Long-term cell culture of electrically active sensory neurons free of glial cells

1977 ◽  
Vol 5 (3-4) ◽  
pp. 153-157 ◽  
Author(s):  
Ellen Rieske ◽  
Georg W. Kreutzberg
Keyword(s):  
Cell Culture ◽  
Sensory Neurons ◽  
Glial Cells

Long-term depression of Aplysia sensorimotor synapses in cell culture: inductive role of a rise in postsynaptic calcium

1996 ◽  
Vol 76 (3) ◽  
pp. 2111-2114 ◽  
Author(s):  
X. Y. Lin ◽  
D. L. Glanzman
Keyword(s):  
Cell Culture ◽  
Synaptic Plasticity ◽  
Sensory Neurons ◽  
Tetraacetic Acid ◽  
Short Term ◽  
Long Term Depression ◽  
Central Synapses ◽  
Postsynaptic Calcium

1. Activation of sensory neurons at 2 Hz for 15 min induces long-term depression (LTD) of isolated Aplysia sensorimotor synapses in cell culture. 2. Prior infusion of the Ca2+ chelator 1,2-bis-(2-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (BAPTA) into the postsynaptic motor neuron blocks the induction of LTD, but not short-term synaptic depression. 3. Invertebrate central synapses possess the capacity for LTD. This form of long-term synaptic plasticity may play an important role in learning in Aplysia.

scholarly journals Long-Term Effects of Axotomy on Excitability and Growth of Isolated Aplysia Sensory Neurons in Cell Culture: Potential Role of cAMP

1998 ◽  
Vol 79 (3) ◽  
pp. 1371-1383 ◽  
Author(s):  
Supinder S. Bedi ◽  
Ali Salim ◽  
Shanping Chen ◽  
David L. Glanzman
Keyword(s):  
Cell Culture ◽  
Sensory Neurons ◽  
Potential Role ◽  
Morphological Changes ◽  
Axonal Injury ◽  
Long Term Effects ◽  
Cellular Processes ◽  
Neuritic Outgrowth

Bedi, Supinder S., Ali Salim, Shanping Chen, and David L. Glanzman. Long-term effects of axotomy on excitability and growth of isolated Aplysia sensory neurons in cell culture: potential role of cAMP. J. Neurophysiol. 79: 1371–1383, 1998. Crushing nerves, which contain the axons of central sensory neurons, in Aplysia causes the neurons to become hyperexcitable and to sprout new processes. Previous experiments that examined the effects of axonal injury on Aplysia sensory neurons have been performed in the intact animal or in the semi-intact CNS of Aplysia. It therefore has been unclear to what extent the long-term neuronal consequences of injury are due to intrinsic or extrinsic cellular signals. To determine whether injury-induced changes in Aplysia sensory neurons are due to intrinsic or extrinsic signals, we have developed an in vitro model of axonal injury. Isolated central sensory neurons grown for 2 days in cell culture were axotomized. Approximately 24 h after axotomy, sensory neurons exhibited a greater excitability—reflected, in part, as a significant reduction in spike accommodation—and greater neuritic outgrowth than did control (unaxotomized) neurons. Rp diastereoisomer of the cyclic adenosine 3′,5′-monophosphorothiate (Rp-cAMPS), an inhibitor of protein kinase A, blocked both the reduction in accommodation and increased neuritic outgrowth induced by axotomy. Rp-cAMPS also blocked similar, albeit smaller, alterations observed in control sensory neurons during the 24-h period of our experiments. These results indicate that axonal injury elevates cAMP levels within Aplysia sensory neurons, and that this elevation is directly responsible, in part, for the previously described long-term electrophysiological and morphological changes induced in Aplysia sensory neurons by nerve crush. In addition, the results indicate that control sensory neurons in culture are also undergoing injury-related electrophysiological and structural changes, probably due to cellular processes triggered when the neurons are axotomized during cell culturing. Finally, the results provide support for the idea that the cellular processes activated within Aplysia sensory neurons by injury, and those activated during long-term behavioral sensitization, overlap significantly.

Distribution and Function of GABAB Receptors in Spider Peripheral Mechanosensilla

2003 ◽  
Vol 90 (4) ◽  
pp. 2571-2580 ◽  
Author(s):  
Izabela Panek ◽  
Shannon Meisner ◽  
Päivi H. Torkkeli
Keyword(s):  
Sensory Neurons ◽  
Glial Cells ◽  
Gaba Receptors ◽  
Synaptic Vesicles ◽  
Sensory Cell ◽  
Gabab Receptors ◽  
Long Term Effects ◽  
And Function ◽  
Receptor Antibodies

The mechanosensilla in spider exoskeleton are innervated by bipolar neurons with their cell bodies close to the cuticle and dendrites attached to it. Numerous efferent fibers synapse with peripheral parts of the mechanosensory neurons, with glial cells surrounding the neurons, and with each other. Most of these efferent fibers are immunoreactive to γ-aminobutyric acid (GABA), and the sensory neurons respond to agonists of ionotropic GABA receptors with a rapid and complete inhibition. In contrast, little is known about metabotropic GABAB receptors that may mediate long-term effects. We investigated the distribution of GABAB receptors on spider leg mechanosensilla using specific antibodies against 2 proteins needed to form functional receptors and an antibody that labels the synaptic vesicles on presynaptic sites. Both anti-GABAB receptor antibodies labeled the distal parts of the sensory cell bodies and dendrites but anti-GABABR1 immunoreactivity was also found in the axons and proximal parts of the cell bodies and some glial cells. The fine efferent fibers that branch on top of the sensory neurons did not show GABAB receptor immunoreactivity but were densely labeled with anti-synapsin and indicated synaptic vesicles on presynaptic locations to the GABAB receptors. Intracellular recordings from sensory neurons innervating the slit sensilla of the spider legs revealed that application of GABAB receptor agonists attenuated voltage-activated Ca2+ current and enhanced voltage-activated outward K+ current, providing 2 possible mechanisms for controlling the neurons' excitability. These findings support the hypothesis that GABAB receptors are present in the spider mechanosensilla where their activation may modulate information transmission.

cAMP and arachidonic acid simulate long-term structural and functional changes produced by neurotransmitters in aplysia sensory neurons

Neuron ◽  
1993 ◽  
Vol 10 (6) ◽  
pp. 1079-1088 ◽  
Author(s):  
Samuel Schacher ◽  
Eric R. Kandel ◽  
PierGiorgio Montarolo
Keyword(s):  
Arachidonic Acid ◽  
Sensory Neurons ◽  
Functional Changes

Sensory Neurons With Activated Caspase-3 Survive Long-Term Experimental Diabetes

Diabetes ◽  
2003 ◽  
Vol 52 (9) ◽  
pp. 2363-2371 ◽  
Author(s):  
C. Cheng ◽  
D. W. Zochodne
Keyword(s):  
Sensory Neurons ◽  
Caspase 3 ◽  
Experimental Diabetes

Long-term sensitization in Aplysia: biophysical correlates in tail sensory neurons

Science ◽  
1987 ◽  
Vol 235 (4789) ◽  
pp. 685-687 ◽  
Author(s):  
K. Scholz ◽  
J. Byrne
Keyword(s):  
Sensory Neurons

Design and development of microbioreactors for long-term cell culture in controlled oxygen microenvironments

2011 ◽  
Vol 14 (1) ◽  
pp. 145-152 ◽  
Author(s):  
Hasan E. Abaci ◽  
Raghavendra Devendra ◽  
Quinton Smith ◽  
Sharon Gerecht ◽  
German Drazer
Keyword(s):  
Cell Culture ◽  
Design And Development

scholarly journals Induction of long-term facilitation in Aplysia sensory neurons by local application of serotonin to remote synapses

1993 ◽  
Vol 90 (23) ◽  
pp. 11411-11415 ◽  
Author(s):  
G A Clark ◽  
E R Kandel
Keyword(s):  
Gene Expression ◽  
Sensory Neurons ◽  
Cell Body ◽  
Sensory Cells ◽  
Target Cells ◽  
Synaptic Terminals ◽  
Dissociated Cell Culture ◽  
Synaptic Changes ◽  
Long Term Facilitation

Long-term synaptic facilitation at the connections of Aplysia sensory neurons onto their target cells involves alterations in gene expression. How then are the relevant cellular signals for the induction and expression of long-term synaptic changes conveyed between the nucleus and remote synaptic terminals? We have explored this question using a set of remote, peripheral terminals of siphon sensory cells, which are approximately 3 cm from the sensory cell body in the abdominal ganglion. We found that these remote synapses, like the proximal synapses previously studied in dissociated cell culture, can exhibit long-term facilitation 24 hr after cell-wide serotonin application. Furthermore, serotonin applications restricted to the remote synaptic terminals nevertheless produced long-term facilitation, indicating that signals generated in synaptic regions can trigger the long-term process, perhaps via retrograde signals to the nucleus to modify gene expression, followed by anterograde signals back to the terminal. Serotonin applications restricted to the cell body and proximal synapses of the sensory neuron also produced long-term facilitation at remote synapses, although to a lesser extent, suggesting that long-term facilitation is expressed cell-wide, but that superimposed on this cell-wide facilitation there appears to be a component that is synapse-specific.

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