scholarly journals Activity-Dependent Potentiation of Synaptic Transmission From L30 Inhibitory Interneurons of Aplysia Depends on Residual Presynaptic Ca2+ But Not on Postsynaptic Ca2+

1997 ◽  
Vol 78 (4) ◽  
pp. 2061-2071 ◽  
Author(s):  
Thomas M. Fischer ◽  
Robert S. Zucker ◽  
Thomas J. Carew
Keyword(s):  
Synaptic Transmission ◽  
Time Course ◽  
Common Property ◽  
Free Calcium ◽  
Inhibitory Interneurons ◽  
Short Term ◽  
Intracellular Ca ◽  
Frequency Facilitation ◽  
Activity Dependent

Fischer, Thomas M., Robert S. Zucker, and Thomas J. Carew. Activity-dependent potentiation of synaptic transmission from L30 inhibitory interneurons of Aplysia depends on residual presynaptic Ca2+ but not on postsynaptic Ca2+. J. Neurophysiol. 78: 2061–2071, 1997. Activity-induced short-term synaptic enhancement (STE) is a common property of neurons, one that can endow neural circuits with the capacity for rapid and flexible information processing. Evidence from a variety of systems indicates that the expression of STE depends largely on the action of residual Ca2+, which enters the presynaptic terminal during activity. We have shown previously that a Ca2+-dependent STE in the inhibitory synapse between interneurons L30 and L29 in the abdominal ganglion of Aplysia californica has a functional role in regulating the gain of the siphon withdrawal circuit through facilitated recurrent inhibition onto the L29s. In the present paper, we further explore the role of Ca2+ in L30 STE by examining two basic issues: 1) What is the role of residual presynaptic Ca2+ in the maintenance of L30 STE? We examine this question by first inducing STE in the L30s then rapidly buffering presynaptic free calcium through the use of the photoactivated Ca2+ chelator diazo-4, which was preloaded into the L30 neurons. Three forms of STE in the L30s were examined: frequency facilitation (FF), augmentation (AUG), and posttetanic potentiation (PTP). In each case, the activation-induced enhancement of the L30 to L29 synapse was reduced to preactivation levels at the first test pulse following photolysis of diazo-4. 2) What is the role of postsynaptic Ca2+ in the induction of L30 STE? We examine whether there is a postsynaptic requirement of elevated Ca2+ for the induction of L30 STE by first injecting the calcium chelator bis-( o-aminophenoxy)- N,N,N′,N′-tetraacetic acid (BAPTA) into the postsynaptic cell L29 (at levels sufficient to block transmitter release from the L29s), to prevent any increase in postsynaptic intracellular Ca2+ that may occur during L30 (presynaptic) activation. We found that BAPTA injection did not effect either the induction or the time course of FF, AUG, or PTP in the L30s. Taken collectively, our data indicate that all forms of STE in the L30s depend on presynaptic free cytosolic Ca2+ for their maintenance but do not require the elevation of postsynaptic Ca2+ for their induction.

scholarly journals Role of Apamin-Sensitive KCa Channels for Reticulospinal Synaptic Transmission to Motoneuron and for the Afterhyperpolarization

2002 ◽  
Vol 88 (1) ◽  
pp. 289-299 ◽  
Author(s):  
Lorenzo Cangiano ◽  
Peter Wallén ◽  
Sten Grillner
Keyword(s):  
Synaptic Transmission ◽  
Nmda Receptors ◽  
Time Course ◽  
Frequency Regulation ◽  
Similar Time ◽  
Calcium Dependent ◽  
Before And After ◽  
Voltage Dependent ◽  
Intracellular Ca

Single motoneurons and pairs of a presynaptic reticulospinal axon and a postsynaptic motoneuron were recorded in the isolated lamprey spinal cord, to investigate the role of calcium-dependent K+ channels (KCa) during the afterhyperpolarization following the action potential (AHP), and glutamatergic synaptic transmission on the dendritic level. The AHP consists of a fast phase due to transient K+ channels (fAHP) and a slower phase lasting 100–200 ms (sAHP), being the main determinant of spike frequency regulation. We now present evidence that the sAHP has two components. The larger part, around 80%, is abolished by superfusion of Cd2+ (blocker of voltage-dependent Ca2+ channels), by intracellular injection of 1,2-bis-( 2-aminophenoxy)-ethane- N,N,N′,N′-tetraacetic acid (BAPTA; fast Ca2+ chelator), and by apamin (selective toxin for KCa channels of the SK subtype). While 80% of the sAHP is thus due to KCa channels, the remaining 20% is not mediated by Ca2+, either entering through voltage-dependent Ca2+ channels or released from intracellular Ca2+ stores. This Ca2+-independent sAHP component has a similar time course as the KCa portion and is not due to a Cl− conductance. It may be caused by Na+-activated K+ channels. Glutamatergic excitatory postsynaptic potentials (EPSPs) evoked by single reticulospinal axons give rise to a local Ca2+ increase in the postsynaptic dendrite, mediated in part by N-methyl-d-aspartate (NMDA) receptors. The Ca2+ levels remain elevated for several hundred milliseconds and could be expected to activate KCa channels. If so, this activation should cause a local conductance increase in the dendrite that would shunt EPSPs following the first EPSP in a spike train. We have tested this in reticulospinal/motoneuronal pairs, by stimulating the presynaptic axon with spike trains at different frequencies. We compared the first EPSP and the following EPSPs in the control and after blockade with apamin. No difference was observed in EPSP amplitude or shape before and after apamin, either in normal Ringer or in Mg2+-free Ringer removing the voltage-dependent block of NMDA receptors. In conclusion, the local Ca2+ entry during reticulospinal EPSPs does not cause an activation of KCa channels sufficient to affect the efficacy of synaptic transmission. Thus the integration of synaptic signals at the dendritic level in motoneurons appears simpler than would otherwise have been the case.

Pharmacological and kinetic characterization of two functional classes of serotonergic modulation in Aplysia sensory neurons

1996 ◽  
Vol 75 (2) ◽  
pp. 855-866 ◽  
Author(s):  
L. L. Stark ◽  
A. R. Mercer ◽  
N. J. Emptage ◽  
T. J. Carew
Keyword(s):  
Synaptic Transmission ◽  
Sensory Neurons ◽  
Time Course ◽  
Behavioral Sensitization ◽  
Input Resistance ◽  
Short Term ◽  
Synaptic Facilitation ◽  
Functional Classes ◽  
Kinetics Of ◽  
Serotonergic Modulation

1. Modulation of mechanoafferent sensory neurons (SNs) by the neutrotransmitter serotonin (5HT) plays a significant role in behavioral sensitization of several withdrawal reflexes in Aplysia. The modulatory effects of 5HT on these SNs include increased excitability, increased input resistance, action potential broadening, and increased synaptic transmission. Based on a previously described dissociation of some of these modulatory effects, revealed with the 5HT-receptor antagonist, cyproheptadine, we investigated whether a similar dissociation could be found by systematically varying the concentration of the endogenous agonist, 5HT. 2. We first applied a range of 5HT concentrations to isolated pleural/pedal ganglia (containing tail SNs and tail motor neurons, respectively), and measured the magnitude of 5HT-induced modulation of spike broadening and increased excitability. The resulting dose-response curve showed that both forms of modulation increase monotonically as a function of 5HT concentration, but that excitability has a lower threshold for modulation by 5HT than does spike duration. 3. We further characterized the modulatory effects of 5HT on Aplysia SNs by comparing the time course of onset of modulation by 5HT and the time course of recovery after washout. Independent of 5HT concentration, modulation of excitability increases rapidly in the presence of 5HT and recovers rapidly (< 3 min) after washout. Similarly, input resistance increases and recovers rapidly, mirroring the profile of increased excitability. However, modulation of spike duration exhibits two profiles, dependent on 5HT concentration. Low concentrations of 5HT (0.5 and 1 microM) induce a rapid-onset and transient-recovery form of spike broadening, which resembles the kinetics of increased excitability and increased input resistance. Higher concentrations of 5HT (2.5 and 5 microM) induce a more slowly developing and prolonged-recovery form of spike broadening (> 9 min). At these higher concentrations, the recovery profile for prolonged spike broadening is significantly different from those observed for both increased excitability and increased input resistance. 4. We next compared the relationship between spike broadening and short-term synaptic facilitation. We found that significant facilitation of synaptic transmission requires a high 5HT concentration, which is comparable with that required to induce prolonged spike broadening. Similarly, the recovery profiles for spike broadening and synaptic facilitation are strikingly similar, recovering in parallel. 5. Our experiments show that the modulatory effects of 5HT in the tail SNs can be dissociated both by their sensitivity to different concentrations of 5HT and by their kinetics of serotonergic modulation. Based on these results, together with extensive evidence from other laboratories, we propose that the short-term modulatory effects of 5HT fall into two distinct functional classes. The first class, which includes excitability, input resistance, and transient spike broadening, has a low threshold for 5HT modulation and recovers rapidly. The second class, which includes prolonged spike broadening and short-term synaptic facilitation, has a higher threshold for modulation and recovers more slowly. It now will be of interest to determine the functional contribution of each of these classes to different aspects of sensitization.

Ryanodine-Sensitive Stores Regulate the Excitability of AH Neurons in the Myenteric Plexus of Guinea-Pig Ileum

2000 ◽  
Vol 84 (6) ◽  
pp. 2777-2785 ◽  
Author(s):  
K. Hillsley ◽  
J. L. Kenyon ◽  
T. K. Smith
Keyword(s):  
Sensory Processing ◽  
Calcium Release ◽  
Excitatory Postsynaptic Potential ◽  
Similar Time ◽  
Intracellular Ca ◽  
Time Courses ◽  
High Concentrations ◽  
Calcium Induced Calcium Release ◽  
Activity Dependent

Myenteric afterhyperpolarizing (AH) neurons are primary afferent neurons within the gastrointestinal tract. Stimulation of the intestinal mucosa evokes action potentials (AP) that are followed by a slow afterhyperpolarization (AHPslow) in the soma. The role of intracellular Ca2+ ([Ca2+]i) and ryanodine-sensitive Ca2+ stores in modulating the electrical activity of myenteric AH neurons was investigated by recording membrane potential and bis-fura-2 fluorescence from 34 AH neurons. Mean resting [Ca2+]i was ∼200 nM. Depolarizing current pulses that elicited APs evoked AHPslow and an increase in [Ca2+]i, with similar time courses. The amplitudes and durations of AHPslow and the Ca2+ transient were proportional to the number of evoked APs, with each AP increasing [Ca2+]i by ∼50 nM. Ryanodine (10 μM) significantly reduced both the amplitude and duration (by 60%) of the evoked Ca2+ transient and AHPslow over the range of APs tested (1–15). Calcium-induced calcium release (CICR) was graded and proportional to the number of APs, with each AP triggering a rise in [Ca2+]i of ∼30 nM Ca2+ via CICR. This indicates that CICR amplifies Ca2+ influx. Similar changes in [Ca2+]i and AHPslow were evoked by two APs in control and six APs in ryanodine. Thus, the magnitude of the change in bulk [Ca2+]i and not the source of the Ca2+ is the determinant of the magnitude of AHPslow. Furthermore, lowering of free [Ca2+]i, either by reducing extracellular Ca2+ or injecting high concentrations of Ca2+buffer, induced depolarization, increased excitability, and abolition of AHPslow. In addition, activation of synaptic input to AH neurons elicited a slow excitatory postsynaptic potential (sEPSP) that was completely blocked in ryanodine. These results demonstrate the importance of [Ca2+]i and CICR in sensory processing in AH neurons. Activity-dependent CICR may be a mechanism to grade the output of AH neurons according to the intensity of sensory input.

scholarly journals Intracellular Ca2+Stores and Ca2+Influx Are Both Required for BDNF to Rapidly Increase Quantal Vesicular Transmitter Release

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Michelle D. Amaral ◽  
Lucas Pozzo-Miller
Keyword(s):  
Transmitter Release ◽  
Time Course ◽  
Pyramidal Neurons ◽  
Receptor Activation ◽  
Trpc Channels ◽  
Styryl Dyes ◽  
Trkb Receptors ◽  
Mepsc Frequency ◽  
Intracellular Ca

Brain-derived neurotrophic factor (BDNF) is well known as a survival factor during brain development as well as a regulator of adult synaptic plasticity. One potential mechanism to initiate BDNF actions is through its modulation of quantal presynaptic transmitter release. In response to local BDNF application to CA1 pyramidal neurons, the frequency of miniature excitatory postsynaptic currents (mEPSC) increased significantly within 30 seconds; mEPSC amplitude and kinetics were unchanged. This effect was mediated via TrkB receptor activation and required both full intracellular Ca2+stores as well as extracellular Ca2+. Consistent with a role of Ca2+-permeable plasma membrane channels of the TRPC family, the inhibitor SKF96365 prevented the BDNF-induced increase in mEPSC frequency. Furthermore, labeling presynaptic terminals with amphipathic styryl dyes and then monitoring their post-BDNF destaining in slice cultures by multiphoton excitation microscopy revealed that the increase in frequency of mEPSCs reflects vesicular fusion events. Indeed, BDNF application to CA3-CA1 synapses in TTX rapidly enhanced FM1-43 or FM2-10 destaining with a time course that paralleled the phase of increased mEPSC frequency. We conclude that BDNF increases mEPSC frequency by boosting vesicular fusion through a presynaptic, Ca2+-dependent mechanism involving TrkB receptors, Ca2+stores, and TRPC channels.

Effect of ionophore A23187 on cytosolic Ca2+ and enzyme secretion

1982 ◽  
Vol 243 (3) ◽  
pp. C196-C199 ◽  
Author(s):  
R. J. Stark ◽  
J. O'Doherty
Keyword(s):  
Cell Activation ◽  
Narrow Range ◽  
Acinar Cells ◽  
Enzyme Secretion ◽  
Free Calcium ◽  
Ionophore A23187 ◽  
Amylase Release ◽  
Intracellular Ca ◽  
The Mean

As the ionophore A23187 is believed to act by increasing cytosolic Ca2+ ([Ca]i), it offers a mechanism for experimentally controlling [Ca]i. Ca2+-selective microelectrodes were employed to examine the effect of A23187 on [Ca]i and the role of [Ca]i in acinar secretion. The mean [Ca]i in acinar cells of the mouse pancreas was determined to be 0.43 +/- 0.03 microM. When the ionophore was added to the saline bathing the acinar cells, 10(-6) M A23187 depolarized the membrane potential (Em) by 5.2 +/- 0.3 mM and the intracellular Ca-electrode potential (ECs) by 9.8 +/- 0.6 while 10(-5) M A23187 depolarized Em by 7.4 +/- 0.3 mV and ECs by 14.1 +/- 0.8. These changes in potentials reflect an increase in [Ca]i to 0.62 +/- 0.03 microM with 10(-6) M and 0.73 +/- 0.05 microM with 10(-5) M A23187. The increase in [Ca]i observed with 10(-6) M A23187 was similar to that found with concentrations of acetylcholine (Ach) that produced maximal enzyme secretion, whereas the increase in [Ca]i with 10(-5) M was similar in magnitude to that observed with ACh concentration that inhibited or reduced secretion. Measurements of amylase release during 30 min exposure of A23187 produced an 88.4% increase in amylase activity over basal levels with 10(-6) M and little or no change with (10(-5) M, indicating that the ionophore influences secretion through changes in [Ca]i in a manner analogous to the natural secretagogue ACh. This report establishes that acinar secretion occurs only within a narrow range of [Ca]i activities and suggests intracellular increases in both "bound" and "free" calcium may occur during cell activation.

scholarly journals Galactocerebroside is expressed by non-myelin-forming Schwann cells in situ.

1985 ◽  
Vol 101 (3) ◽  
pp. 1135-1143 ◽  
Author(s):  
K R Jessen ◽  
L Morgan ◽  
M Brammer ◽  
R Mirsky
Keyword(s):  
Schwann Cells ◽  
Time Course ◽  
In Utero ◽  
Sympathetic Trunk ◽  
Short Term ◽  
Cultured Schwann Cells ◽  
Cervical Sympathetic ◽  
Time Courses

Interest in the glycosphingolipid galactocerebroside (GC) is based on the consensus that in the nervous system it is expressed only by myelin-forming Schwann cells and oligodendrocytes, and that it has a specific role in the elaboration of myelin sheaths. We have investigated GC distribution in two rat nerves--the sciatic, containing a mixture of myelinated and non-myelinated axons, and the cervical sympathetic trunk, in which greater than 99% of axons are non-myelinated. Immunohistochemical experiments using mono- and polyclonal GC antibodies were carried out on teased nerves and cultured Schwann cells, and GC synthesis was assayed biochemically. Unexpectedly, we found that mature non-myelin-forming Schwann cells in situ and in short-term cultures express unambiguous GC immunoreactivity, comparable in intensity to that of myelinated fibers or myelin-forming cells in short-term cultures. GC synthesis was also detected in both sympathetic trunks and sciatic nerves. In the developing sympathetic trunk, GC was first seen at day 19 in utero, the number of GC-positive cells rising to approximately 95% at postnatal day 10. In contrast, the time course of GC appearance in the sciatic nerve shows two separate phases of increase, between day 18 in utero and postnatal day 1, and between postnatal days 20 and 35, at which stage approximately 94% of the cells express GC. These time courses suggest that Schwann cells, irrespective of subsequent differentiation pathway, start expressing GC at about the same time as cell division stops. We suggest that GC is a ubiquitous component of mature Schwann cell membranes in situ. Therefore, the role of GC needs to be reevaluated, since its function is clearly not restricted to events involved in myelination.

scholarly journals Loss of Ryanodine Receptor 2 impairs neuronal activity-dependent remodeling of dendritic spines and triggers compensatory neuronal hyperexcitability

2020 ◽  
Vol 27 (12) ◽  
pp. 3354-3373
Author(s):  
Fabio Bertan ◽  
Lena Wischhof ◽  
Liudmila Sosulina ◽  
Manuel Mittag ◽  
Dennis Dalügge ◽  
...  
Keyword(s):  
Ryanodine Receptor ◽  
Neuronal Activity ◽  
Dendritic Spines ◽  
Pyramidal Neurons ◽  
Excitatory Synapses ◽  
Structural And Functional Properties ◽  
Intracellular Ca ◽  
Memory Acquisition ◽  
Activity Dependent

AbstractDendritic spines are postsynaptic domains that shape structural and functional properties of neurons. Upon neuronal activity, Ca2+ transients trigger signaling cascades that determine the plastic remodeling of dendritic spines, which modulate learning and memory. Here, we study in mice the role of the intracellular Ca2+ channel Ryanodine Receptor 2 (RyR2) in synaptic plasticity and memory formation. We demonstrate that loss of RyR2 in pyramidal neurons of the hippocampus impairs maintenance and activity-evoked structural plasticity of dendritic spines during memory acquisition. Furthermore, post-developmental deletion of RyR2 causes loss of excitatory synapses, dendritic sparsification, overcompensatory excitability, network hyperactivity and disruption of spatially tuned place cells. Altogether, our data underpin RyR2 as a link between spine remodeling, circuitry dysfunction and memory acquisition, which closely resemble pathological mechanisms observed in neurodegenerative disorders.

Role of Membrane Potential in Calcium Signaling During Rhythmic Bursting in Tritonia Swim Interneurons

2007 ◽  
Vol 97 (3) ◽  
pp. 2204-2214 ◽  
Author(s):  
Evan S. Hill ◽  
Paul S. Katz
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Laser Scanning ◽  
Time Course ◽  
Motor Pattern ◽  
Confocal Laser Scanning Microscope ◽  
Confocal Laser ◽  
Intracellular Ca ◽  
Potential Waveform

Rhythmic bursting in neurons is accompanied by dynamic changes in intracellular Ca2+ concentration. These Ca2+ signals may be caused by membrane potential changes during bursting and/or by synaptic inputs. We determined that membrane potential is responsible for most, if not all, of the cytoplasmic Ca2+ signal recorded during rhythmic bursting in two neurons of the escape swim central pattern generator (CPG) of the mollusk, Tritonia diomedea: ventral swim interneuron B (VSI) and cerebral neuron 2 (C2). Ca2+ signals were imaged with a confocal laser scanning microscope while the membrane potential was recorded at the soma. During the swim motor pattern (SMP), Ca2+ signals in both neurons transiently increased during each burst of action potentials with a more rapid decay in secondary than in primary neurites. VSI and C2 were then voltage-clamped at the soma, and each neuron's own membrane potential waveform recorded during the SMP was played back as the voltage command. In all regions of VSI, this completely reproduced the amplitude and time course of Ca2+ signals observed during the SMP, but in C2, the amplitude was lower in the playback experiments than during the SMP, possibly due to space clamp problems. Therefore in VSI, the cytoplasmic Ca2+ signal during the SMP can be accounted for by its membrane potential excursions, whereas in C2 the membrane potential excursions can account for most of the SMP Ca2+ signal.

scholarly journals Attenuated Late-PhaseArcTranscription in the Dentate Gyrus of Mice LackingEgr3

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Amanda Maple ◽  
Rachel E. Lackie ◽  
Diana I. Elizalde ◽  
Stephanie L. Grella ◽  
Chelsey C. Damphousse ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Time Course ◽  
Wild Type ◽  
Short Term ◽  
Unique Role ◽  
Late Protein ◽  
Dependent Learning

The dentate gyrus (DG) engages in sustainedArctranscription for at least 8 hours following behavioral induction, and this time course may be functionally coupled to the unique role of the DG in hippocampus-dependent learning and memory. The factors that regulate long-term DGArcexpression, however, remain poorly understood. Animals lackingEgr3show lessArcexpression following convulsive stimulation, but the effect ofEgr3ablation on behaviorally inducedArcremains unknown. To address this,Egr3−/−and wild-type (WT) mice explored novel spatial environments and were sacrificed either immediately or after 5, 60, 240, or 480 minutes, andArcexpression was quantified by fluorescence in situ hybridization. Although short-term (i.e., within 60 min)Arcexpression was equivalent across genotypes, DGArcexpression was selectively reduced at 240 and 480 minutes in mice lackingEgr3. These data demonstrate the involvement ofEgr3in regulating the late protein-dependent phase ofArcexpression in the DG.

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