Introduction: Spreading depression (SD) is a bioelectrical event in the central nervous system and involves in the pathophysiology of some neurological disorders. In this present study, we indicate enhancement of long-term potentiation of hippocampus tissue in juvenile rats faced to cortical spreading depression repetitively. Materials and Methods: Silver recording electrodes as well as a cannula were implanted over the brain of juvenile rats. Repetitive cortical SD events were induced by KCl 3 M weekly injection through the cannula. The brains were removed after 4 weeks. Transverse sections were prepared and incubated in artificial cerebrospinal fluid. Single electrical stimulations were applied through a bipolar electrode placed on to the hippocampal Schaffer collaterals. The field excitatory postsynaptic potentials (fEPSP) were elicited by adjusting the intensity of stimulation to 50% of that at which population spikes began to appear. Results: Repetitive SD enhanced the long-term potentiation in CA1 hippocampal area. The data indicate that repetitive cortical SD in juvenile rats significantly increases the amplitude of the fEPSP form the baseline. Conclusion: This may clarify the pathophysiology of memory deficit were seen in some neurological disorders in children.

Introduction: Memory is ability to acquisition, maintenance and retrieval of information, which is classified through different ways. Complex mechanisms play a role in learning and memory that ultimately leads to biochemical, morphological and physiological changes at the level of synaptic and neural networks. The basic mechanisms involved in the formation and stabilization of memory are synaptic facilitation, long term potentiation and long term depression. Conclusion: Considering the importance of glutamate receptors (especially NMDA subtype), calcium homeostasis, balance between kinases and phosphatases, calcineurin, cellular adhesion molecules, extracellular matrix, glial cells, and different neurotransmitters in process of memory formation, this study evaluate the cellular and molecular pathways involved in learning and memory.

Long-term potentiation (LTP) is a process that certain types of synaptic stimulation lead to a long-lasting enhancement in the strength of synaptic transmission. Studies in recent years indicate the importance of molecular pathways in the development of memory and learning. Tropomyosin receptor kinase B (TrkB) is a member of the neurotrophin receptor tyrosine kinase family, that its ligand is brain-derived neurotrophic factor (BDNF). In recent years, Research has been shown that TrkB has an important role in LTP formation in hippocampus and after ligand binding activates several intracellular signaling cascades. Three important intracellular signaling cascades are triggered by the TrkB receptor includes: Ras–mitogen activated protein kinase (MAPK) pathway, phosphatidylinositol 3‑kinase (PI3K)-Akt pathway and PLCγ-Ca 2+ pathway.
 

Long-term potentiation (LTP) is a reflection of synaptic plasticity that induced by specific patterns of synaptic activity and has an important role in learning and memory. The first clue of the potential role of glutamate receptors in LTP was in 1991 with the observation that the mGluR agonists 1-amino-1, 3-cyclopentanedicarboxylic acid (ACPD), increased LTP. Studies have shown that ACPD induce LTP in CA1 and in the dentate gyrus. Scientists suggest that the modulatory impact of mGluR activation on LTP varied in N-methyl-D-aspartic acid (NMDA)-dependent and NMDA-independent pathways because LTP was unimpaired in mutant mice with mGluR1 mutation and produced with full strength in NMDA-dependent pathways of the hippocampus but was attenuated in NMDA-independent LTP in the mossy fiber synapses on CA3. Consequently, research has shown that in mutant mice lacking mGluR5 the potentiation of the NMDA response was absent but the potentiation of the AMPA response was maintained. The findings suggest that mGluR5 activation plays an important role in expression of NMDA receptor-dependent LTP.
 

Long-term potentiation (LTP) is a form of activity-dependent plasticity that occurs during learning. Potassium channels are the most diverse group of all ion channels that related to synaptic plasticity. Small-conductance calcium-activated potassium channels (SKs) are found in hippocampal CA1 neurons and by inhibiting of postsynaptic potentials are involved in synaptic transmission impairment. Studies have been shown that blockage of SKs result in increase of LTP so that blocking of these channels increased LTP process and vice versa. Large-conductance calcium-activated potassium channels (BKs) also are found in hippocampal CA1 neurons and by influencing synaptic plasticity play an important role in learning and memory.
 

Synaptic plasticity in the central nervous system (CNS) of mammals has been discussed for many years. Several forms of synaptic plasticity of mammal’s CNS have been identified, such as those that occur in long-term potentiation (LTP). Different types of LTP have been observed in distinctive areas of the CNS of mammals. The hippocampus is one of the most important areas in the CNS that plays an important role in learning and memory formation and LTP. LTP of synaptic strength occurs during learning and the examination of the molecular and cellular mechanisms underlying these types of synaptic plasticity have been studied by several scientists. In this review, emphasis is focused on the role of synaptic ion channels, ionotropic and metabotropic glutamate receptors as well as TrkB receptor in LTP, and the importance and significance of these elements in understanding of the molecular biology of learning and memory.

Long-term potentiation (LTP) is a biological process of learning and memory after a high-frequency train of electrical stimulations. By binding of brain-derived neurotrophic factor (BDNF) to Tropomyosin receptor kinase B (TrKB) receptors in postsynaptic neurons, tyrosine kinase Fyn is bound to these receptors and hereby plays a mediating role to binding and activation of N-methyl-D-aspartic acid receptors (NMDARs). TrkB receptor can be initiated three different pathway includes: MAPK pathway, PI3K-Akt  pathway and PLCγ-Ca 2+ pathway. So Fyn by playing a mediating role between TrkB signaling pathway and NMDARs has an important role in LTP induction.

Long-term potentiation (LTP) is a reflection of synaptic plasticity that has an important role in learning and memory. LTP is a long-lasting increase of synaptic activity due to enhancement of excitatory synaptic transmission after a high-frequency train of electrical stimulation. The role of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in excitatory synaptic transmission and LTP formation uncovered over recent decades. The activity regulation of AMPA receptors (AMPARs) has a significant role in the LTP induction. AMPARs are homomeric or heteromeric receptors combined of four subunits GLUA1 to GLUA4. GluR1 have a critical role in LTP formation in the CA1 region of hippocampus and is necessitated for synaptic delivery of AMPA receptors.

Long-term potentiation (LTP) is a form of activity dependent plasticity that induced by high-frequency stimulation or theta burst stimulation and results in synaptic transmission. Several Studies have been shown that LTP is one of the most important processes in the CNS that plays an important role in learning and memory formation. Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a major synaptic protein that involved in many signaling cascades and has an important role in the induction of LTP and certain forms of learning. This kinase consist of 12 subunits (alpha and beta) and activated by calcium-calmodulin and expressed presynaptically and postsynaptically. In one of the most important pathways, CaMKII is phosphorylated α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) and increased conductance of the ion-channels. On the other hand, CaMKII increased the insertion of AMPARs at the postsynaptic membrane and enhanced the density of receptors at the neurons. Therefore, CaMKII seems prone to be a mediator of essential significance in connecting transient calcium signs to neuronal plasticity.

Introduction: Long-term potentiation (LTP) is a generic term that applies to a form of activity-dependent plasticity that induced by high-frequency or theta burst stimulation and results in enhancement of synaptic transmission. LTP has a key role in learning and memory. Different types of LTP have been observed in distinctive areas of the central nervous system. Hippocampal CA1 area is vital for the formation of long-term memory. Conclusion: Several studies have been shown the importance of signaling pathways in the development of memory and learning. In this review is intended to present an overview of the role of synaptic ion channels, ionotropic and metabotropic glutamate receptors as well as TrkB receptor in LTP formation of learning and memory.