When "don't perform the trainer-desired behavior, go buy the reward at the store yourself" becomes an available behavior, it can get reinforced pretty fast.

It is a simple truth of economics that what one rewards, one gets more of.

What is extremely hard to do is determine what exactly one is rewarding when one responds positively to a particular behavior. When my toddler asks to be picked up, is he seeking approval, attention, or escape from whatever task I've just set for him (e.g. "Sit on the potty chair"). If you don't carefully determine the function of a behavior, you won't be able to accurately determine whether your response is reinforcing or punishing. And if you reinforce what you intended to punish, you'll get more of the behavior instead of less.

To put it slightly differently, one might think that the purpose of teenage rebellion is changing the norms. Or the purpose might be to shock others (and thereby obtain attention). What responses will decrease the frequency of of rebellious behavior depends a great deal on which reason is true in a particular case.

Are you referring to the diction, or stating there is no description of how associations are created? I created a footnote to address the latter.

The Little Albert example really makes the point.

I would judge it as 90% good. Which means: good.

Possible improvement: If the core of the article is less than one screen long, it either does not need a summary, or it needs much shorter summary. The length of summary should be cca 10% of the article length, not 30%. And perhaps (other readers may disagree with this) the summary should be at the end of the article, not at the beginning.

I thought about that; the original DragonBox example involved operant conditioning instead of classical.

Fortunately Richard's quote provided in footnote three offers an example of operant conditioning. Should I say thus in the footnote itself?

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.