How does the human brain store memory?

Question

This was inspired by somebody asking how much can it hold, but I want to know how?

Thankya!

Answer 1

At present, the exact mechanism for memory formation and storage is unknown. There is clear evidence that the connections (synapses) between specific neurons in the brain change their physiology after having been exposed to particular signals in a particular order. The problem lies in the fact that while we can identify molecular changes between cells in response to specific stimuli, it is not at all clear as to how or why certain synaptic changes should or do lead to memory formation.

It is known from animal studies and examinations of humans with various types of lesions in the brain that we can identify.the specific brain structures that are important for specific types of memory (i.e. short term vs long term memory; episodic vs semantic memory, etc.), However, the actual mechanism by which memories are created, processed and stored remains largely a mystery. One whose answers lie in the neural networks of the brain.

Answer 2

I think memories are stored as little packets each having a list of triggers, thousands of triggers. You activate a memory by matching one or more triggers. Maybe a colour, a word, a phrase, scene, sound or maybe a face. Maybe a song and maybe a thousand other things.

So each memory has thousands of triggers and each trigger has a sensitivity. Lets say the sensitivity is between 0 and 10. Recent or traumatic events are likely to have a high sensitivity and older and less important events will have a lower sensitivity.

So some memories will trigger often and some will trigger rarely.

I think the brain is constantly bombarded with triggers from the world you live in. Thousands of triggers a second triggering thousands of memories perhaps. These memories parade past in your conscious or subconscious mind (what am I a psychiatrist).

Answer 3

It is a very lengthy and complected answer. To sum up, memories are stored as electrical pulses and currents. Short term memory (like were you parked your car) is held in a fast moving current, while long term memory (how to walk) is a chemical reaction and the synapses go through a serious of firings for these things. The more you practice them the faster the signals get and therefore, you get better at it.

Answer 4

Apparently two ways.

Short term memory appears to be chemical. When signals are transmitted down neural pathways (like after you saw something), the residual neurotransmitter chemicals remain in the pathway, temporarily strengthening it.

Long term memory seems to be caused by growing new connections in the brain between neurons (in response to these residual chemicals)

Answer 5

How Does the Brain Store Memories?


Alzheimer's disease, Huntington's disease, epilepsy, weaking of memory as a result of aging all originate from disruption of the function of the hippocampus. The movie "Memento"(TM) where the main character cannot remember what happened to him more than five minutes prior suffers from an inability to make new long term memories, a unique form of amnesia. An epileptic patient named HM had portions of his hippocampus removed because anti-convulsant drugs were simply not preventing seizures. The result was that he no longer could make long term declarative (those memories unassociated with motor skill) memories. Thus, so much rides on a successfully operating hippocampus although it seems a small part of the brain as a whole.




Pictured above is a cartoon of a labeled hippocampus to the detail of general pathway locations.(Kandel, Science, 2001) The pathways are part of a memory stabilization process known as long term potentiation (LTP).

Our memories make us who we are. Cognitive psychology points to one's collection of long term memories as the definition of the self. Our childhood, our tragedies, our triumphs, the people we love, the people we dislike and all that we can recall with even the slightest cognition is all that we as humans can know about our selves. We can be nowhere but at the center of our own universe. Therefore, it would be desirable to know the science underlying this memory formation. Modern human science is now returning more and more to genetics for its answers.




Depolarization relieves the magnesium blockage of the n-methyl-D-aspartate channels. Calcium is allowed to then flow into the post-synaptic cell and promote LTP.(Malenka et al. Science, 1999)
Thus, it is necessary to study those microscopic processes occuring on the cellular level. An applied mathematician with even the slightest knowledge of a few aspects of biology is endlessly valuable to a biological research scientist. I have worked with Paul Smolen on a recent project in biology which is understanding a specific gene that regulates memory. The gene regulates memory at the level of individual nerve cells. The point at which nerve cells are joined, the synapse is the building block of memory systems within the hippocampus. Info comes across the synapse and second messengers bring that info inside the cell from the outside. One 2nd messenger in particular is cyclic adenosine monophosphate (cAMP). The primary neurotransmitter here is calcium. A rise in calcium promotes a rise in cAMP. This in turn activates kinases. Kinases can be thought of as machines for switching on genes. The way that kinases switch genes on is by adding phosphate groups to sites on transcription factors. Transcription factors promote production of gene product by messenger ribonucleic acid (mRNA). Gene product promotes cellular function.




Above is a molecular model for LTP at the synaptic cleft.(Abel et al, Cell, 1997)
In the case of long term memory, the occurence that converts short to long term memory is synaptic growth. The cAMP response element binding protein (CREB) names the gene cascade responsible for nerve cells actually growing more synapses. More synapses means a more stable memory. My job was to model the behaviors of some of the elements in this gene network. A common method for modeling gene networks is with a system of ODEs. The ODEs for this system in particular had a common form most of the time


However, a lot of progress has been made which may be useful for you. First of
all, Ivan Pavlov's theorised that a memory trace is layed down in the brain
during conditioning as the bases of the memory. A breakthrough was made by T.V.P.
Bliss in 1973 when he found long-term potentiation (LTP) of excitatory
postsynaptic potentials in the hippocampus; such phenomena also supported the
theories proposed by Hebb (1949) who suggested that memory storage is the
activity-dependent changes of the efficacy of synaptic transmission. Today, there
are thousands of papers published about LTP. Now, most neurobiologists agree that
LTP may be the best cellular model for learning and memory.

There are two parts to the signaling that occurs in the nervous system. The first
part are called action potentials, which either fire or don't fire, all or none,
i.e. No or Yes. Therefore, action potentials carry information by their frequency
of occurance. The second half is synaptic transmission. The action potentials
trigger neurotransmitter release which results in excitatory or inhibitory
postsynaptic potentials which are graded signals. The action potential pretty
much acts as a binary code, but we can't predict the graded signal of the
postsynaptic potential.

There are many research works showing that the areas of memory storage
are the prefrontal cortex (Goldman-Rakic, Yale Univ.) and the hippocampus
(Scoville and Milner). O'Keefe (1971) found that there are place cells in the
hippocampus which associate with a spatial map. So, based on these developments,
we believe that synpatic plasticity underlies the storage of information by brain
areas such as the hippocampus during learning.

The storage capacity is very difficulty to guess. Some people guess
that our brain could store 10^13-10^14 bits. Based on the fact that there are
about 10^10 neurons in our brain and each neuron has several thousands of
synapses to communicate with other neurons.





K1'(t)=kpK1(t)K2(t)-kdK1(t).

Here, we have a phosphorylation or activation constant and a dephosphorylation or deactivation constant. Additionally K1(t) is the concentration of the modeled kinase or phosphorylation site or even gene product. K2 is like an agent in the activation here. The model I worked with had 10-15 ODEs of this style. As they were nonlinear, coupled ODEs, they were most easily solvable by a numerical ODE solver. Plots were then fit by selecting appropriate activation and deactivation constants to fit experimental data. This was done both by hand and with a least squares solver.
For a more in depth approach to this topic, this paper explains a history behind the derivation of the CREB gene network and an explanation of the ODE system. References below are also excellent reading material on the topic.

Answer 6

If they could figure THAT out, they could download all your thoughts onto disk.
Awesome.

Answer 7

it holds mamory the same way a lamp does, amazingly.

Answer 8

dude i have no idea but im gonna look to see also =] lol

Answer 9

I FORGET!!!