We haven’t really found the answer to that yet, to be honest. There are certain brain regions, like the hippocampus, that when damaged, lesioned, or hijacked by the HPA axis effect a perturbation of memory formation or recall. According to the most prevalent current theory on how associations are stored, neurones or small clusters of neurones may somehow convey the recall of a memory through synchronous activation; hippocampal damage interferes with cortical capacity for recall of the type of memories the hippocampus specializes in helping learn. More recent findings that some glia respond to neurotransmitters may indicate glia also have some role to play in cortical functioning as well. There have been some attempts to identify the structure of cortex-wide neuronal pathways, but to my knowledge no theory is yet accepted by the field as a whole.
In a bit more detail:
The hypothalamo-pituitary adrenal axis, involved in stress response, effects an increase in the synthesisation of cortisol by the adrenal glands of the kidneys, which helps the body respond to a threat by decreasing immune function and increasing the amount of readily available glucose. Its operations begin with a(n environmental) stimulus, which is relayed to the hypothalamus by the amygdala and various other inputs. The hypothalamus then secretes CRH (corticotropin releasing hormone), which is received by the anterior pituitary gland, which secretes ACTH (adrenocorticotropin-releasing hormone), which is picked up by the adrenal glands, which secrete cortisol.
The process is halted (inhibited) by the hippocampus; it has a large number of glucocorticoid receptors (GR), which are all over the body, but particularly on the hippocampus. The hippocampus plays an important role in memory formation—specifically short-term memory (STM) and context-heavy memories; if you can’t form a memory short-term, long term memory thus is also affected. The GR of the hippocampus, when activated, hijack the structure’s normal processes; GR are activated by cortisol. GR are proximal to the parts of the hippocampus critical to its function in memory, so when GR are activated, the hippocampus can’t quite execute those functions properly. Keep in mind, though, that it takes but an infinitesimal amount of time for GR to process cortisol; afterwards, the hippocampus signals the hypothalamus to stop producing CRH (the hypothalamus is inhibited), ending the cycle. Only when GR are hyper-active, when the blood contains an exorbitant amount of cortisol, could function of the hippocampus be hindered. Rather more often the case GR are over-activated by excessive and persistent levels of cortisol in the blood, leading to their failure—as they are part of the hippocampus, the structure itself degenerates and loses volume. This is chronic stress. Degeneration of the hippocampus effects a decrease in one’s capacity for STM and recall of context-heavy memories.
I describe the HPA axis to show how we know where associations are created. When the hippocampus cannot exercise its role in memory formation and recall, synchronous firing of both newly allocated and recalled associations (neurone clusters) cannot occur; thus perturbations of memory result. On an fMRI scan, one would seen two (or more) spatially separated regions ‘light up’, signifying increased blood-oxygen flow to, and thus increased activation of, those regions. What do these associations look like on the cellular level? Right now that depends on your imaging techniques. No definitive answer to that question has yet been accepted by the field.
Research on OCD (which is an addictive behaviour) has found that the neuronal pathways in regions related to addictive behaviour (like the Ventral-Tegmental Area) have more activation—are more brightly lit on an fMRI scan—than in humans without OCD; id est, the pathways are more like an interstate than a country road (not my analogy). The more one indulges the OCD-associated behaviour, the theory then goes, the broader the pathway becomes.
*We refers broadly to humans, and specifically to neuroscientists.
I guess what I’m getting at though is, if we can’t point at something & say, “This is an association. It weighs 5 grams & consumes 0.5% of the brain’s energy”, then how do we quantify an association? Are we referring to behavior? A subjective feeling? A concept? What?
Think of it as an inter-connexion of neurones and neurites (dendrites and axonal fibers). When an association is created, concepts become related.
We have yet to be able to pin down a specific neurone cell body, or a small cluster of neurones, and say, “This neurone contains the face of Bob, and this cluster of neurones stores Bob’s name and data on how you know him.”
You can look into connectionist models of how neurones operate if interested.
Personally I think the models aren’t an accurate representation of cortical processes—though they might have helped in the recent Blue Brain results. The models are accurate to an extent, but I do not think them comprehensive enough to adequately describe, and then predict, all cortical processes. Again, that is just personal speculation.
Where are associations created & what do they look like?
In brief:
We haven’t really found the answer to that yet, to be honest. There are certain brain regions, like the hippocampus, that when damaged, lesioned, or hijacked by the HPA axis effect a perturbation of memory formation or recall. According to the most prevalent current theory on how associations are stored, neurones or small clusters of neurones may somehow convey the recall of a memory through synchronous activation; hippocampal damage interferes with cortical capacity for recall of the type of memories the hippocampus specializes in helping learn. More recent findings that some glia respond to neurotransmitters may indicate glia also have some role to play in cortical functioning as well. There have been some attempts to identify the structure of cortex-wide neuronal pathways, but to my knowledge no theory is yet accepted by the field as a whole.
In a bit more detail:
The hypothalamo-pituitary adrenal axis, involved in stress response, effects an increase in the synthesisation of cortisol by the adrenal glands of the kidneys, which helps the body respond to a threat by decreasing immune function and increasing the amount of readily available glucose. Its operations begin with a(n environmental) stimulus, which is relayed to the hypothalamus by the amygdala and various other inputs. The hypothalamus then secretes CRH (corticotropin releasing hormone), which is received by the anterior pituitary gland, which secretes ACTH (adrenocorticotropin-releasing hormone), which is picked up by the adrenal glands, which secrete cortisol.
The process is halted (inhibited) by the hippocampus; it has a large number of glucocorticoid receptors (GR), which are all over the body, but particularly on the hippocampus. The hippocampus plays an important role in memory formation—specifically short-term memory (STM) and context-heavy memories; if you can’t form a memory short-term, long term memory thus is also affected. The GR of the hippocampus, when activated, hijack the structure’s normal processes; GR are activated by cortisol. GR are proximal to the parts of the hippocampus critical to its function in memory, so when GR are activated, the hippocampus can’t quite execute those functions properly. Keep in mind, though, that it takes but an infinitesimal amount of time for GR to process cortisol; afterwards, the hippocampus signals the hypothalamus to stop producing CRH (the hypothalamus is inhibited), ending the cycle. Only when GR are hyper-active, when the blood contains an exorbitant amount of cortisol, could function of the hippocampus be hindered. Rather more often the case GR are over-activated by excessive and persistent levels of cortisol in the blood, leading to their failure—as they are part of the hippocampus, the structure itself degenerates and loses volume. This is chronic stress. Degeneration of the hippocampus effects a decrease in one’s capacity for STM and recall of context-heavy memories.
I describe the HPA axis to show how we know where associations are created. When the hippocampus cannot exercise its role in memory formation and recall, synchronous firing of both newly allocated and recalled associations (neurone clusters) cannot occur; thus perturbations of memory result. On an fMRI scan, one would seen two (or more) spatially separated regions ‘light up’, signifying increased blood-oxygen flow to, and thus increased activation of, those regions. What do these associations look like on the cellular level? Right now that depends on your imaging techniques. No definitive answer to that question has yet been accepted by the field.
Research on OCD (which is an addictive behaviour) has found that the neuronal pathways in regions related to addictive behaviour (like the Ventral-Tegmental Area) have more activation—are more brightly lit on an fMRI scan—than in humans without OCD; id est, the pathways are more like an interstate than a country road (not my analogy). The more one indulges the OCD-associated behaviour, the theory then goes, the broader the pathway becomes.
*We refers broadly to humans, and specifically to neuroscientists.
Thanks for the thorough reply.
I guess what I’m getting at though is, if we can’t point at something & say, “This is an association. It weighs 5 grams & consumes 0.5% of the brain’s energy”, then how do we quantify an association? Are we referring to behavior? A subjective feeling? A concept? What?
Think of it as an inter-connexion of neurones and neurites (dendrites and axonal fibers). When an association is created, concepts become related.
We have yet to be able to pin down a specific neurone cell body, or a small cluster of neurones, and say, “This neurone contains the face of Bob, and this cluster of neurones stores Bob’s name and data on how you know him.”
You can look into connectionist models of how neurones operate if interested.
Personally I think the models aren’t an accurate representation of cortical processes—though they might have helped in the recent Blue Brain results. The models are accurate to an extent, but I do not think them comprehensive enough to adequately describe, and then predict, all cortical processes. Again, that is just personal speculation.