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 Sensory
memory is the memory that results from our perceptions
automatically and generally disappears in less than a second.
It includes two sub-systems: iconic memory of visual perceptions
and echoic memory of auditory perceptions. [3]
Short-term memory
depends on the attention paid to the elements of sensory memory.
Short-term memory lets you retain a piece of information for
less than a minute and retrieve it during this time. One typical
example of its use is the task of repeating a list of items
that has just been read to you, in their original order. In
general, you can retain 5 to 9 items (or, as it is often put,
7±2 items) in short-term memory. [3]
Working memory
is a more recent extension of the concept of short-term memory.
As techniques for studying memory have become more refined,
it has become increasingly apparent that the original conception
of short-term memory as a mere temporary receptacle for long-term
memory is too simplistic. In fact, it is becoming increasingly
clear that there is no strict line of demarcation between
memories and thoughts. In order to test some hypotheses that
may provide a better understanding of this complex phenomenon,
the concept of working memory has therefore been advanced.
[3]
Long-term
memory
Explicit (declarative)
memory: your memory of all those things that you
are aware of remembering and that you can describe in words,
such as your birthday, or the meaning of the word "cradle",
or what you ate last night. This form of memory is also called
explicit memory, because you can name and describe each of
these remembered things explicitly. There are two types of
explicit memory: episodic and semantic.
Episodic memory lets you remember events that you
personally experienced at a specific time and place. It includes
memories such as the meal you ate last night, or the name
of an old classmate, or the date of some important public
event.
Semantic memory is the system that you use to store
your knowledge of the world. It is a knowledge base that we
all have and much of which we can access quickly and effortlessly.
It includes our memory of the meanings of words–the kind
of memory that lets us recall not only the names of the world’s
great capitals, but also social customs, the functions of
things, and their colour and odour. Semantic memory also includes
our memory of the rules and concepts that let us construct
a mental representation of the world without any immediate
perceptions. Its content is thus abstract and relational and
is associated with the meaning of verbal symbols. [3]
Implicit (non-declarative)
memory is expressed by means other than words.
For example, when you ride a bike, juggle some balls or simply
tie your shoelaces, you are expressing memories of motor skills
that do not require the use of language. Such "motor
memories" are just one type of implicit memory
Procedural memory enables people to acquire
motor skills and gradually improve them. Procedural memory
is unconscious, not in the Freudian sense of suppressed memories,
but because it is composed of automatic sensorimotor behaviours
that are so deeply embedded that we are no longer aware of
them.
Implicit memory is also where many of our conditioned reflexes
and conditioned emotional responses are stored. The associative
learning that constitutes the basis for these forms of memory
is a very old process, phylogenetically speaking, and can
take place without the intervention of the conscious mind.
We form implicit memories without being aware that we are
doing so. Scientists try to uncover them by indirect methods,
such as "priming". In priming, researchers try to
increase the speed or accuracy with which their subjects make
a decision by first exposing them to information that relates
to the same context, but without the subjects' having any
other particular reason to retrieve the piece of information
concerned. For example, subjects will take less time to decide
that the string of letters "doctor" is a word if
they have first been shown the word "nurse" than
if they have first been shown an irrelevant word, such as
"north", or a nonsense word, such as "nuber".
[3]
 Hebb's
theory (1949). Neuron activities continue
even after the termination of stimulus, inducing structural
changes. Different neurons are linked via this activity and
form neural circuits that can fire with minimal stimulation.
When a nerve impulse repeatedly go from one neuron to another
then metabolic change takes place in both cells. Memory is
specific patterns of activity across a network of neurons.
Synapses (connections between neurons) become more extensive
during the learning. This is a "mechanism" of long-term
memory.
Picture: D.O. Hebb (1905 - 1985)
Reconsolidation.
There is some evidence that the very act of recalling a stored
memory erases it from storage and to preserve it, it must
be stored anew (rather as if a "SAVE" of an unchanged
computer file actually replaced the original just as a "SAVE
AS" with the same name does). This phenomenon has been
named reconsolidation. Source.
Long-term memory
can involve the formation of new synaptic connections.
Source.
Learning is
related to synaptic growth and the development of new dendritic
spines. [1]
Neural circuits
can be associative, such that a variety of memories are linked
as a whole and in parallel and they may also be temporal-sequential.
Different axons and dendrites must be highly active whereas
yet others must be silence and at the same time for these
exclusionary networks to form, thus creating networks for
specific memories. [1]
Neuron activity.
The activity between a number of specific presynaptic and
post synaptic surfaces be correlated and thus linked together,
whereas others remain at a low level of excitation so that
they do not become linked with the emerging network. A large
number of specific axons and dendrites must be actived simultaneously
which in turn allows these pathways to consolidate whereas
yet others are silenced. [1]
Dendrite
connections A single dendrite may receive
input from hundreds of axons, each of which may be concerned
with different perceptual, emotional, behavioral, or cognitive
functions. A dendrite which is repeatedly stimulated becomes
more complex and grows new dendritic spines. [1]
Neuroplasticity
The brain continues to reorganize itself by forming new neural
connections throughout life. This phenomenon, called neuroplasticity,
allows the neurons in the brain to compensate for injury and
adjust their activity in response to new situations or changes
in their environment. source
Memory
activation is a variety of cues, each of which
can trigger activation of a portion or the entire neural circuit.
[1]
Long-Term Potentiation
(LTP) is a long lasting post synaptic depolarization,
which is induced through the repetitive stimulation and summation
of excitatory post-synaptic potentials.
LTP1 Long-term
potentiation for about 6 hours. LTP1 is due to the increase
of kinases in the post synaptic dendrite. [1]
LTP2 Long-term
potentiation for about 10 hours. LTP2 is due to a buildup
in dopamine and activation of glutamate receptors. [1]
LTP3 Long-term
potentiation for weeks. LTP3 is due to dendritic growth, and
thus reflects genetic activity and protein synthesis. [1]
Origin of LTP
LTP can be a function of increased transmitter levels
(due to the release of more vesicles) as well as the changes
in the post synaptic receptors which appear to increase in
size which allows them to absorb more of the excess transmitter.
[1]
LTP may result from:
- Increased number of new AMPA receptors during stimulation
- Alteration of synaptic structure
- The dendritic spines form “perforated” synapses
with the presynaptic terminals
- Structural changes depend on entry of calcium ions and on
the calcium kinase (CaM-KII)
- Activation of NMDA receptors that increases the activity
of nitric oxide
- Nitric oxide diffuses into presynaptic terminals and may
increase glutamate release from the presynaptic terminal [2]
Mechanism of LTP
What happens is that when the axons are exposed to a
high-frequency stimulus.
 Glutamate,
the neurotransmitter released into these synapses, binds to
several different sub-types of receptors on the post-synaptic
neuron. Two of these sub-types, the receptors for AMPA and
NMDA, are especially important for LTP.
The AMPA receptor is paired with an ion channel so
that when glutamate binds to this receptor, this channel lets
sodium ions enter the post-synaptic neuron. This influx of
sodium causes the post-synaptic dendrite to become locally
depolarized, and if this depolarization reaches the critical
threshold to trigger an action potential, the nerve impulse
is transmitted to the next neuron.
The NMDA receptor is also paired with an ion channel,
but this channel admits calcium ions into the post-synaptic
cell. When this cell is at resting potential, the calcium
channel is blocked by magnesium ions (Mg2+), so that even
if glutamate binds to the receptor, calcium cannot enter the
neuron. For these magnesium ions to withdraw from the channel,
the dendrite’s membrane potential must be depolarized.
[3]
More about mechanism of
LTP Long-term potentiation (LTP) is a process in
which synapses are strengthened. It has been the subject of
much research, because of its likely role in several types
of memory. LTP is the opposite of long-term depression (LTD).
In LTP, after intense stimulation of the presynaptic neuron,
the amplitude of the post-synaptic neuron’s response
increases. The stimulus applied is generally of short duration
(less than 1 second) but high frequency (over 100 Hz). In
the postsynaptic neuron, this stimulus causes sufficient depolarization
to evacuate the magnesium ions that are blocking the NMDA
receptor, thus allowing large numbers of calcium ions to enter
the dendrite.
 These
calcium ions are extremely important intracellular messengers
that activate many enzymes by altering their conformation.
One of these enzymes is calmoduline, which becomes active
when four calcium ions bind to it. It then becomes Ca2+/calmodulin,
the main second messenger for LTP. Ca2+/calmodulin then in
turn activates other enzymes that play key roles in this process,
such as adenylate cyclase and Ca2+/calmodulin-dependent protein
kinase II (CaM kinase II). These enzymes in turn modify the
spatial conformation of other molecules, usually by adding
a phosphate ion to them. This common catalytic process is
called phosphorylation.
Thus, the activated adenylate cyclase manufactures cyclic
adenosine mono-phosphate (cAMP), which in turn catalyzes the
activity of another protein, kinase A (or PKA). In other words,
there is a typical cascade of biochemical reactions which
can have many different effects.
For example, PKA phosphorylates the AMPA receptors, allowing
them to remain open longer after glutamate binds to them.
As a result, the postsynaptic neuron becomes further depolarized,
thus contributing to LTP.
Other experiments have shown that CREB protein is another
target of PKA. CREB plays a major role in gene transcription,
and its activation leads to the creation of new AMPA receptors
that can increase synaptic efficiency still further.
The other enzyme activated by Ca2+/calmodulin, CaM kinase
II, has a property that is decisive for the persistence of
LTP: it can phosphorylate itself! Its enzymatic activity continues
long after the calcium has been evacuated from the cell and
the Ca2+/calmodulin has been deactivated.
CaM kinase II can then in turn phosphorylate the AMPA receptors
and probably other proteins such as MAP kinases, which are
involved in the building of dendrites, or the NMDA receptors
themselves, whose calcium conductance would be increased by
this phosphorylation.
To give some idea of the complexity of the metabolic sequences
responsible for LTP, we will mention three of the other enzymes
currently being studied. Protein kinase C (PKC) appears to
phosphorylate AMPA receptors at the same site as CaM kinase
II. Inhibitor 1 (ou I1) seems to be activated by PKA and prevent
phosphatase 1 from dephosphorylating AMPA receptors. And tyrosine
kinase SRC may be activated directly by the AMPA receptors,
and then phosphorylate the NMDA receptors. [3]
Degree of LTP
The degree of LTP induced was greatest at the synapse which
was first stimulated, intermediate for the second, and least
of all for the third. Hence, LTP binds those neurons, which
initially share parallel activity - a process that must occur
in numerous synapses which are activated simultaneously to
process the same event [1]
Integration interval
(Singer, 1990) The integration interval during which
presynaptic and postsynaptic activation must coincide in order
to lead to stabilization of a pathway and excitatory and inhibitory
inputs to the same dendrite must be activated and silenced
respectively. The efficiency of stimuli to induce modifications
of cortical circuitry will increase to the extent that the
stimuli not only match the response properties, but also conform
with the resonance properties of more distributed neuronal
assemblies. [1]
Silence of neural network
(Xu et al. 1998) It is necessary for neural networks to become
silenced so that specific circuits can be formed. Extensive
long-lasting decreases in synaptic efficacy may act in tandem
with enhancements at selected synapses to allow the detection
and storage of new information by the hippocampus. [1]
Long-term depression
(Artola & Singer, 1993) If two neurons form synapses with
the same dendrite but with different dendritic spines, the
more active of the two may inhibit the activity of the other.
Even synaptic links that have developed LTP may be inhibited
and develop long-term depression - which may be associated
with forgetting. [1]
Mechanism of long-term
depression Long-term depression (LTD) may be regarded
as a complementary mechanism to long-term potentiation (LTP).
In the hippocampus, the role of LTD is  thought
to be to return synapses that have been potentiated by LTP
to a normal level so that they will be available to store
new information. But elsewhere in the brain, LTD may be actively
responsible for the storage of new information.
LTD develops when a presynaptic neuron is active at low frequencies
(1 to 5 Hz) without the postsynaptic neuron’s being subjected
to strong depolarization, as it is with LTP. This lack of
association between the two neurons raises the concentration
of calcium in the postsynaptic neuron, but much less than
in LTP.
Consequently, instead of proteins such as CaM kinase II or
kinase A being activated, enzymes called phosphatases are
activated. These enzymes remove certain phosphate groups from
the AMPA receptors; in other words, they dephosphorylate them.
The AMPA receptor GluR1 subunit, which has two sites that
can be phosphorylated (Ser831, phosphorylated by CaM kinase
II, and Ser845, phosphorylated by PKA), appears to be the
target for phosphatases 1, 2A, and 2B. In the hippocampus,
the effect of this dephosphorylation of the AMPA receptor
would be to reduce the amplitude of the postsynaptic potential
to the normal level where it was before LTP.
It is also believed that the number of AMPA receptors decreases
during LTD. These receptors would be removed from the postsynaptic
membrane and placed in reserve: in short, the opposite of
what happens in LTP, when additional receptors are inserted
into the membrane.
Memory activation
When one region of the neural network is activated,
associated neurons within the circuit are likely to become
aroused in parallel or sequentially. [1]
Isolated memories
Certain memories may be shared between circuits, or confined
to a specific neural network. If there are few other memories
associated with that circuit, then this memory can come to
be isolated and may not easily retrieved. That is, only a
selective and quite narrow assortment of thoughts or associations
or future experiences may trigger memory recall, in the absence
of which the memory may appear to be forgotten. [1]
Permanence of memory
(Gloor, 1997) The neurons are involved in a variety
of circuits. Individual neurons can die, or be eliminated
from the circuit without significantly disrupting associated
memory. [1]
Sources and additional
reading
1. Joseph Rhawn, in Neuropsychiatry, Neuropsychology,
Clinical Neuroscience (Williams & Wilkins, 1996)
2. Allyn
& Bacon (2001)
3. The
brain from top to bottom
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