Introduction
Infantile amnesia is one of the phenomena that have been extensively studied for decades. Explanations have been sought with multiple empirical studies focusing either on human or nonhuman subjects. The term infantile amnesia has been defined as the condition where adults are unable to remember their early-life experiences. Much of the current literature focuses on empirical evidence from laboratory experimentation with rats, and a few have studies actual human beings. Regardless of the research subjects, consistency in the findings has offered a generalized view of the causes of infantile amnesia. According to Glenberg and Hayes (2016), infantile amnesia is characterized by faster forgetting of childhood events up until seven years of age. Most importantly, this problem occurs across all altricial species, which is why even the studies on rats can be generalized to human populations. As will be highlighted in this literature review, some materials address memory formation and learning or the genetic and or biological process related to memory.
The purpose of this literature review is to explore why infantile amnesia occurs. An online search for empirical research and review articles on the subject has been conducted to achieve this objective. The literature review will describe the methods, approaches, and outcomes of experiments and other research work and use the information to answer why infantile amnesia occurs. In the process, a detailed definition and description of this phenomenon are explored as it has been presented in the research materials obtained. An important point to note is that when exploring the causes of infantile amnesia, some studies may offer experiments on specific genetic and biological processes, which should form a background to the problem of infantile amnesia.
Review of Literature
What mechanisms underlie infantile amnesia and memories appear to be the best starting point in this review. A similar query has been made in a study by Travaglia, Bisaz, Sweet, Blitzer, and Alberini (2017), who seek to link infantile amnesia to hippocampal learning. The basis for their research was that the memories formed during adulthood tend to be remembered for years. However, the salient episodic memories in childhood are rapidly and easily forgotten. The hypothesis generated in the study is that the infant’s brain is immature, which is seen as the main cause of amnesia. The idea behind this hypothesis is that neural substances and cell or circuitry composition of the hippocampal, cortical, or other areas that process episodic memories are underdeveloped, which means that they lack functional competence. Therefore, what causes amnesia, according to this hypothesis, is the underdevelopment of infant’s brains.
Empirical evidence from tests using such animal subjects as rats is rampant and common among the researchers. To test their hypothesis, Travaglia et al. (2017) have used inhibitory avoidance to show that the acquisition and storage of episodic threatening experiences tend to require hippocampal mechanisms. It is important to emphasize that their study seeks to answer why infantile memories are forgotten, yet they tend to influence adult life. Therefore, Travaglia et al. (2017) find that early life memories remain latent and that later reminders can help the subjects recall. Regarding what causes infantile amnesia, the explanation of the hypothesis of the hippocampal mechanism has been retained. The experiments have involved training rats and measuring their memories at designated periods. To test the hypothesis of hippocampal mechanisms, the researchers used hippocampal implants and injections, after which manipulations were made. The general conclusion is that the critical developmental period in infants is a key determinant of the possibility of infantile amnesia. In other words, the condition results from the inability of the infants to form long-term associative memories.
Hippocampal mechanisms have become the focus of many empirical studies whose experiments seek to determine object location learning and memory formation. Similar to Travaglia et al. (2017), research by Travaglia, Steinmetz, Miranda, and Alberini (2018) has also explored the role of the hippocampus in object learning and memory formation in infant rats. It has been expressed earlier that many empirical studies, mostly in the form of laboratory experiments, use nonhuman subjects, mostly rats. The similarities between these two studies go beyond the use of rats – they also hold the same hypothesis regarding hippocampal mechanisms and the use of later reminders to reinstate lost infant memories. Additionally, similar methodological approaches, including the measurements and periods of observation, are used in Travaglia et al. (2018), which means that similar results can be expected. Therefore, it can be concluded that the hippocampal mechanisms are responsible for the loss of episodic memories and the onset of infantile amnesia.
Even though the similarity is found between the above studies regarding the experimental approaches, it is important to highlight that the subjects determine the choice of methods. For example, postnatal days 17 and 24 (PN17 and PN24, respectively) are selected in the studies because they correspond to various phases of hippocampal maturation. Therefore, the studies found a possibility to recapitulate infantile amnesia at PN17 and not PN24 (Travaglia et al., 2017; Travaglia et al., 2018). An explanation for this finding is that memories formed during these two time periods can be reinstated with reminders, even though they would still be lost after a day. The findings by Travaglia et al. (2018) regarding hippocampal injections were also indicative of the role of the hippocampus.
Most importantly, the injections were intended to facilitate maturity and improve functional competency, which yielded positive results. In other words, the injections after training at PN17 were associated with higher levels of memory retention. Therefore, brain immaturity and functional incompetence in infants are the main reason that infantile amnesia occurs.
The association of infantile amnesia with hippocampal mechanisms has resulted in many experiments and studies extensively studying the hippocampus and its role in memory retention. The term hippocampal amnesia has been used by Argyropoulos et al. (2019). They hypothesized that network abnormalities are the basis for understanding the inconsistencies in the debates surrounding the role of the hippocampus in amnesia. Their study expressed that the damages in the hippocampus explain the variations in memory loss across the cohort of patients. The researchers used patients from autoimmune limbic encephalitis, a syndrome related to the focal structural hippocampal pathology. In such patients, the study identified an impaired recall, remote autobiographical amnesia, and recognition and maintenance of new information. Therefore, Argyropoulos et al.’s (2019) research are one of the few studies that have used neuroscience to explain human memory. However, it is unclear what the relationships are between infantile amnesia and hippocampal amnesia. Even so, the literature examine above indicates that the hippocampal mechanisms are critical determinants of memory formation and retention.
Therefore, it can be acknowledged that most empirical studies on the hippocampus and its role in memory can be used to explain the mechanisms behind infantile amnesia. However, it is also important to distinguish between the empirical evidence on infantile amnesia as expressed in such studies as Travaglia et al. (2017) and Travaglia et al. (2018) and the hippocampal amnesia discussed by Argyropoulos et al. (2019). First, infantile amnesia is seen as the result of underdeveloped brains and the hippocampus in children. On the other hand, hippocampal amnesia is caused by damages in the hippocampus due to certain illnesses. Therefore, while both streams of research explain how the hippocampus relates to memory, the sole focus on infantile amnesia should pay more attention to the development of the hippocampal mechanisms themselves instead of damages observable in elder patients. However, it does not mean that the research by Argyropoulos et al. (2019) is irrelevant. On the contrary, further information regarding the functioning of the hippocampus serves to explain just how important the hippocampus is to memory creation and retention.
As mentioned earlier, all studies on hippocampal mechanisms and their role in memory can be used are references in studying infantile amnesia. The concept of developmental amnesia has been studied by Elward, Rugg, and Vargha-Khadem (2021). They have established that this condition is associated with early damages in the hippocampus and the subsequent episodic amnesia. It can be argued that while their study does not necessarily directly the problem of infantile amnesia, Elward et al. (2021) pay adequate attention to memory and learning, which are the two main elements involving the hippocampal mechanisms. Therefore, their research led to the conclusion that patients with developmental amnesia displayed impaired scene memory, a condition that is almost similar to forgetting childhood experiences in infantile amnesia. The fact that the two concepts, infantile and developmental amnesia, deal with memory means that the hippocampal hypothesis has been proven by Elward et al. (2021). Therefore, it can be seen that most empirical studies reach the same conclusion that infantile amnesia is the result of the defects in the hippocampus.
Some studies have focused on humans, while others have used nonhuman research subjects, depending on the research methods and approaches used. Both Elward et al. (2021) and Argyropoulos et al. (2019) have used human subjects as observational research methods. In other words, their studies have observed the conditions in the human brain and how it affects memory. On the other hand, experimental studies used by Travaglia et al. (2017) and Travaglia et al. (2018) means that rat subjects have been used. Experimentations often involve the manipulation of variables to cause changes in others. Specifically, the two experimental studies manipulated the hippocampus to produce changes in amnesia in rats. Such procedures cannot be performed on humans, making rats were the ideal subjects. However, the experimental studies have offered a better view of the relationship between variables. The causal nature of the association between the variables can be determined. In observational studies, it isn’t easy to establish the causal relationship because only general links can be developed. However, the bottom line is that all studies have shown hippocampal mechanisms to be the key determinants of childhood amnesia.
So far, the hippocampus is the most critical element in infantile amnesia. A study by Cowan, Stylianka, and Richardson (2018) has deviated from this hypothesis and argues that early life experiences are responsible for this phenomenon. However, examples of early experiences given have included brain development, microbiota, and early-life stress. Regarding brain development, a connection has been made to hippocampal development. In other words, the research result in their study reveals that early stresses are related to more mature patterns of emotional stimuli and stronger connectivity in the hippocampal network. Therefore, the same hypothesis seems to me sustained regarding hippocampal mechanisms in memory development and retention. The key point to note with Cowan et al. (2018) is that the causes of brain damage or determinants of brain development have been highlighted and linked with the problem of amnesia. Neuronal development is also offered in addition to the hippocampus, where fear-related neuronal structures, including the amygdala, are related to the early onset of infantile amnesia.
Neurogenesis is another concept that has been associated with forgetting and is related to the hypothesis of the hippocampal mechanism. Research by Epp, Mera, Kohler, Josselyn, and Frankland (2016) that established memories can interfere with the encoding of new memories, especially when the new ones overlap in content with the existing ones. Such a hypothesis can support an argument that some of the childhood memories are forgotten because new ones have been created. The study by Epp et al. (2016) attempts to show that manipulating the levels of hippocampal neurogenesis can regulate the proactive interferences to memory retention. The findings have indicated that increasing hippocampal neurogenesis tends to weaken existing memories in mice. Therefore, it is not necessarily that hippocampal damage or developmental incompetence in the brain causes infantile amnesia. In most cases, the growth of the hippocampus results in the creation of new memories, which causes the older ones to be forgotten. This study has illustrated that regardless of the stand taken by the researchers, the role of the hippocampus in memory retention is a theme that is impossible to skip when examining the causes of infantile amnesia.
The available empirical studies have been the foundation of most other scholarly works, especially commentaries and literature reviews on the subject of infantile amnesia. Such an argument is rationalized because other materials cite the empirical evidence and comment and or criticize the various hypotheses. Infantile amnesia has been described as a riddle by Glenberg and Hayes (2016), especially when considering the question of why the hippocampus matures at a certain time and not another. Even with the mention of hippocampal development, Glenberg and Hayes (2016) develop a hypothesis rooted in the theories of embodied cognition to explain both infantile amnesia and hippocampal development. Most importantly, locomotion has been seen as a critical factor because it influences the alignment of the hippocampus place cells to the environment. In other words, locations tend to become critical cues for memories, which means that new environments lead to new memories. Such arguments can be perceived as aligned with the hypothesis of early life experiences proposed by Cowan et al. (2018). Therefore, the child’s development, experiences, and environment are all responsible for infantile amnesia.
Several authors have explored the role of the environment in the development of learning and memory. According to Callaghan (2020), the environment can program learning and memory, a subject that has captured the attention of psychiatry and psychology due to the clinical implications. However, the focus here is on the causes of infantile amnesia, which these authors agree that the early conditions in the environment have a key role to play. The arguments have been founded on past experiments with rats, which have established that molecular markers in the brain are associated with infantile amnesia. Most importantly, the environment has been shown to shape early experiences, including stress. Such experiences are referred to as sensitive periods of memory and learning. An example of an experiment used is where rats have been conditioned to behave in certain ways in response to fear and threat-predictive cues. Such experiences tend to influence the developments in the amygdala and frontal cortex, regions of the brain that play a significant role in creating and retaining memory.
Infantile amnesia has been described as the inability to remember childhood memories. Some scholars call these memories autobiographical or episodic and have established that they are heavily reliant on the hippocampus. Other terminologies often used in literature include hippocampus-dependent memories, suggesting a consensus that childhood memories all depend on the hippocampus. In other words, much of the literature has presented an argument that defects and damages in the hippocampus are the major cause of infantile amnesia. According to Donato et al. (2021), infant memories are processed by the hippocampus-dependent memory systems. Based on the experiments done using rat subjects, Donato et al. (2021) have presented a comprehensive overview of the functioning of the brain and the role of the hippocampus. Differences between the growth trajectories between rats and humans are also expressed, which also serve to highlight the periods when childhood memories are formed and lost. Neurogenesis is also highly referenced, which supports the argument that most reviews tend to combine findings and hypotheses from empirical studies to elaborate on the theoretical aspects of infantile amnesia.
Infantile amnesia has been extensively studied for several decades due to growing interests in the ontogeny of memory. However, some scholars feel that while most of the research has focused on the characterization of psychological determinants, the neurobiology of memory persistence has grossly been ignored (Ramsaran, Schlichting, & Frankland, 2019). Neurological and psychological perspectives are used in the arguments presented by these scholars. However, it can be seen that their hypotheses also include hippocampal mechanisms from the neurological perspective. The behavioral phenotypes are also not a new theoretical construct added into the literature by Ramsaran et al. (2019) because the focus has been on the past experiences shaping new behavior and forming new memory. Therefore, it can be argued that Ramsaran et al. (2019) have reviewed the literature from all theoretical approaches to express the need to divert attention to the ontogeny of memory.
However, it is important to acknowledge that even the literature reviews have raised new themes or offered better scientific explanations to the phenomena associated with infantile amnesia. The empirical studies have largely proven a link between infantile amnesia and hippocampal mechanisms and other elements. However, detailed explanations are largely absent compared to works by such scholars as Ramsaran et al. (2019). These researchers have explained hippocampal neurogenesis, a process where increases in synaptic junctions following learning tend to impede responses previously learned. In other words, new synapses in the hippocampus are continually added through the addition of new neurons, which occur in the dentate gyrus throughout mammalian life.
Additionally, Ramsaran et al. (2019) elaborate that neurogenesis is regulated by age, which means infants face constant remodeling in their hippocampus. The main difference between such scholars as Travaglia e al. (2017) is that they ask questions and use experiments to answer them. On the other hand, reviews often seem to use the evidence from the experiments to offer more details, especially the hippocampus’s underlying mechanisms.
The evidence from the literature can lead to one major conclusion: that infantile amnesia represents a critical period in learning and remembering. Such sentiment has been expressed by Alberini and Travaglia (2017), whose paper can be seen as a reiteration of the key points regarding infantile amnesia. For example, they have defined infantile amnesia as the inability of adults to recollect episodic childhood memories. Additionally, they have emphasized such hypotheses as to the role of brain development in amnesia and the early life experiences as the key determinants of infantile amnesia. The most important points expressed is the mechanisms of the hippocampus-dependent memories. Additionally, it has been reiterated that the hippocampus does not fuction on its own. On the contrary, it tends to cooperate with other such regions as the cortical and the medial temporal lobe. However, it important to acknowledge that the hippocampal mechanisms still dominate all literature on the causes of infantile amnesia. This is because despiteb the approach taken or the methodologies deployed in both the empirical and review studies, the hippocampus has emerged as a common theme as the key determinant of infantile amnesia.
Summary
The focus of this literature review was to address the question of why infantile amnesia occurs. A description of this phenomenon has been presented, where the main definition has been the inability of adults to remember childhood memories. Several empirical studies have been explored, all of which have presented first-hand data from experiments and other research approaches. Two groups have been observed: one uses experiments with nonhuman subjects, specifically rats, while the other uses human subjects. However, it has been expressed that regardless of the methodological approaches, all empirical studies have illustrated the relationship between infantile amnesia and hippocampal mechanisms. Therefore, the defects and damages in the brain are the major determinants of infantile amnesia. However, it is also important to acknowledge that some studies could only be used for inferences in the association between hippocampus and memory. For example, those studies exploring memory loss in adults after surgeries only inform on how brain damage can complicate memory formation and retention.
Another key observation is that other studies, majorly reviews and commentaries on the subject, have drawn heavily from the empirical studies. However, there has been no deviation from the primary hypothesis linking the hippocampus to infantile amnesia. A few other concepts may have been mentioned, but they all led to the brain and the regions involved in learning and memory. Examples include early life experiences and the environment, as expressed in several studies, but even these have expressed that the experiences and the environment influences hippocampal development and alignment. Therefore, the answer to the research question is that infantile amnesia is caused by defective brain development among infants, where the hippocampus and other brain regions play a critical role. This answer is founded on the common themes established across all the studies explored in this literature review.
References
Alberini, C., & Travaglia, A. (2017). Infantile amnesia: A critical period of learning to learn and remember. Journal of Neurscience, 37(24), 5783-5795. Web.
Argyropoulos, G., Loane, C., Roca-Fernandez, A., Lage-Martinez, C., Gurau, O., Irani, S., & Butler, C. (2019). Network-wide abnormalities explain memory variability in hippocampal amnesia. eLife, 8, 1-38. Web.
Callaghan, B. (2020). Nested sensitive periods: How plasticity across the microbiota-gut-brain axis interacts to affect the development of learning and memory. Behavioral Sciences, 36, 1-8. Web.
Cowan, C., Stylianka, A., & Richardson, R. (2018). Early-life stress, microbiota, and brain development: Probiotics reverse the effects of maternal separation on neural circuits underpinning fear expression and extinction in infant rats. Developmental Cognitive Neuroscience, 37, 1-10. Web.
Donato, F., Alberini, C., Amso, D., Dragoi, G., Dranovsky, A., & Newcombe, N. (2021). The ontogeny of hippocampus-dependent memories. The Journal of Neuroscience, 41(5), 920-926. Web.
Elward, R., Rugg, M., & Vargha-Khadem, F. (2021). When the brain, but not the person, remembers: Cortical reinstatement is modulated by retrieval goal in developmental amnesia. Neuropsychologia, 154, 1-12. Web.
Epp, J., Mera, R., Kohler, S., Josselyn, S., & Frankland, P. (2016). Neurogenesis-mediated forgetting minimizes proactive interference. Nature Communications, 7, 1-8. Web.
Glenberg, A., & Hayes, J. (2016). Contribution of embodiment to solving the riddle of infantile amnesia. Frontiers in Psychology, 7(10), 1-6. Web.
Ramsaran, A., Schlichting, M., & Frankland, P. (2019). The ontogeny of memory persistence and specificity. Developmental Cognitive Neuroscience, 36, 1-15. Web.
Travaglia, A., Bisaz, R., Sweet, E., Blitzer, R., & Alberini, C. (2017). Infantile amnesia reflects a developmental critical period for hippocampal learning. Nature Neuroscience, 19(9), 1225-1233. Web.
Travaglia, A., Steinmetz, A., Miranda, J., & Alberini, C. (2018). Mechanisms of critical period in the hippocampus underlie object location learning and memory in infant rats. Learning and Memory, 25(4), 176-182. Web.