Amiloride suppresses the induction of long-term potentiation in the mossy fiber pathway but not in the commissural/associational pathway of the hippocampal CA3 region

Synapse ◽  
1989 ◽  
Vol 3 (3) ◽  
pp. 286-287 ◽  
Author(s):  
Haruyuki Kamiya
Keyword(s):  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Hippocampal Ca3 ◽  
Mossy Fiber Pathway ◽  
Ca3 Region

Associative long-term potentiation (LTP) among extrinsic afferents of the hippocampal CA3 region in vivo

2002 ◽  
Vol 940 (1-2) ◽  
pp. 86-94 ◽  
Author(s):  
Carlo O. Martinez ◽  
Viet H. Do ◽  
J.L. Martinez ◽  
Brian E. Derrick
Keyword(s):  
Long Term Potentiation ◽  
Term Potentiation ◽  
Hippocampal Ca3 ◽  
Ca3 Region

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.

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

Effects of l-threo-DOPS, a noradrenaline precursor, on the long-term potentiation in the rat hippocampal mossy fiber-CA3 region

1991 ◽  
Vol 567 (2) ◽  
pp. 267-273 ◽  
Author(s):  
Norio Sakai ◽  
Masashi Sasa ◽  
Kumatoshi Ishihara ◽  
Osamu Komure ◽  
Chikako Tanaka ◽  
...  
Keyword(s):  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Ca3 Region

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

AMPA Silencing Is a Prerequisite for Developmental Long-Term Potentiation in the Hippocampal CA1 Region

2008 ◽  
Vol 100 (5) ◽  
pp. 2605-2614 ◽  
Author(s):  
Therése Abrahamsson ◽  
Bengt Gustafsson ◽  
Eric Hanse
Keyword(s):  
Developmental Stages ◽  
Long Term Potentiation ◽  
Synaptic Strength ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Silent Synapses ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca3

AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) unsilencing is an often proposed expression mechanism both for developmental long-term potentiation (LTP), involved in circuitry refinement during brain development, and for mature LTP, involved in learning and memory. In the hippocampal CA3–CA1 connection naïve (nonstimulated) synapses are AMPA signaling and AMPA-silent synapses are created from naïve AMPA-signaling (AMPA-labile) synapses by test-pulse synaptic activation (AMPA silencing). To investigate to what extent LTPs at different developmental stages are explained by AMPA unsilencing, the amount of LTP obtained at these different developmental stages was related to the amount of AMPA silencing that preceded the induction of LTP. When examined in the second postnatal week Hebbian induction was found to produce no more stable potentiation than that causing a return to the naïve synaptic strength existing prior to the AMPA silencing. Moreover, in the absence of a preceding AMPA silencing Hebbian induction produced no stable potentiation above the naïve synaptic strength. Thus this early, or developmental, LTP is nothing more than an unsilencing (dedepression) and stabilization of the AMPA signaling that was lost by the prior AMPA silencing. This dedepression and stabilization of AMPA signaling was mimicked by the presence of the protein kinase A activator forskolin. As the relative degree of AMPA silencing decreased with development, LTP manifested itself more and more as a “genuine” potentiation (as opposed to a dedepression) not explained by unsilencing and stabilization of AMPA-labile synapses. This “genuine,” or mature, LTP rose from close to nothing of total LTP prior to postnatal day (P)13, to about 70% of total LTP at P16, and to about 90% of total LTP at P30. Developmental LTP, by stabilization of AMPA-labile synapses, thus seems adapted to select synaptic connections to the growing synaptic network. Mature LTP, by instead strengthening existing stable connections between cells, may then create functionally tightly connected cell assemblies within this network.

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