scholarly journals Different Calcium Sources Are Narrowly Tuned to the Induction of Different Forms of LTP

2002 ◽  
Vol 88 (1) ◽  
pp. 249-255 ◽  
Author(s):  
Clarke R. Raymond ◽  
Stephen J. Redman
Keyword(s):  
Calcium Influx ◽  
Ryanodine Receptors ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Ip3 Receptors ◽  
Term Potentiation ◽  
Voltage Dependent ◽  
Calcium Sources

The essential role of calcium in the induction of long-term potentiation (LTP) has been well established. In particular, calcium influx via the N-methyl-d-aspartate (NMDA) receptor (NMDAR) is important for LTP induction in many pathways. However, the specific roles of other calcium sources in hippocampal LTP are less clear. The aim of the present study was to determine the appropriate conditions and extent to which non-NMDAR Ca2+ sources contribute to the induction of different forms of LTP in area CA1 of hippocampal slices. Increasing numbers of theta-burst trains (1, 4, and 8 TBS) induced LTP of increasing magnitude and persistence. Inhibition of ryanodine receptors caused inhibition of weak LTP induced by 1 TBS, but had no effect on more robust forms of LTP. Inhibition of IP3 receptors inhibited moderate LTP induced by 4 TBS, but had no effect when 1 TBS or 8 TBS were used. Inhibition of L-type voltage–dependent Ca2+ channels inhibited strong LTP induced by 8 TBS, but had no effect on weaker forms of LTP. These results show that different Ca2+ sources have different thresholds for activation by TBS trains. Furthermore, each Ca2+ source appears to be tuned to the induction of a different form of LTP. Such tuning could reflect an important link between different LTP induction and maintenance mechanisms.

scholarly journals Role of Voltage-Dependent Calcium Channel Long-Term Potentiation (LTP) and NMDA LTP in Spatial Memory

2000 ◽  
Vol 20 (24) ◽  
pp. 9272-9276 ◽  
Author(s):  
Albert M. Borroni ◽  
Harlan Fichtenholtz ◽  
Brian L. Woodside ◽  
Timothy J. Teyler
Keyword(s):  
Spatial Memory ◽  
Calcium Channel ◽  
Long Term Potentiation ◽  
Voltage Dependent Calcium Channel ◽  
Term Potentiation ◽  
Voltage Dependent

Aging Differentially Alters Forms of Long-Term Potentiation in Rat Hippocampal Area CA1

1998 ◽  
Vol 79 (1) ◽  
pp. 334-341 ◽  
Author(s):  
Subbakrishna Shankar ◽  
Timothy J. Teyler ◽  
Norman Robbins
Keyword(s):  
Calcium Channel ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Voltage Dependent Calcium Channel ◽  
Area Ca1 ◽  
Age Related ◽  
Term Potentiation ◽  
Voltage Dependent ◽  
Hippocampal Area

Shankar, Subbakrishna, Timothy J. Teyler, and Norman Robbins. Aging differentially alters forms of long-term potentiation in rat hippocampal area CA1. J. Neurophysiol. 79: 334–341, 1998. Long-term potentiation (LTP) of the Schaffer collateral/commissural inputs to CA1 in the hippocampus was shown to consist of N-methyl-d-aspartate receptor (NMDAR) and voltage-dependent calcium channel (VDCC) dependent forms. In this study, the relative contributions of these two forms of LTP in in vitro hippocampal slices from young (2 mo) and old (24 mo) Fischer 344 rats were examined. Excitatory postsynaptic potentials (EPSP) were recorded extracellularly from stratum radiatum before and after a tetanic stimulus consisting of four 200-Hz, 0.5-s trains given 5 s apart. Under control conditions, a compound LTP consisting of both forms was induced and was similar, in both time course and magnitude, in young and old animals. NMDAR-dependent LTP (nmdaLTP), isolated by the application of 10 μM nifedipine (a voltage-dependent calcium channel blocker), was significantly reduced in magnitude in aged animals. The VDCC dependent form (vdccLTP), isolated by the application of 50 μM d,l-2-amino-5-phosphonvalerate (APV), was significantly larger in aged animals. Although both LTP forms reached stable values 40–60 min posttetanus in young animals, in aged animals vdccLTP increased and nmdaLTP decreased during this time. In both young and old animals, the sum of the two isolated LTP forms approximated the magnitude of the compound LTP, and application of APV and nifedipine or genestein (a tyrosine kinase inhibitor) together blocked potentiation. These results suggest that aging causes a shift in synaptic plasticity from NMDAR-dependent mechanisms to VDCC-dependent mechanisms. The data are consistent with previous findings of increased L-type calcium current and decreased NMDAR number in aged CA1 cells and may help explain age-related deficits in learning and memory.

Role of voltage-dependent calcium channel subtypes in spinal long-term potentiation of C-fiber-evoked field potentials

Pain ◽  
2011 ◽  
Vol 152 (3) ◽  
pp. 623-631 ◽  
Author(s):  
Soichiro Ohnami ◽  
Mitsuo Tanabe ◽  
Shunji Shinohara ◽  
Keiko Takasu ◽  
Akira Kato ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Long Term Potentiation ◽  
Field Potentials ◽  
Voltage Dependent Calcium Channel ◽  
Evoked Field Potentials ◽  
Term Potentiation ◽  
C Fiber ◽  
Voltage Dependent

Caffeine-Mediated Presynaptic Long-Term Potentiation in Hippocampal CA1 Pyramidal Neurons

2003 ◽  
Vol 89 (6) ◽  
pp. 3029-3038 ◽  
Author(s):  
Eduardo D. Martín ◽  
Washington Buño
Keyword(s):  
Nmda Receptors ◽  
Glutamate Release ◽  
Ryanodine Receptors ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Cellular Mechanisms ◽  
Pipette Solution ◽  
Term Potentiation

We report a new form of long-term potentiation (LTP) in Schaffer collateral (SC)-CA1 pyramidal neuron synapses that originates presynaptically and does not require N-methyl-d-aspartate (NMDA) receptor activation nor increases in postsynaptic-free Ca2+. Using rat hippocampal slices, application of a brief “pulse” of caffeine in the bath evoked a nondecremental LTP (CAFLTP) of SC excitatory postsynaptic currents. An increased probability of transmitter release paralleled the CAFLTP, suggesting that it originated presynaptically. The P1 adenosine receptor antagonist 8-cyclopentyltheophylline and the P2 purinoreceptor antagonists suramin and piridoxal-5′-phosphate-azophenyl 2′,4′-disulphonate blocked the CAFLTP. Inhibition of Ca2+ release from caffeine/ryanodine stores by bath-applied ryanodine inhibited the CAFLTP, but ryanodine in the pipette solution was ineffective, suggesting a presynaptic effect of ryanodine. Previous induction of the “classical” LTP did not prevent the CAFLTP, suggesting that the LTP and the CAFLTP have different underlying cellular mechanisms. The CAFLTP is insensitive to the block of NMDA receptors by 2-amino-5-phosphonopentanoic acid and to Ca2+ chelation with intracellular 1,2-bis (2-aminophenoxy) ethane- N,N,N′ ,N′-tetraacetic acid, indicating that neither postsynaptic NMDA receptors nor increases in cytosolic-free Ca2+ participate in the CAFLTP. We conclude that the CAFLTP requires the interaction of caffeine with presynaptic P1, P2 purinoreceptors, and ryanodine receptors and is caused by an increased probability of glutamate release at SC terminals.

Electrical Stimuli Patterned After the Theta-Rhythm Induce Multiple Forms of LTP

2001 ◽  
Vol 86 (3) ◽  
pp. 1289-1296 ◽  
Author(s):  
S. L. Morgan ◽  
T. J. Teyler
Keyword(s):  
Calcium Influx ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Natural Activity ◽  
Term Potentiation ◽  
Voltage Dependent ◽  
Acceptable Model ◽  
Voltage Dependent Calcium Channels ◽  
Frequency Stimulation

The induction of long-term potentiation (LTP) by high-frequency stimulation is considered an acceptable model for the study of learning and memory. In area CA1 calcium influx through N-methyl-d-aspartate receptors (NMDARs; nmdaLTP) and/or L-type voltage-dependent calcium channels (vdccLTP) results in distinct forms of LTP. In the light of significant accumulation of knowledge about patterns of naturally occurring activity in the intact animal, we examined whether the application of stimuli patterned after natural activity induced nmdaLTP and/or vdccLTP. In rat hippocampal slices we examined LTP induced by three types of patterned stimulation short (S-TBS), long (L-TBS), and high-intensity long theta-patterned stimulation (HL-TBS). The patterns of stimulation were applied in control, nifedipine (blocks vdccLTP),d,l-2-amino-5-phosphonovaleric acid (APV; blocks nmdaLTP), or APV and nifedipine containing media. We found that S-TBS resulted in LTP that was completely attenuated in the presence of APV but was unaffected by nifedipine. Thus S-TBS results in the selective induction of nmdaLTP. L-TBS resulted in LTP that was completely blocked by APV and only partially blocked by nifedipine. Therefore L-TBS results in a compoundLTP consisting of both nmdaLTP and vdccLTP components. In the presence of APV, HL-TBS resulted in vdccLTP, and when APV and nifedipine were both present, LTP was completely blocked. Thus HL-TBS results in a vdccLTP in isolation when APV is present. We also examined saturation of S-TBS–induced LTP (nmdaLTP) by applying S-TBS at short intervals. When nifedipine was present, multiple S-TBS trains resulted in a substantially smaller final LTP as compared with controls. We conclude that multiple bursts of S-TBS eventually summate to result in compoundLTP. Stimuli patterned after innate rhythms in the hippocampus effectively induce nmdaLTP (S-TBS), compoundLTP (L-TBS), or vdccLTP (HL-TBS).

Characterisation of the Role of Calcium in AlF4-Induced Long-Term Potentiation in Area CA1 of Rat Hippocampus

1997 ◽  
Vol 17 (2) ◽  
pp. 209-218
Author(s):  
N. A. Breakwell ◽  
S. J. Publicover
Keyword(s):  
Calcium Influx ◽  
Long Term Potentiation ◽  
Rat Hippocampus ◽  
Protein Activator ◽  
Area Ca1 ◽  
Term Potentiation ◽  
Bath Application ◽  
The Mean

We investigated calcium influx in the long lasting potentiation induced in area CA1 of rat hippocampus by brief bath application of the G-protein activator AlF4−(NaF/AlCl3). Brief (10 min) bath application of AlF4− in standard saline (with 2mM Ca2+) consistently induced a long lasting potentiation which was not observed if AlF4− was bath-applied in nominally calcium free saline. Increasing the potential calcium influx, either by raising extracellular calcium concentration to 3.5 mM or by addition of the voltage operated calcium channel (VOCC) agonist BayK8644. failed to increase the number of slices exhibiting potentiation or the mean level of potentiation. Bath application of AlF4− in the presence of the VOCC antagonist failed to block the potentiation and AlF4− readily induced a long lasting potentiation under voltage clamp conditions, strongly suggesting that the calcium influx required for AlF4-induced potentiation is not through NMDA receptors or VOCC channels. It is suggested that the calcium required may be provided by an ongoing recharging and emptying of IP3 sensitive intracellular Ca2+ stores.

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