Science of Spaced Learning

The role of memory and learning has been well documented as being an important factor when learning and remembering information. Though there have been many models which have looked at addressing memory and learning, fully understanding some of the neurological and neurochemical principles would enable the educator to best set up their lesson to transfer the information they are presenting into the long-term memory of the student. It has been suggested by Toppino and Gerbier (2014) that one of the most robust and fundamental phenomena seen today regarding learning and memory is the spacing effect, however according to Gerbier and Toppino (2015), although many cognitive models have been proposed to account for the spacing effect, the neural representations contributing to it is still under discussion. One such model is the encoding variability hypothesis which according to Glenberg (1979) assumes that the greater variability that exists across learning repetitions provides more routes to effective retrieval, this is due to greater contextual changes and thus more variable encoding, resulting in the better memory performance. A second popular model is the study-phase retrieval hypothesis which proposes that each repetition serves as a retrieval cue to reactivate and then strengthen the representation of the prior experience (Thios and D'Agostino, 1976). This said, even though cognitive models have been hypothesised to explain the spacing effect, the neurological and neurochemical process of what occurs within the brain is still being researched. The current research however is suggesting that a transcription factor named CREB played a key role in converting short-term memory into long-term memory (Yin and Tully, 1996). According to Ortega-Martinez (2015), Transcription factors are seen as dominant proteins found inside the nucleus cell and whose role it is to find and bind to specific sequences of DNA which become on/off switches that control a gene's transcription. Morris (1997) stated that activation of CREB protein becomes the catalyst for the manufacturing of synapse-strengthening proteins that transform a short-term memory into a long-term one. This synapse-strengthening process has been suggested by Hebb (1949) that connections among neurons that get fired at the same time should become strengthened that form a cellular circuit. This increased strength of neuronal connections, triggered by CREB and synapse-strengthening from a process termed long-term potentiation (Choi et al 2009) can be relatively short-lived. It has been mentioned by Ikeda et al (2003) that after high-frequency stimuli have been generated within the brain the voltage produced by the synapse slowly diminishes back to its original strength within a few hours, reducing the ability of short-term memories to become long term memories the longer the time drifts. However, Fields (2005) mentions that if the same high-frequency stimulus is applied repeatedly with regular intervals of inactivity for 10-15 minutes the synapse becomes strengthened permanently, a state called late long-term potentiation. This process of the high-frequency situation was carried out by Frey and Morris (1997) who showed that synapse-strengthening proteins would affect any temporarily strengthened synapse. The researchers firstly stimulated a synapse briefly to induce early long-term potentiation, which would normally last just hours, they then fired a second synapse on the same neuron in a way that would induce late long-term potentiation that synapse. The researchers did this by inducing three bursts of activity separated by 10 minutes of waking rest, the results highlighted that both synapses were permanently strengthened with the stronger stimulus being sent a signal to the nucleus calling for memory-protein manufacture, in which the proteins then found any synapse that was already primed to use them. As with the stimulation of CREB. synapse-strengthening proteins and their relationship to long-term potentiation, the brain binds these new sequences of synapse connections into a framework of different representations and consolidations (Albouy et al, 2015) a key aspect of human evolution (Jacobacci et al, 2020) and what Genzel et al (2020) calls neural replay or more precise, hippocampal-neocortical replay, the temporally compressed reactivation of neural activity patterns representing behavioural sequences during rest to compress and imprint the information upon the neuronal framework (Terada, 2020). It has been suggested by Creswell et al, 2015) that neural underpinnings of waking rest from work demonstrate changes in activity and connectivity (Tambini et al, 2010) following encoding. This has been seen specifically right dorsolateral prefrontal cortex and left visual cortex [Creswell et al, 2019). A role of the dorsolateral prefrontal cortex is to support the control and organizational processes in associative encoding and retrieval (Blumenfeld and Ranganath, 2007) suggesting local reactivation and encoded memory representations. This dynamic process can be termed consolidation theory as it posits that a long-term memory trace is more efficiently stabilised or strengthened by spaced trials and waking rest (Wickelgren, 1972). Importantly, this form of wakeful memory consolidation has been suggested to be approximately 4-fold greater in magnitude than classically studied overnight consolidation, which requires sleep (Jacobacci et al., 2020) and is preserved even when practice experience is reduced by half (Bönstrup et al., 2020). As spoken about in the research by Frey and Morris (1997) it is important to recognise that when learning occurs over multiple optimally spaced trials, molecular signaling initiated in the first trial can extend the temporal window of enhanced neuronal excitability (Silva, 2009) which is said to increase the likelihood of the same ensemble being reactivated in subsequent activity (Pignatelli, 2019). Spaced learning would then in turn strengthen the internal synaptic connectivity and render the memory more resilient to homeostatic mechanisms that can result in forgetting which increases the probability of retrieval (Rao-Ruiz, 2019). According to Wamsley (2019) many of the same neurobiological mechanisms thought to underlie sleep’s effect on memory are shared by waking rest. First, cellular-level memory “reactivation” occurs during quiescent waking rest, in the hippocampus and it is during this process that, sequences of neuronal firing representing recent experiences are reiterated offline. Secondary Warmsley (2019) countries and suggest that acetylcholine levels are substantially reduced from active waking levels, thought to promote hippocampal-cortical communication dynamics that benefit consolidation, this in turn active process of consolidation, facilitated by the offline reactivation and synaptic plasticity.