scholarly journals Photolysis of Postsynaptic Caged Ca2+ Can Potentiate and Depress Mossy Fiber Synaptic Responses in Rat Hippocampal CA3 Pyramidal Neurons

2004 ◽  
Vol 91 (4) ◽  
pp. 1596-1607 ◽  
Author(s):  
Jun Wang ◽  
Mark F. Yeckel ◽  
Daniel Johnston ◽  
Robert S. Zucker
Keyword(s):  
Tyrosine Kinases ◽  
Pyramidal Neurons ◽  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Ca1 Neurons ◽  
Term Potentiation ◽  
Hippocampal Ca3 ◽  
Ca3 Pyramidal Neurons ◽  
Cell Somata

The induction of mossy fiber-CA3 long-term potentiation (LTP) and depression (LTD) has been variously described as being dependent on either pre- or postsynaptic factors. Some of the postsynaptic factors for LTP induction include ephrin-B receptor tyrosine kinases and a rise in postsynaptic Ca2+ ([Ca2+]i). Ca2+ is also believed to be involved in the induction of the various forms of LTD at this synapse. We used photolysis of caged Ca2+ compounds to test whether a postsynaptic rise in [Ca2+]i is sufficient to induce changes in synaptic transmission at mossy fiber synapses onto rat hippocampal CA3 pyramidal neurons. We were able to elevate postsynaptic [Ca2+]i to approximately 1 μm for a few seconds in pyramidal cell somata and dendrites. We estimate that CA3 pyramidal neurons have approximately fivefold greater endogenous Ca2+ buffer capacity than CA1 neurons, limiting the rise in [Ca2+]i achievable by photolysis. This [Ca2+]i rise induced either a potentiation or a depression at mossy fiber synapses in different preparations. Neither the potentiation nor the depression was accompanied by consistent changes in paired-pulse facilitation, suggesting that these forms of plasticity may be distinct from synaptically induced LTP and LTD at this synapse. Our results are consistent with a postsynaptic locus for the induction of at least some forms of synaptic plasticity at mossy fiber synapses.

Quantal mechanism of long-term potentiation in hippocampal mossy-fiber synapses

1994 ◽  
Vol 71 (6) ◽  
pp. 2552-2556 ◽  
Author(s):  
Z. Xiang ◽  
A. C. Greenwood ◽  
E. W. Kairiss ◽  
T. H. Brown
Keyword(s):  
Pyramidal Neurons ◽  
Mossy Fiber ◽  
Classical Method ◽  
Brain Slices ◽  
Long Term Potentiation ◽  
Quantal Size ◽  
Term Potentiation ◽  
Before And After ◽  
Whole Cell Recordings

1. The quantal mechanism underlying the expression of long-term potentiation (LTP) was studied in the mossy-fiber (mf) synapses of the rat hippocampus. Whole-cell recordings were used to measure the excitatory postsynaptic currents (EPSCs) before and after LTP induction in brain slices maintained at 31 +/- 1 degrees C. 2. Evoked EPSCs were recorded from 473 CA3 pyramidal neurons. The mf synapses were stimulated using paired pulses (40-ms interpulse interval) repeated every 2–10 s. At least 400 pairs of mf responses were obtained before and during the expression of LTP, which was produced by high-frequency (100 Hz) mf stimulation. Sufficiently stationary data were obtained from five neurons that exhibited LTP and that also satisfied strict criteria and procedures that are necessary for eliciting and identifying unitary mf responses. 3. Three independent lines of evidence implicated a presynaptic component to the mechanism underlying mf LTP. The first was based on a graphical version of the classical method of variance. The graphical variance (GV) method was evaluated by clamping the cell at two different holding potentials during paired-pulse facilitation (PPF). The results indicated that the GV method can distinguish changes in mean quantal content m and mean quantal size q in rat mf synapses. The same analysis, when applied to PPF before and after LTP induction, indicated that both result from an increase in m. 4. The second line of evidence was based on the classical method of failures. Consistent with the inference that mf LTP is due to an increase in m, there was a statistically significant reduction in the number of quantal release failures.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Synaptic plasticity and cognitive function are disrupted in the absence of Lrp4

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Andrea M Gomez ◽  
Robert C Froemke ◽  
Steven J Burden
Keyword(s):  
Long Term Potentiation ◽  
Neurological Deficits ◽  
Spine Density ◽  
Ca1 Neurons ◽  
Form And Function ◽  
Term Potentiation ◽  
Hippocampal Ca3 ◽  
And Function ◽  
Apical Dendrites

Lrp4, the muscle receptor for neuronal Agrin, is expressed in the hippocampus and areas involved in cognition. The function of Lrp4 in the brain, however, is unknown, as Lrp4−/− mice fail to form neuromuscular synapses and die at birth. Lrp4−/− mice, rescued for Lrp4 expression selectively in muscle, survive into adulthood and showed profound deficits in cognitive tasks that assess learning and memory. To learn whether synapses form and function aberrantly, we used electrophysiological and anatomical methods to study hippocampal CA3–CA1 synapses. In the absence of Lrp4, the organization of the hippocampus appeared normal, but the frequency of spontaneous release events and spine density on primary apical dendrites were reduced. CA3 input was unable to adequately depolarize CA1 neurons to induce long-term potentiation. Our studies demonstrate a role for Lrp4 in hippocampal function and suggest that patients with mutations in Lrp4 or auto-antibodies to Lrp4 should be evaluated for neurological deficits.

scholarly journals Postsynaptic Expression of a New Calcium Pathway in Hippocampal CA3 Neurons and Its Influence on Mossy Fiber Long-Term Potentiation

2002 ◽  
Vol 22 (11) ◽  
pp. 4312-4320 ◽  
Author(s):  
Wataru Kakegawa ◽  
Nobuaki Yamada ◽  
Masae Iino ◽  
Kimihiko Kameyama ◽  
Tatsuya Umeda ◽  
...  
Keyword(s):  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Hippocampal Ca3 ◽  
Ca3 Neurons

scholarly journals Synapsin I deficiency results in the structural change in the presynaptic terminals in the murine nervous system.

1995 ◽  
Vol 131 (6) ◽  
pp. 1789-1800 ◽  
Author(s):  
Y Takei ◽  
A Harada ◽  
S Takeda ◽  
K Kobayashi ◽  
S Terada ◽  
...  
Keyword(s):  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Synapsin I ◽  
Term Potentiation ◽  
Gene Mutant ◽  
Associated Proteins ◽  
Hippocampal Ca3

Synapsin I is one of the major synaptic vesicle-associated proteins. Previous experiments implicated its crucial role in synaptogenesis and transmitter release. To better define the role of synapsin I in vivo, we used gene targeting to disrupt the murine synapsin I gene. Mutant mice lacking synapsin I appeared to develop normally and did not have gross anatomical abnormalities. However, when we examined the presynaptic structure of the hippocampal CA3 field in detail, we found that the sizes of mossy fiber giant terminals were significantly smaller, the number of synaptic vesicles became reduced, and the presynaptic structures altered, although the mossy fiber long-term potentiation remained intact. These results suggest significant contribution of synapsin I to the formation and maintenance of the presynaptic structure.

Maintenance of long-term potentiation in hippocampal mossy fiber-CA3 pathway requires fine-tuned MMP-9 proteolytic activity

Hippocampus ◽  
2013 ◽  
Vol 23 (6) ◽  
pp. 529-543 ◽  
Author(s):  
Grzegorz Wiera ◽  
Grazyna Wozniak ◽  
Malgorzata Bajor ◽  
Leszek Kaczmarek ◽  
Jerzy W. Mozrzymas
Keyword(s):  
Proteolytic Activity ◽  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Term Potentiation
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