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Introduction:

Infantile amnesia is a puzzling
phenomenon which occurs throughout two early phases in our lives. During the
first, we cannot remember anything from the first 2 or 3 years of life, and
during the second phase our memories are also very scattered (age 3 up till 7)
(Pillemer and White 1989; Bruce et al. 2005). Theories considering our
cognitive mechanisms argue that our capability to form and store declarative
memories in our long term store is associated with language development and
theory of mind. However, further complicating the subject, we also know that
animals show signs of infantile amnesia suggesting that there are other factors
involved. Biological explanations look at the development of certain brain
regions after birth which have been previously associated as important for
maintaining information in our long term memory, such as the hippocampus. In
this essay, I will critically evaluate these two approaches by digging deeper
into completed research.

There has been a great deal of
controversy surrounding this. We know that our functioning memory develops over
our lifetime (Ofen and Shing 2013). This is intriguing because, firstly, early
events and memories are believed to be a determinant of our personality, sense
of identity and core beliefs in the present (McAdams et al., 2006). Secondly, young
children seem to have the capacity to form and recall memories and events.
Hence, the question must be asked why the majority of these become inaccessible
as we mature.

 

 

 

 

 

Changes in
Child’s Neurological Make up:

This approach suggests that key neural regions are not yet developed
enough to process memories, i.e. “immature brains”. Previous research has shed
light on the fact that postnatal development of the hippocampus and dentate
gyrus (DG), in different species including humans and rats, is protracted (Eriksson
et al. 1998; Knoth et al. 2010; Sierra et al. 2011). New neurons are added to
the DG layer of the hippocampus shortly after we’re born, decaying the memories
already stored. Either; increasing excitability reduces the stability of
memories stored in the hippocampus, or the pre-existing synaptic circuits are replaced.
“Ongoing brain maturation” theories, say that the memories lost are a result of
the cortex being offline in young children (Pillemer
and White 1989). As infants go through puberty, cortical aspects mature, such
as larger synaptic density, giving more stability to memories (Bauer 2008).

 

 

1)       Inverse Relationship Between Levels of Postnatal
Neurogenesis and Memory Persistence

2)       Increasing Neurogenesis Promotes Forgetting in
Adult Mice

1)       While these data are consistent with the idea
that high levels of hippocampal neurogenesis promote forgetting, nonetheless,
the a-CaMKII mutation produces other alterations (e.g., impaired cortical
plasticity Frankland et al. 2001 and infradian activity patterns Yamasaki et
al. 2008) that could also impair memory consolidation.

2)      Therefore, the suggestion that increasing
neurogenesis in adult animals might actually destabilize existing
hippocampus-dependent memories is, perhaps, counter-intuitive. Are these two
ideas—that adult neurogenesis contributes to both memory degradation (Feng et
al. 2001; Deisseroth et al. 2004) as well as storage (e.g., Shors
2008)—compatible?

 

 

The Development of Language:

·        
Fenson (1994) said that it shouldn’t be seen as a
coincidence that the period of language development occurs at the same time as
when we experience childhood amnesia. The rapid development of language must be
associated as part of the reason for why we struggle to recall memories during
that time. Hayne and Rovee-Collier (1995) suggested that memories encoded
without language are likely to entail retrieval failure because the child is attempting
to access memories that were experienced based primarily on perceptually based
attributes. Language acquisition makes two significant contributions to
children’s memory. i) Having conversations about the past, and ii) the child’s
ability to use language as a retrieval cue of memories (Hudson 1990; Nelson 1993).

 

1)     
Building on the position of K. Nelson (1993)
and of Hudson (1990), we hypothesize that the inability to translate early,
preverbal experiences into language prevents these experiences from becoming a
part of autobiographical memory. In this way, language development may be the
rate-limiting step in the offset of childhood amnesia.  

2)      -Children’s
verbal reports of the event were frozen in time, re?ecting their verbal skill
at the time of encoding, rather than at the time of the test. This ?nding is
clearly limited to the verbal recall of preverbal items. That is, at the time
of the test, the children recognized photographs and performed actions for
which they did not have the relevant vocabulary at the time of original
encoding.

 

1)      Unfortunately, however, the bulk of
this claim rests on anecdotal (Todd & Perlmutter, 1980) or retrospective
(Myers, Clifton, & Clarkson, 1987; Myers, Perris, & Speaker, 1994;
Perris, Myers, & Clifton, 1990) reports of children’s memory.

2)      In
the handful of studies that were speci?cally designed to assess the relation
between language acquisition and memory development, the objects that were part
of the original event were present during the test, making it impossible to
differentiate between children’s verbal recall of a preverbal memory and their
on-line descriptions of objects or actions at the time of the test (Bauer,
Kroupina, Schwade, Dropik, & Wewerka, 1998; Bauer & Wewerka, 1995,
1997). Furthermore, children’s preverbal status is often inferred on the basis
of their age alone or on the basis of general language measures that may or may
not include the vocabulary relevant to the memory task at hand. Thus, whether
or not children can actually translate their preverbal experiences into
language is not known

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