Learning Mechanisms and Memory Formation in Neural Networks
The learning brain changes its structure at the cellular and molecular level. Particularly the neural synapses` connectivity may strengthen or weaken during the learning which refers to as synaptic plasticity. The synaptic plasticity in brain controls the mechanisms of the learning and encoding processes for the memory and retrieval of the memory stored. The synaptic changes and reconfiguration happen throughout the whole brain but the changes due to the education and the learning are more localized at the hippocampus. The mechanism which controls the synaptic changes due to the education as a stimulus are technically referred to as Long Term Potentiation (LTP) and also Long-Term Depression (LTD). These mechanism takes place at the synaptic gap of the neurons of the hippocampus and complex interactions controls learning and encodes the memory. At the synaptic gap, there exists a vital protrusion, dendritic spine, that its dynamic and rapid creation and annihilation plays a significant role on the memory formation after the learning. As these tiny protrusions which evade even the most high-resolution optical microscopy plays a vital role in memory formation then their deficit also plays a crucial role in many neuropsychiatric and neurological disorders such as Alzheimer disease which its cognitive decline has been linked to the dendritic spine.
In this review, the focus has been on how education triggers as a potent stimulus to instigate the cascade of the events that lead to the formation of memories and discusses how it can alter the learning mechanism and memory formation within the neural cortex.
To review the papers which explore and investigate the fundamental mechanism involving the learning and memory in the brain, using the minimal amount of the terminologies in biology and psychology was inevitable, however in rare cases where some terminologies seem elusive, proper explanation has been provided with enough details but it is assumed that the reader has the basic knowledge of the neural structures.
Education and pedagogic methods and methodologies cannot be investigated in depth and related theories cannot be depended on without a scientific benchmark which should stand as a point of reference.
The point of the reference however, should provide a basis not only to prove the existing methodologies but also to provide opportunities that help the academics and educational theorecien to predict the efficiency and efficacy of their theories and ensure of their responsiveness of their theories for the educational purposes.
Science, particularly the science which explores the brain and mind, both from the biological and biochemical perspective can provide the reference point and frame for the educational theories and methods. The validity and acceptability of the educational theories then can be benchmarked with the science which demonstrate the impact of those methods with respect the mechanisms in the brain and neuronal circuits which form the learning and encode the memory.
In this review the efficacy and efficiency of the educational theories are investigated through the prism of the neuroplasticity and in finer details the synaptic plasticity. This may help the educators to devise education strategies where the output has a long-lasting impact on the student’s memory formation.
Learning Mechanism and Memory Formation
At the end of the 19th century, scientists recognized that the number of the neurons in the brain did not increase significantly with age which gave the scientists a reason to believe that memories were not the result of the new neuron creation.  Then as a result the theories on learning and memory formation which was based on the idea that neurons are created to store the memories were essentially obsolete.
The Spanish neuroanatomist Santiago Ramon Cajal proposed a mechanism of learning that did not require the formation of new neurons. He postulated that memories might instead be formed by strengthening or weakening of the connections between existing neurons. This theory later was emphasized by the Donald Hebb nowadays referred to as Hebbian theory on learning and memory to state that neural cells may grow completely new connections and generate new synaptic connections or enhance their ability to communicate. 
All the traditional views and postulates on the learning mechanism and memory become more scientifically relevant by the advent of the concept of the long-term potentiation LTP which literally is the persistent strengthening of the neuronal connections based on the recent pattern of the activity.
The long term potentiation in the brain is one the most important phenomena that results in the synaptic plasticity and is widely considered one the major cellular reactions that underlines learning and memory.
Memory encoding and learning starts when the signals either from the visual or auditory stimuli enters first enters the dentate gyrus of the hippocampus and then granule neurons of the dentate gyrus transmits the signals which they are essentially the information obtained in the learning process to the axons of the neuros in the CA1 region of the hippocampus which is called Schaffer Collaterals to the CA1 pyramidal cells. 
For example, the process of studying and preparing for an upcoming exam or test, activates certain but various neural pathways within the brain, the continued and persistent activation of these specific pathways that is what that leads to memory retention for long periods of time and sometimes for the life time. 
Long term memory of the humans in the brain anatomy is associated with a structure which resembles a horse shoe deep inside the brain as it is referred to hippocampus, this complex structure involved in many complex aspect of cognition is found in both hemisphere of the brain within the medial temporal lobe which plays two crucial role in the cognition which is retention and retrieval of memories and also heavily involved in the mechanism of the learning within the context of the education. 
The medial temporal lobe although critical for learning and memory formation, has severe consequences for cases where the medial temporal lobe dysfunctions. The most occurring case of disorders is the Pick`s disease (frontotemporal dementia) which is caused by the atrophy of the frontotemporal lobe, the symptoms of this disease is normally immediate mood changes, extremely poor attention span and aggressive behavior towards themselves and others.  However, there are many other symptoms such as language deficit and loss of vocabulary in which further diagnosis requires psychological tests but the personality and emotional change as well as the deterioration of the language is the initial hallmark of the Pick`s disease without going further into details in the pathological aspect of the disease . Although it may sound bizarre that the dementia is generally a type of neurological disorder that hit the patients at old age, the Pick`s disease can start as early as teenage period with unknown cure for it yet and unfortunately for some severe cases of the frontotemporal dementia the patient passes away after several years of the diagnosis. 
Other curious case for the importance of the temporal lobe of the brain within the context of the learning and education comes from the interesting syndrome as Savant Syndrome, which may be caused by the damage to the anterior portion of the left temporal lobe.
Savant Syndrome is type of the neurodevelopmental disability which is like autism spectrum and has been the inspiration of making the movie Rain Man, students diagnosed with this disorder although has mental disorder but demonstrate certain abilities far in excess of average, these abilities may include artistic ability, rapid calculation or musical abilities. 
Although, the savant syndrome can be induced either following a severe brain injury causing the lesions on the left anterior temporal lobe or ultimately can be induced artificially by using the transcranial magnetic stimulation (TMS) in order to temporarily disable the lower left anterior temporal lobe. 
Coming back to the memory formation, Hippocampus has 3 major structures which each one coordinates with each other for the processing of the memory and learning new information which are dentate gyrus, CA1 and ultimately CA3.
But when you are exposed to new information or the new stimuli, how the learning and memory processing begins?
When the signals are back to the internoral cortex at the CA1 region the process which is termed long term, potentiation is mainly responsible for the learning process and the formation of the memory which is essentially a long lasting and enduring enhancement of the signal transmission between two neurons after the repeated stimulation. The impact of the LTP has been extensively studied for the synapse which are formed between the Schaffer collateral axons of the CA3 neurons and the CA1 pyramidal cells. 
At the post synaptic cells there are two sites that receive the signal transmitted to them, the NMDA and APMA receptors, which are activated by opening their channels by the influence and binding the powerful excitatory neurotransmitter and the most abundant in the brain glutamate. The AMPA receptors which they are widely scattered on the post synaptic site of the neurons after binding of the glutamate receptors to them becomes permeable to the sodium ions. [10-21]
When the signals which carries the stimuli due to the learning reaches the presynaptic site, it releases a small amount of the neurotransmitter glutamate which triggers the release and entering of the sodium ions inside the post synaptic neurons through the activated open AMPA receptors which this gradient of the positive charge inside the cells which is the depolarization
However, at the same time the glutamate neurotransmitters are binding to the NMDA receptors but as the channel of the receptor is locked the magnesium ions and the number of the glutamine is not enough, no sodium ions pass through the NMDA receptor which contributes nothing to the polarization of the inner cell with respect to the outer cell environment, which essentially equivalent of not having higher intensity LTD. This can be easily understood and comprehended when students study a material for a short time and only a few times with not enough repeating which at the neuronal level and mechanism of the learning few times study session do not contribute to persistent long lasting LTD at the synaptic level to result in a long-term memory.
But on the other hand, when studying is persistent, a higher frequency signal is travelling through the Schafer collateral which induces higher density of glutamate neurons at the synaptic level which is like when students study for a longer period. [10-21]
The stronger signal transmission from the Schafer collateral causes the release of the higher intensity of the glutamate and the channels through the AMPA receptors stays open for longer resulting of the flow of the higher density of the sodium ions into the post synaptic region and a higher depolarization level and these higher intensity of the sodium ions inside the post synaptic cleft repels the magnesium positive ion which locks the NMDA receptor by the electrostatic force .At this stage the NMDA receptor bounded to the glutamate receptor lets the flow of the calcium ions inside the post synaptic cleft. [10-21]
The flux of the calcium ions inside the post synaptic regions of the hippocampus neurons causes a cascade of the many other secondary reactions before the formation of the memory as a result of the learning. The increase of the calcium contributes to two different stages of long term potentiation LTP. At the early phase of the LTP, the calcium ions binds to a specific protein which results in the fixation of more AMPA receptors of the membrane of the post synaptic neurons for the purpose of the sodium ions uptake at the CA1 region of the hippocampus. However, prolonged study time, causes the longer presence of the calcium ions inside the intracellular neurons, these calcium ions which stays longer inside the neurons contributes to the synthesis of the protein leading to the final synthesis of the more AMPA receptor clinging to the membrane of the neurons at the post synaptic and contributing to more and more flux of the sodium ions and as a result more depolarization. [10-21]
On the other hand, increased gradient of the calcium ions inside the cytoplasm of the post synaptic neurons due to a stronger signal or action potential of prolonged study period causes the formation and synthesis of a protein called growth factor. The growth factor protein through a cascading events involves in the formation of the new synapses or the dendritic spines between the CA1 and CA3 synapses allowing the stronger connection between the two neurons. The strengthening of the synaptic connections which is vital for remembering and recalling the information namely as memory provides the basis also for the neuroplasticity and synaptic plasticity. [10-21]
The dynamics of these newly formed dendritic spines which are the result of the cascading events inside the cytoplasm of the post synaptic neurons due to the growth factor proteins then plays an important role in the maintenance of the memory over a life time. [10-21]
The dendritic spines are morphologically very diverse and they vary in shape and structure and can be classified as cup-shaped, mushroom, stubby, thin or filopodial spines. 
However, the changes of dendritic spine number on the post synaptic neurons, their size and morphology which are collectively termed “structural synaptic plasticity” are significantly correlated with the abundance of post synaptic density and organization and localization of the AMPA-type glutamate receptors at the post synaptic sites of the neuronal connectivity
These changes of the number and their size results in the connectivity and the strength of the synaptic connection and consequently the efficiency of the signal transmission between the connecting neurons which is termed “functional synaptic plasticity”. 
Structural synaptic plasticity, particularly those related to the changes in dendritic spine density and their shapes is critical for the learning and memory mechanism as outlined above. for example enhanced spine formation is associated with the improved performance after learning  as an example motor learning experience induces the very rapid formation of the dendritic spines in the mouse motor cortex ( the region of the brain involved in planning , control and execution of the voluntary movements ) and also the long continuation of the training task stabilizes the learning induced spines and interestingly , the repetitive post synaptic depolarization which leads to the long term potentiation LTP promotes dendritic spine enlargement 
The synaptic strength and the efficiency of the signal transmission between the neuronal connectivity between CA3 and CA1 in the hippocampus as noted earlier depends then on many structural factors in the neuronal connection, as volumes of the synaptic buttons of the presynaptic neurons and the density of the dendritic spines of the post synaptic neurons, thedensity of the synaptic vesicles carrying the bulk of the glutamate neurotransmitter, the areas of the active zones in the and eventually the composition of the post synaptic density 
The concurrent increases in the size of the dendritic spines, presynaptic boutons and eventually the post synaptic density are critical for synaptic plasticity which suggests that dendritic spine morphology plays a vital and important role in synaptic plasticity 
Recent evidences also, implicates synapses at dendritic spines as important substrate of pathogenesis of many neuropsychiatric disorders including autism spectrum disorder. For example, increased dendritic spine density has been observed in the frontal, temporal and parietal lobes of human ADS brains and recent studies indicate a defect in dendritic spine pruning from 13-18 years of age which is proposed that this pruning deficit may contribute to abnormalities in the cognitive functions that human acquire in their late childhood, teenage or early adult years. 
Memory loss and cognitive decline which are the symptoms of some neurological disorders such as Alzheimer`s disease also has been correlated with chemical mechanism at the synaptic gap that leads to the loss of dendritic spines 
Understanding the learning mechanism and memory formation in the neural networks provides an essential knowledge for the educators and theoreticians of the education to assess and evaluate their pedagogical method against the science behind the learning and ask themselves the incorporation of new methodologies or incorporation of the new changes how and in what possible way can impact the neural mechanism of the brain by invoking the building blocks of the learning and memory which are the long term potentiation and the growth of the dendritic spines due to the exposure to environment stimuli and teaching materials.
If these consideration be taken into account, then when it comes to answer the questions within the education context, such as whether there should be homework or not , the answer without equivocation can come from the science behind that involves the memory formation.
Dendritic spine: is a small membranous protrusion from a neuron’s dendrite that typically receives input from a single axon at the synapse. Dendritic spines serve as a storage site for synaptic strength and help transmit electrical signals to the neuron’s cell body.
Dentate Gyrus: The dentate gyrus is part of a brain region known as the hippocampus (part of the hippocampal formation). The dentate gyrus is thought to contribute to the formation of new episodic memories, the spontaneous exploration of novel environments, and other functions.
Granule Neurons: Cerebellar granule cells form the thick granular layer of the cerebellar cortex and are among the smallest neurons in the brain. (The term granule cell is used for several unrelated types of small neurons in various parts of the brain.)
Long Term Potentiation: In neuroscience, long-term potentiation is a persistent strengthening of synapses based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons.
Neural Pathways: A neural pathway is the connection formed by axons that project from neurons to make synapses onto neurons in another location, to enable a signal to be sent from one region of the nervous system to another. Neurons are connected by a single axon, or by a bundle of axons known as a nerve tract, or fasciculus.
Neurotransmitters: are endogenous chemicals that enable neurotransmission. It is a type of chemical messenger which transmits signals across a chemical synapse
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
-  Santiago Ry (1894). “The Croonian Lecture: La Fine Structure des Centres Nerveux”. Proceedings of the Royal Society of London. 55 (331–335): 444–468
-  Caporale N; Dan Y (2008). “Spike timing-dependent plasticity: a Hebbian learning rule”. Annual Review of Neuroscience. 31: 25–46.
-  Bliss TV, Collingridge GL (January 1993). “A synaptic model of memory: long-term potentiation in the hippocampus”. Nature. 361 (6407): 31–9.
-  Doyere, V. & Laroche, S. Hippocampus 2, 39–48 (1992).
-  Van Harreveld, A. & Fifkova, E. Swelling of dendritic spines in the fascia dentata after stimulation of the perforant fibers as a mechanism of post-tetanic potentiation. Exp. Neurol. 49, 736–749 (1975)
-  Bliss, T. V. & Lomo, T. Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. J. Physiol. (Lond.) 232, 331–356 (1973)
-  Yamakawa, K; Takanashi M; Watanabe M; Nakamura N; Kobayashi T; Hasegawa M; Mizuno Y; Tanaka S; Mori H (2006). “Pathological and biochemical studies on a case of Pick disease with severe white matter atrophy”. Neuropathology. 26 (6): 586–591
-  Hughes JR (2012). “The savant syndrome and its possible relationship to epilepsy”. Advances in Experimental Medicine and Biology. 724: 332–43
-  Allan Snyder, Explaining and inducing savant skills: privileged access to lower level, less-processed information, Phil. Trans. R. Soc. B (2009) 364, 1399–1405
-  Frey U, Morris RG (February 1997). “Synaptic tagging and long-term potentiation”. Nature. 385 (6616): 533–6.
-  2. Chater TE, Goda Y: The role of AMPA receptors in postsynaptic mechanisms of synaptic plasticity. Front. Cell. Neurosci. 2014, 8:401. 3.
-  Saneyoshi T, Fortin DA, Soderling TR: Regulation of spine and synapse formation by activity-dependent intracellular signaling pathways. Curr. Opin. Neurobiol. 2010, 20:108-115.  MacGillavry HD, Hoogenraad CC: The internal architecture of dendritic spines revealed by super-resolution imaging: what did we learn so far? Exp. Cell Res. 2015, 335:180-186
-  Maiti P, Manna J, Ilavazhagan G, Rossignol J, Dunbar GL: Molecular regulation of dendritic spine dynamics and their potential impact on synaptic plasticity and neurological diseases. Neurosci. Biobehav. Rev. 2015, 59:208-23
-  Saneyoshi T, Fortin DA, Soderling TR: Regulation of spine and synapse formation by activity-dependent intracellular signaling pathways. Curr. Opin. Neurobiol. 2010, 20:108-115.
-  Um K, Niu S, Duman JG, Cheng JX, Tu YK, Schwechter B, Liu F, Hiles L, Narayanan AS, Ash RT et al.: Dynamic control of excitatory synapse development by a Rac1 GEF/GAP regulatory complex. Dev. Cell 2014, 29:701-715
-  Chen Y, Wang Y, Erturk A, Kallop D, Jiang Z, Weimer RM, Kaminker J, Sheng M: Activity-induced Nr4a1 regulates spine density and distribution pattern of excitatory synapses in pyramidal neurons. Neuron 2014, 83:431-443.
-  Okamoto K, Bosch M, Hayashi Y: The roles of CaMKII and Factin in the structural plasticity of dendritic spines: a potential molecular identity of a synaptic tag? Physiology (Bethesda) 2009, 24:357-366
-  Spence EF, Soderling SH: Actin out: regulation of the synaptic cytoskeleton. J. Biol. Chem. 2015, 290:28613-28622.  Matsuzaki M, Honkura N, Ellis-Davies GC, Kasai H: Structural basis of long-term potentiation in single dendritic spines. Nature 2004, 429:761-766.
-  Lei W, Omotade OF, Myers KR, Zheng JQ: Actin cytoskeleton in dendritic spine development and plasticity. Curr. Opin. Neurobiol. 2016, 39:86-92.
-  Maiti P, Manna J, Ilavazhagan G, Rossignol J, Dunbar GL: Molecular regulation of dendritic spine dynamics and their potential impact on synaptic plasticity and neurological diseases. Neurosci. Biobehav. Rev. 2015, 59:208-237.
-  Tanaka J, Horiike Y, Matsuzaki M, Miyazaki T, Ellis-Davies GC, Kasai H: Protein synthesis and neurotrophin-dependent structural plasticity of single dendritic spines. Science 2008, 319:1683-1687.
-  Yang G, Pan F, Gan WB: Stably maintained dendritic spines are associated with lifelong memories. Nature 2009, 462:920-924.
-  Xu T, Yu X, Perlik AJ, Tobin WF, Zweig JA, Tennant K, Jones T, Zuo Y: Rapid formation and selective stabilization of synapses for enduring motor memories. Nature 2009, 462:915-919.
-  Matsuzaki M, Honkura N, Ellis-Davies GC, Kasai H: Structural basis of long-term potentiation in single dendritic spines. Nature 2004, 429:761-766.
-  Caroni P, Donato F, Muller D: Structural plasticity upon learning: regulation and functions. Nat. Rev. Neurosci. 2012, 13:478-490.
-  Meyer D, Bonhoeffer T, Scheuss V: Balance and stability of synaptic structures during synaptic plasticity. Neuron 2014, 82:430-443
-  Meraj Joensuu, Vanessa Lanoue,Pirta Hotulainen , Denderitic spine actin cytoskeleton in autism spectrum disorder , Progress in Neuropharmacology and Biological Psychiatry 2018,362-381
-  Spires-Jones T, Knafo S: Spines, plasticity, and cognition in Alzheimer’s model mice. Neural Plast. 2012, 2012:319836.