WordNet

situated or running side by side; "collateral ridges of mountains"
a security pledged for the repayment of a loan
serving to support or corroborate; "collateral evidence" (同)confirmative, confirming, confirmatory, corroborative, corroboratory, substantiating, substantiative, validating, validatory, verificatory, verifying
descended from a common ancestor but through different lines; "cousins are collateral relatives"; "an indirect descendant of the Stuarts" (同)indirect
accompany, concomitant; "collateral target damage from a bombing run"

PrepTutorEJDIC

並び合った / 二次的な,付随的な(secondary) / 証券類を担保とした / 傍系の,直系でない / 担保,低当,見返り物資

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/10/29 20:48:50」(JST)

wiki en

Schaffer collaterals are axon collaterals given off by CA3 pyramidal cells in the hippocampus. These collaterals project to area CA1 of the hippocampus^[1] and are an integral part of memory formation and the emotional network of the Papez circuit, and of the hippocampal trisynaptic loop. It is one of the most studied synapses in the world and named after the Hungarian anatomist-neurologist Károly Schaffer.

As a part of the hippocampal structures, Schaffer collaterals develop the limbic system, which plays a critical role in the aspects of learning and memory. The signals of information from the contralateral CA3 region leave via the Schaffer collateral pathways for the CA1 pyramidal neurons. Mature synapses contain fewer Schaffer collateral branches than those synapses that are not fully developed.^[2] Many scientists try to use the Schaffer collateral synapse as a sample synapse, a typical excitatory glutamatergic synapse in the cortex that has very well been studied in order to try to identify the rules of both the patterns of stimulation in electrical rules and the chemical mechanisms by which synapses get persistently stronger and which synapses get persistently weaker as well and to develop medication and treatment to cure the chronic diseases, such as dementia and Alzheimer's disease. Moreover, they believe that studying the Schaffer collateral can provide a whole range of understanding how Schaffer collaterals allow us to intervene with drug-treatments and with electrical-stimulation so that the quality of human experience can be improved.

Development

"Schaffer collateral is the conductor of the orchestra, but not the actual instrument that plays the music" - Dr. Patrick K. Stanton [3].

An individual needs the functional hippocampus to store long-term memories as synaptic plasticity in terms of storing information. Once those memories are stored, they remain stored in very long time. However, they slowly fade away, which means that there are some roles for the hippocampus when talking to the neocortex in order to prevent diminishing those memories away. It is clear that whatever plastic changes occurring in the hippocampus involve in directing the process by which memories get stored.

The Schaffer collateral is involved in activity-dependent plasticity and the information processes that always are processed through the hippocampus all the time. The Schaffer collateral clearly affects whether the target cells fire action potentials or not. However, at the same time, it is triggering the process that takes much longer whereby some synapses get stronger and some get weaker, and overall the patterns of synaptic strength of the network all evolve over time.

Moreover, Schaffer collateral axons develop excitatory synapses that are scattered over the dendritic arborization^[3] of hippocampal CA1 pyramidal neurons.^[4] In the early stage of long-term potentiation, Schaffer collaterals release glutamate that binds to AMPA receptors of CA1-dendrites. The process of developing a network of CA3-to-CA1 recurrent excitatory glutamatergic synapses alters the frequency of spontaneous action potentials in Schaffer collaterals. By adulthood, CA3 recurrent network activity is reduced, the frequency of spontaneous action potentials is decreased in Schaffer collaterals, and a single release locus synapse with one dendritic spine on a given CA1 pyramidal neuron can be developed by Schaffer collateral axons.^[2]

Location

The Schaffer collateral is located between the CA1 region and CA3 region in the hippocampus. Schaffer collaterals are the axons of pyramidal cells that connect two neurons (CA3 and CA1) and transfer information from CA3 to CA1.^[5]^[6] The entorhinal cortex sends the main input to the dentate gyrus (perforant pathway). From the granule cells of the dentate gyrus, connections are made to the CA3 regions of the hippocampus via mossy fibers. CA3 sends the information signals to CA1 pyramidal cells via the Schaffer collateral and commissural fibers from the contralateral hippocampus as well.

Function

Throughout the memory process in the hippocampus, Schaffer collaterals seem not to play a major role in the formation of actual memory, but it is clear that Schaffer collaterals assist the activity-dependent plasticity and the information processes that are always altered over the course of memory development in the hippocampus. Schaffer collaterals alter the development of the limbic system that is critical for learning and memory. The contralateral CA3 region sends information through Schaffer collateral to the CA1 pyramidal neurons.

Schaffer collateral and hippocampal synaptic plasticity

Plastic changes occurring in the hippocampus are involved in directing the process by which memories get stored. Schaffer collaterals affect the hippocampus to develop short (Short-term Plasticity) and long term synaptic plasticity (Long-term Plasticity) in terms of storing information and changing in the efficiency of synaptic transmission following previous synaptic activity.

Long-term plasticity

Long-term potentiation (LTP) in the hippocampal formation is an example model for neural plasticity.^[7] Schaffer collateral synapses have been used as a sample synapse, a typical excitatory glutamatergic synapse in the cortex that has very well been studied in order to try to identify the rules of both the patterns of stimulation in electrical rules and the chemical mechanisms by which synapses get persistently stronger and which synapses get persistently weaker as well. LTPs are involved in how people store information and how they retrieve information and involve networks of memories that are involved in facts and in emotions as well because the hippocampus is the part of the limbic system connected to the amygdala.

LTP in the hippocampus is an important model for neural plasticity that contributes to learning and memory.^[7] The study on Schaffer collateral is important because the Schaffer collaterals are the axons of the neurons in the CA3 regions of the hippocampus that form synapses in the CA1 regions.

The hippocampus is a part of the feedback process that sends signals to stop cortisol production. Thus, a damaged hippocampus can cause memory loss and inability of cognitive function. Furthermore, as the hippocampus is the region controlling learning and memory processes, the roles of Schaffer collateral are potential to find treatments for diseases related to the hippocampus or its neural processing pathways such as Alzheimer's disease, a neurodegenerative disorder.

Long-term potentiation (LTP) of synaptic strength at Schaffer collateral synapses has largely been attributed to changes in the number and biophysical properties of AMPA receptors (AMPARs).^[8] Neuropsin has a regulatory effect on Schaffer collateral LTP in the rat hippocampus^[7]

The functional hippocampus needs to store long-term memories. Once the memories are stored, they remain stored in very long time. Long-term changes in synaptic efficacy in the hippocampus can be induced by different patterns of stimulation generating presynaptic and postsynaptic depolarization^[9] The theta burst stimulation of Schaffer collaterals can be sufficient to induce LTP by promoting the formation of filamentous actin in CA1 dendrites.^[10] Within the mammalian brain, some patterns of synaptic activity produce long-term potentiation (LTP) which is a long-lasting increase in synaptic strength and long-term depression (LTD) which is a long-lasting decrease in synaptic strength.

LTP at Schaffer collateral-CA1 synapses and "SK2 channel plasticity"

Long-term plasticity in synapses of the hippocampus can be induced by different patterns of stimulation generating pre- and post-synaptic depolarization. These synaptic changes can clearly lead to modification in circuit function and to behavioral plasticity. Some patterns of synaptic activity produce an extensive increase in synaptic strength, also known as Long-Term Potentiation (LTP). In the hippocampus, LTP at Schaffer collateral-CA1 modulates the biophysical properties of AMPA receptors. Moreover, SK2, small-conductance Ca2+-activated K+ channel, changes the shape of excitatory postsynaptic potentials (EPSPs) by coupling with N-methyl D-aspartate receptors (NMDA receptors). The research by Lin MT, et al. was designed to investigate whether SK2 channels participate in synaptic changes when an activity-dependent decrease contributes to LTP.^[11]

SK2 channels are ion channels that are activated by an increasing in the concentration of intracellular calcium and as a result of allowing K+ cation to cross the cell membrane. The double immunogold labeling identified that SK2 channels and NMDA cohabit within the postsynaptic density (PSD) of CA1 regions of the hippocampus. The authors used theta-burst pairing (TBP) to produce a rapid potentiation of synaptic strength and to evoke LTP that is induced simultaneously but whose expression levels vary inversely over time, and the result of the TBP induction was compared to the control group. The result showed that the TBP induction of LTP significantly increased EPSPs level. When the stimulus strength was reduced below the action potential threshold, apamin, a neurotoxin, was added to assess the contribution of SK2 activity to EPSPs. It resulted in an increase in the level of EPSPs with blockage of SK2 channels. The TBP induction of LTP abolishes SK2 channel contribution to EPSPs. When the induction of chemical LTP was applied, immunoparticles for SK2 were not found within the PSD of asymmetrical synapses. However, the SK2 immunoparticles were observed within intracellular membranes. The activation of protein kinase A (PKA) downregulates the surface expression of SK2 because PKA regulates the surface expression of AMPA receptors, a non-NMDA-type ionotropic transmembrane receptor, in the hippocampus. Therefore, PKA decreases the activity of LTP-dependent of SK2 channels.Schaffer collateral#Long-term Plasticity

Short-term plasticity

Short-term synaptic plasticity undergoes important age-dependent changes that have crucial implications during the development of the nervous system^[2]

Vesicular release at "Schaffer Collateral"

The way transmitter release works is every terminal at every pre-synapse in your brain has a large pool of vesicles that are filled with glutamate and that can be used to release a neurotransmitter. However, in any given time, most of them are not being used. This is known as the reserve pool. The readily recyclable pool or rapidly recycling pool is 10% of what is being used all the time. When a transmitter is released, a vesicle does not just get thrown away. The vesicles are actually resealed, and they get recycled back around and stuck preferentially back into the rapidly recycling pool, not the reserve pool, so they can be used again. Most of the vesicles in the reserve pool are released only when it is activated at the maximum strength like by polarizing them with high potassium or by driving with the high frequency of action potentials. The little recycling vesicles can't keep up. Then, signals tell the reserve pool to release what it stores in itself. The acting zone of the reserve pool has its certain length with so many docking sites. The vesicles have to dock to the sealed complex. They have to bind to the right place. When calcium comes in, it binds, releases the vesicle, and opens up to release a neurotransmitter. Therefore, how fast endocytosis occurs means how fast the vesicles get back into the recycling pool.^[12]

Multivesicular release (MVR) occurs at Schaffer collateral-CA1 synapses when P is elevated by facilitation and that MVR may be a phenomenon common to many synapses throughout the central nervous system.^[13]

References

^ Vago DR, Kesner RP(2008). Disruption of the direct perforant path input to the CA1 subregion of the dorsal hippocampus interferes with spatial working memory and novelty detection. Behav. Brain Res. 189(2): 273–83
^ ^a ^b ^c Schiess AR, Scullin C & Partridge LD (2010). Maturation of Schaffer collateral synapses generates a phenotype of unreliable basal evoked release and very reliable facilitated release. European Journal of Neuroscience. 31:1377-1387.
^ [1]
^ Smith MA, Ellis-Davies GC & Magee JC (2003). Mechanism of the distance-dependent scaling of Schaffer collateral synapses in rat CA1 pyramidal neurons. Journal of Physiology. 548.1:245-258
^ Lebeau G, DesGroseillers L, Sossin Wayne & Lacaille J (2011). mRNA binding protein staufen 1-dependent regulation of pyramidal cell spine morphology NMDA receptor mediated synaptic plasticity. BioMed central. 4(22)
^ Arrigoni E & Greene RW (2004). Schaffer collateral and perforant path inputs activate different subtypes of NMDA receptors on the same CA1 pyramidal cell. British Journal of Pharmacology. 142: 317-322
^ ^a ^b ^c Komai S, Matsuyama T, Matsumoto K, Kato K, Kobayashi M, Imamura K, Yoshida S, Ugawa S & Shiosaka S (2000). Neuropsin regulates an early phase of Schaffer-collateral long-term potentiation in the murine hippocampus. European Journal of Neurosience. 12:1479-1486
^ Lin MT, Lujan R, Watanabe M, Adelman JP & Maylie J (2007). SK2 channel plasticity contributes to LTP at Schaffer collateral-CA1 synapses. Nature Neuroscience. 11(2): 170-176
^ Hoffman DA, Sprengel R & Sakmann B (2002). Molecular dissection of hippocampal theta-burst pairing potentiation. PNAS.99 (11): 7740-7745
^ Meighan PC, Meighan SE, Davis CJ, Wright JW & Harding JW (2007). Effects of matrix metalloproteinase inhibition on short-and long-term plasticity of Schaffer collateral/CA1 synapses. Journal of Neurochemistry. 102:2085-2096
^ Lin MT, Lujuan R, Watanabe M, Adelman JP, Maylie J (2008). SK2 channel plasticity contributes to LTP at Schaffer collateral-CA1 synapses. Nature. 11 (2): 170-177
^ Stanton PK, Winterer J, Zhang X & Muller W (2005). Imaging LTP of presynaptic release of FM1-43 [2] from the rapidly recycling vesicle pool of Schaffer collateral-CA1 synapses in rat hippocampal slices. European Journal of Neuroscience. 22:2451-2461
^ Christie JM and Jahr CE (2006). Multivesicular Release at Schaffer Collateral-CA1 Hippocampal synapses. The Journal of Neuroscience. 26(1):210-216

External links

Wikimedia Commons has media related to: Schaffer Collateral (Neuroanatomy)

Excitatory amino acids in synaptic transmission in the Schaffer collateral-commissural pathway of the rat hippocampus. by Collingridge GL. et al.
Involvement of Protein Synthesis and Degradation in Long-Term Potentiation of Schaffer Collateral CA1 Synapses by Karpova A. et al.

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1. 冠側副循環 coronary collateral circulation
2. 膝内側側副靱帯損傷 medial collateral ligament injury of the knee
3. 急性膝関節痛または損傷がみられる小児または思春期のアスリートに対するアプローチ approach to the child or adolescent athlete with acute knee pain or injury
4. 小児または思春期のアスリートにおける肘関節損傷 elbow injuries in the child or adolescent athlete
5. 尺側側副靱帯損傷（ゲームキーパー母指またはスキーヤー母指） ulnar collateral ligament injury gamekeepers or skiers thumb

English Journal

Melatonin inhibits voltage-sensitive Ca(2+) channel-mediated neurotransmitter release.

Choi TY1, Kwon JE1, Durrance ES1, Jo SH2, Choi SY3, Kim KT4.Author information 1Department of Physiology, Dental Research Institute, Seoul National University School of Dentistry, Seoul 110-749, Republic of Korea.2Department of Physiology, Institute of Bioscience and Biotechnology, BK21 Plus Graduate Program, Kangwon National University College of Medicine, Chuncheon 200-701, Republic of Korea.3Department of Physiology, Dental Research Institute, Seoul National University School of Dentistry, Seoul 110-749, Republic of Korea; Department of Life Sciences, Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea. Electronic address: sychoi@snu.ac.kr.4Department of Life Sciences, Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea. Electronic address: ktk@postech.ac.kr.AbstractMelatonin is involved in various neuronal functions such as circadian rhythmicity and thermoregulation. Melatonin has a wide range of pharmacologically effective concentration levels from the nanomolar to millimolar levels. Recently, the antiepileptic effect of high dose melatonin has been the focus of clinical studies; however, its detailed mechanism especially in relation to neurotransmitter release and synaptic transmission remains unclear. We studied the effect of melatonin at high concentrations on the neurotransmitter release by monitoring norepinephrine release in PC12 cells, and excitatory postsynaptic potential in rat hippocampal slices. Melatonin inhibits the 70mM K(+)-induced Ca(2+) increase at millimolar levels without effect on bradykinin-triggered Ca(2+) increase in PC12 cells. Melatonin (1mM) did not affect A2A adenosine receptor-evoked cAMP production, and classical melatonin receptor antagonists did not reverse the melatonin-induced inhibitory effect, suggesting G-protein coupled receptor independency. Melatonin inhibits the 70mM K(+)-induced norepinephrine release at a similar effective concentration range in PC12 cells. We confirmed that melatonin (100µM) inhibits excitatory synaptic transmission of the hippocampal Schaffer collateral pathway with the decrease in basal synaptic transmission and the increase in paired pulse ratio. These results show that melatonin inhibits neurotransmitter release through the blocking of voltage-sensitive Ca(2+) channels and suggest a possible mechanism for the antiepileptic effect of melatonin.
Brain research.Brain Res.2014 Apr 4;1557:34-42. doi: 10.1016/j.brainres.2014.02.023. Epub 2014 Feb 18.
Melatonin is involved in various neuronal functions such as circadian rhythmicity and thermoregulation. Melatonin has a wide range of pharmacologically effective concentration levels from the nanomolar to millimolar levels. Recently, the antiepileptic effect of high dose melatonin has been the focus
PMID 24560601

Is replenishment of the readily releasable pool associated with vesicular movement?

Bui L, Glavinović MI.Author information Department of Physiology, McGill University, 3655 Sir William Osler Promenade, Montreal, H3G 1Y6 Canada.AbstractAt the excitatory synapse of rat hippocampus the short-term synaptic depression observed during long high-frequency stimulation is associated with slower replenishment of the readily-releasable pool. Given that the replenishment rate is also not [Ca(++)]o sensitive this puts into question a widely held notion that the vesicles-constrained by the cytoskeleton and rendered free from such constraints by Ca(++) entry that renders them more mobile-are important in the replenishment of the readily-releasable pool. This raises a question-Is vesicular replenishment of the readily releasable pool associated with significant movement? To answer this question we evaluated how okadaic acid and staurosporine (compounds known to affect vesicular mobility) influence the replenishment rate. We used patterned stimulation on the Schaffer collateral fiber pathway and recorded the excitatory post-synaptic currents (EPSCs) from rat CA1 neurons, in the absence and presence of these drugs. The parameters of a circuit model with two vesicular pools were estimated by minimizing the squared difference between the ESPC amplitudes and simulated model output. [Ca(2+)]o did not influence the progressive decrease of the replenishment rate during long, high frequency stimulation. Okadaic acid did not significantly affect any parameters of the vesicular storage and release system, including the replenishment rate. Staurosporine reduced the replenishment coupling, but not the replenishment rate, and this is owing to the fact that it also reduces the ability of the readily releasable pool to contain quanta. Moreover, these compounds were ineffective in influencing how the replenishment rate decreases during long, high frequency stimulation. In conclusion at the excitatory synapses of rat hippocampus the replenishment of the readily releasable pool does not appear to be associated with a significant vesicular movement, and during long high frequency stimulation [Ca(++)]o does not influence the progressive decrease of vesicular replenishment.
Cognitive neurodynamics.Cogn Neurodyn.2014 Apr;8(2):99-110. doi: 10.1007/s11571-013-9264-y. Epub 2013 Jul 30.
At the excitatory synapse of rat hippocampus the short-term synaptic depression observed during long high-frequency stimulation is associated with slower replenishment of the readily-releasable pool. Given that the replenishment rate is also not [Ca(++)]o sensitive this puts into question a widely h
PMID 24624230

Neurophysiological modification of CA1 pyramidal neurons in a transgenic mouse expressing a truncated form of disrupted-in-schizophrenia 1.

Booth CA1, Brown JT, Randall AD.Author information 1School of Physiology and Pharmacology, University of Bristol, Medical Sciences Building, University Walk, Bristol, BS8 1TD, UK.AbstractA t(1;11) balanced chromosomal translocation transects the Disc1 gene in a large Scottish family and produces genome-wide linkage to schizophrenia and recurrent major depressive disorder. This study describes our in vitro investigations into neurophysiological function in hippocampal area CA1 of a transgenic mouse (DISC1tr ) that expresses a truncated version of DISC1 designed to reproduce aspects of the genetic situation in the Scottish t(1;11) pedigree. We employed both patch-clamp and extracellular recording methods in vitro to compare intrinsic properties and synaptic function and plasticity between DISC1tr animals and wild-type littermates. Patch-clamp analysis of CA1 pyramidal neurons (CA1-PNs) revealed no genotype dependence in multiple subthreshold parameters, including resting potential, input resistance, hyperpolarization-activated 'sag' and resonance properties. Suprathreshold stimuli revealed no alteration to action potential (AP) waveform, although the initial rate of AP production was higher in DISC1tr mice. No difference was observed in afterhyperpolarizing potentials following trains of 5-25 APs at 50 Hz. Patch-clamp analysis of synaptic responses in the Schaffer collateral commissural (SC) pathway indicated no genotype-dependence of paired pulse facilitation, excitatory postsynaptic potential summation or AMPA/NMDA ratio. Extracellular recordings also revealed an absence of changes to SC synaptic responses and indicated input-output and short-term plasticity were also unaltered in the temporoammonic (TA) input. However, in DISC1tr mice theta burst-induced long-term potentiation was enhanced in the SC pathway but completely lost in the TA pathway. These data demonstrate that expressing a truncated form of DISC1 affects intrinsic properties of CA1-PNs and produces pathway-specific effects on long-term synaptic plasticity.
The European journal of neuroscience.Eur J Neurosci.2014 Apr;39(7):1074-90. doi: 10.1111/ejn.12549.
A t(1;11) balanced chromosomal translocation transects the Disc1 gene in a large Scottish family and produces genome-wide linkage to schizophrenia and recurrent major depressive disorder. This study describes our in vitro investigations into neurophysiological function in hippocampal area CA1 of a t
PMID 24712988

Japanese Journal

Cholinergic modulation for hippocampal long-term potentiation

SUZUKI ETSUKO
動物心理学研究 64(1), 37-41, 2014
… We addressed the involvement of the inhibition of Kv7/M K+ channels, which are a target of mAChR modulation, during mAChR activation-induced enhancement of long-term potentiation (LTP) at rat hippocampal Schaffer collateral (SC)-CA1 synapses. …
NAID 130004938658

脳の非線形ダイナミクスと情報処理機構

林初男
電子情報通信学会基礎・境界ソサイエティ Fundamentals Review 8(2), 102-114, 2014
工学でも大きな興味が持たれている脳のニューロンや神経回路網は非線形なシステムである．ニューロンは規則的に発火するだけでなく，膜電位あるいは刺激の強さや周波数に依存して不規則に発火することがある．この不規則な発火はカオスと呼ばれる決定論的な力学則に従う非周期振動である．神経回路網の場合は，ニューロンの集団活動を反映した電場電位が周期刺激に対して引き込みやカオス応答を起こす．すなわち，ニューロン集団の …
NAID 130004697142

Effects of subchronic aluminum exposure on spatial memory, ultrastructure and L-LTP of hippocampus in rats

Zhang Lifeng,Jin Cuihong,Liu Qiufang [他],LU Xiaobo,WU Shengwen,YANG Jinghua,DU Yanqiu,ZHENG Linlin,CAI Yuan
Journal of toxicological sciences 38(2), 255-268, 2013-04-01
… The induction and maintenance of L-LTP in area of Schaffer collateral- CA1 synapse was recorded by extracellular microelectrode recording technology in hippocampus of experimental rats. …
NAID 10031151429

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★リンクテーブル★

リンク元	「シャファー側枝」「Schaffer側枝」
関連記事	「collateral」

「シャファー側枝」

　　[★]

英: Schaffer collateral
同: シェファー側枝、シャッファー側枝、シェーファー側枝、Schaffer側枝、シャッファー側副枝
関: 海馬、大錐体細胞 CA3、小錐体細胞 CA1

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海馬CA3からCA1に投射する軸索

「Schaffer側枝」

　　[★]

英: Schaffer collateral
関: シェファー側枝、シャファー側枝

「collateral」

　　[★]

側枝、傍系の

関: lateral shoot

[Vago-0] Vago DR, Kesner RP(2008). Disruption of the direct perforant path input to the CA1 subregion of the dorsal hippocampus interferes with spatial working memory and novelty detection. Behav. Brain Res. 189(2): 273–83

[Schiess-1] Schiess AR, Scullin C & Partridge LD (2010). Maturation of Schaffer collateral synapses generates a phenotype of unreliable basal evoked release and very reliable facilitated release. European Journal of Neuroscience. 31:1377-1387.

[2] [1]

[Smith-3] Smith MA, Ellis-Davies GC & Magee JC (2003). Mechanism of the distance-dependent scaling of Schaffer collateral synapses in rat CA1 pyramidal neurons. Journal of Physiology. 548.1:245-258

[Lebeau-4] Lebeau G, DesGroseillers L, Sossin Wayne & Lacaille J (2011). mRNA binding protein staufen 1-dependent regulation of pyramidal cell spine morphology NMDA receptor mediated synaptic plasticity. BioMed central. 4(22)

[Arrigoni-5] Arrigoni E & Greene RW (2004). Schaffer collateral and perforant path inputs activate different subtypes of NMDA receptors on the same CA1 pyramidal cell. British Journal of Pharmacology. 142: 317-322

[Komai-6] Komai S, Matsuyama T, Matsumoto K, Kato K, Kobayashi M, Imamura K, Yoshida S, Ugawa S & Shiosaka S (2000). Neuropsin regulates an early phase of Schaffer-collateral long-term potentiation in the murine hippocampus. European Journal of Neurosience. 12:1479-1486

[Lin-7] Lin MT, Lujan R, Watanabe M, Adelman JP & Maylie J (2007). SK2 channel plasticity contributes to LTP at Schaffer collateral-CA1 synapses. Nature Neuroscience. 11(2): 170-176

[Hoffman-8] Hoffman DA, Sprengel R & Sakmann B (2002). Molecular dissection of hippocampal theta-burst pairing potentiation. PNAS.99 (11): 7740-7745

[Meighan-9] Meighan PC, Meighan SE, Davis CJ, Wright JW & Harding JW (2007). Effects of matrix metalloproteinase inhibition on short-and long-term plasticity of Schaffer collateral/CA1 synapses. Journal of Neurochemistry. 102:2085-2096

[Lin_MT-10] Lin MT, Lujuan R, Watanabe M, Adelman JP, Maylie J (2008). SK2 channel plasticity contributes to LTP at Schaffer collateral-CA1 synapses. Nature. 11 (2): 170-177

[Stanton-11] Stanton PK, Winterer J, Zhang X & Muller W (2005). Imaging LTP of presynaptic release of FM1-43 [2] from the rapidly recycling vesicle pool of Schaffer collateral-CA1 synapses in rat hippocampal slices. European Journal of Neuroscience. 22:2451-2461

[Christie-12] Christie JM and Jahr CE (2006). Multivesicular Release at Schaffer Collateral-CA1 Hippocampal synapses. The Journal of Neuroscience. 26(1):210-216

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Schaffer collateral