically distinct from encoding. In this registered report we conducted a pre-registered and rigorous test between these accounts of forgetting. Specifically, we used microarray to characterize the transcriptional correlates of a new memory (1 day after training), a forgotten memory (8 days after training), and a savings memory (8 days after training but with a reminder on day 7 to evoke a long-term savings memory) for sensitization in Aplysia californica (n = 8 samples/group). We found that the re-activation of sensitization during savings does not involve a substantial transcriptional response. Thus, savings is transcriptionally distinct relative to a newer (1-day old) memory, with no co-regulated transcripts, negligible similarity in regulation-ranked ordering of transcripts, and a negligible correlation in training-induced changes in gene expression (r = .04 95% CI [-.12, .20]). Overall, our results suggest that forgetting of sensitization memory represents retrieval failure.

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