Шаффер коллатералдары: Жады мен лимбикалық жүйедегі рөлі

Schaffer collaterals are axon collaterals given off by CA3 pyramidal cells in the hippocampus. These collaterals project to area CA1 of the hippocampus 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. of hippocampal CA1 pyramidal neurons. 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. 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.

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.

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 potentiation (LTP) in the hippocampal formation is an example model for neural plasticity. 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. Neuropsin has a regulatory effect on Schaffer collateral LTP in the rat hippocampus. The theta burst stimulation of Schaffer collaterals can be sufficient to induce LTP by promoting the formation of filamentous actin in CA1 dendrites. 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.

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.

Transmitters are released from pre synaptic terminals through fusion of vesicles to the membrane, that are filled with neurotransmitters such as glutamate. Vesicles are exocytosed, with neurotransmitters reentering the presynaptic terminal for reuse. These fused vesicles then reenter preferentially back into the rapidly recycling pool for reuse. Additional vesicles within the reserve pool of the presynaptic terminal are released according to stronger amplitude depolarizations of the presynaptic axon due to greater spatial or temporal summation of action potentials, corresponding to greater calcium influx polarizing. Rate of endocytosis is dependent on rate at which vesicles are recycled into the recycling pool. 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.