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"Schaffer Collaterals"

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 named after the Hungarian anatomist-neurologist Károly Schaffer.

In the early stage of long term potentiation Schaffer collaterals release glutamate that binds to AMPA receptors of CA1-dendrites.

Development

Location

In the hippocampus, Schaffer collaterals are given off by the CA3 region and project to the CA1 area.

Hippocampus

Schaffer collaterals are the axons of prymidal cells that connect two neurons (CA3 and CA1) and transfer information from CA3 to CA1^[2]^[3].

Inner Hippocampal Pathways

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.

Hippocampal Synaptic Plasticity

The hippocampus exhibits shor and long term synaptic plasticity in terms of a change in the efficiency of synaptic transmission following previous synaptic activity.

Short-term Plasticity

Short-term synaptic plasticity undergoes important age-dependent changes that have crucial implications during the development of the nervous system^[4]

Long-term Plasticity

Long-term changes in synaptic efficacy in the hippocampus can be induced by different patterns of stimulation generating pre- and postsynaptic depolarization^[5]

Schaffer collateral LTP

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)^[6]. Neuropsin has a regulatory effect on Schaffer collateral LTP in the rat hippocampus^[7]

Schaffer collateral LTD

Long-Term Synaptic Plasticity and Schaffer Collaterals

Within the mammlian 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 postsynaptic 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 (NMDA) receptorsNMDA 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^[8]. 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 immunoglod 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.

Importance of LTP and Schaffer collateral

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 hippocampuse 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 hippocamps 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.

Multivesicular release at Schaffer Collateral

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 systema^[9].

Schaffer collateral commissural pathway

Excitatory amino acids in synaptic transmission

By the stimulation of Schaffer collateral-commissural proection, the effects of excitatory amino acids and some antagonists applied by ionophoresis to stratum radiatum in the CA1 region of rat hippocampal slices are examined on the locally recorded field EPSP^[10]

Additional images

References

External Links

^ 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
^ 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
^ Schiess ARB, Scullin C & Partridge LD(2010). Maturation of Schaffer collateral synapses generates a phenotype of unreliable basal evoked release and very reliable facilitated release. Eu. Journal of Neuroscience. 31: 1377-1387
^ Hoffman DA, Sprengel R & Sakmann B(2002). Molecular dissection of hippocampal theta-burst pairing potentiation. PNAS.99(11): 7740-7745
^ 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
^ ^a ^b 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. Eu. Neuroscience Association. 12: 1479-1486 Cite error: The named reference "Komai" was defined multiple times with different content (see the help page).
^ 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
^ Christie JM and Jahr CE (2006). Multivesicular Release at Schaffer Collateral-CA1 Hippocampal synapses. The Journal of Neuroscience. 26(1):210-216
^ Collingridge GL, Kehl SJ and McLennan H(1983). The Journal of Physiology. 334:33-46.

Category:Cerebrum Category:Neuroanatomy

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[Vago-1] 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

[Lebeau-2] 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-3] 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

[Schiess-4] Schiess ARB, Scullin C & Partridge LD(2010). Maturation of Schaffer collateral synapses generates a phenotype of unreliable basal evoked release and very reliable facilitated release. Eu. Journal of Neuroscience. 31: 1377-1387

[Hoffman-5] Hoffman DA, Sprengel R & Sakmann B(2002). Molecular dissection of hippocampal theta-burst pairing potentiation. PNAS.99(11): 7740-7745

[Lin-6] 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

[Komai-7] 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. Eu. Neuroscience Association. 12: 1479-1486 Cite error: The named reference "Komai" was defined multiple times with different content (see the help page).

[Lin_MT-8] 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

[Christie-9] Christie JM and Jahr CE (2006). Multivesicular Release at Schaffer Collateral-CA1 Hippocampal synapses. The Journal of Neuroscience. 26(1):210-216

[Collingridge-10] Collingridge GL, Kehl SJ and McLennan H(1983). The Journal of Physiology. 334:33-46.

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