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As far as "pleasure" is concerned, there have been numerous studies on sensitization to drugs that have addictive potential. But in that area, things are more muddy because "behavioral sensitization" doesn't really separate the "like" and "want" components, which have some common pathways in the brain (the famous dopamine mesolimbic/NAc) but also distinct for various "likes" (e.g. those for sweet taste have been fairly well identified) and it seems it is mainly other neurotransmitters are mainly involved in the latter (e.g. MOR-receptor agonists, like endorphins and also orexin for taste. Things are complicated in that regard because merely eating something that does not subjectively register as pleasant will also release pretty much the same neurotransmitters; there are apparently subtle differences to consider in what regions of the brain where they are released.) Behaviorally studied, preferences can have many confounders besides actual "like"; see e.g. [amusing perhaps] controversy on sugars vs cocaine, which was even the stuff of tabloids some years back (as "cupcakes vs cocaine" or thereabout).

While sensitization of D2 [dopamine] receptors involved in the feedback loop of addiction is fairly well understood (e.g. see all the D2High research), I'm not sure there's been comparable effort to understand if there is easily and separately triggerable sensitization in receptors involved in e.g. sweet tasting, although in general, mu opioid receptors can be sensitized as well.

As far as "pleasure" is concerned, there have been numerous studies on sensitization to drugs that have addictive potential. But in that area, things are more muddy because "behavioral sensitization" doesn't really separate the "like" and "want" components, which have some common pathways in the brain (the famous dopamine mesolimbic/NAc) but also distinct for various "likes" (e.g. those for sweet taste have been fairly well identified) and it seems it is mainly other neurotransmitters are mainly involved in the latter (e.g. MOR-receptor agonists, like endorphins and also orexin for taste. Things are complicated in that regard because merely eating something that does not subjectively register as pleasant will also release pretty much the same neurotransmitters; there are apparently subtle differences to consider in what regions of the brain where they are released.) Behaviorally studied, preferences can have many confounders besides actual "like"; see e.g. [amusing perhaps] controversy on sugars vs cocaine, which was even the stuff of tabloids some years back (as "cupcakes vs cocaine" or thereabout).

While sensitization of D2 [dopamine] receptors involved in the feedback loop of addiction is fairly well understood (e.g. see all the D2High research), I'm not sure there's been comparable effort to understand if there is easily and separately triggerable sensitization in receptors involved in e.g. sweet tasting, although in general, mu opioid receptors can be sensitized as well.

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could an existing adult mind/brain be modified to perceive pleasure/pain signals more intensely than otherwise

It depends what you mean by "modified", but even without going to any genetic (or surgical, e.g. implants) modifications, the central mechanisms involved in pain can be sensitized merely by experience/exposure to a certain level of stimuli; see e.g. (fairly cited) review paper on central sensitization.

The nociceptor-induced sensitization of the somatosensory system is adaptive in that it makes the system hyperalert in conditions in which a risk of further damage is high, for example, immediately after exposure to an intense or damaging stimulus. This sensitization is the expression of use-dependent synaptic plasticity triggered in the central nervous system (CNS) by the nociceptor input and was the first example of central sensitization, discovered [in 1983]. Since then, we have learned that a number of different forms of functional, chemical, and structural plasticity can sensitize the central nociceptive system to produce pain hypersensitivity under both normal and pathological circumstances, some of which are persistent.

[...]

To induce central sensitization, the noxious stimulus must be intense, repeated, and sustained. Input from many fibers is required over tens of seconds; a single stimulus, such as a pinch, is insufficient. Peripheral tissue injury is not necessary, although the degree of noxious stimulation that produces frank tissue injury almost always induces central sensitization, so that the phenomenon is very prominent after post-traumatic or surgical injury.

The mechanism[s] by which this happens are on one hand very diverse as far as initiation, but seem to converge in one final pathway (dorsal horn neurons):

multiple different triggers can contribute to the establishment of this form of central sensitization: glutamate acting on NMDAR, but also on AMPAR and mGluR, the neuropeptides substance P and CGRP, the kinin bradykinin, as well as BDNF and NO. [...] The reason so many different transmitters, modulators, and their receptors are involved is that it is not their specific action that is important but rather that they are released directly from or induced in response to nociceptor afferent activity, and each can separately or together initiate the activation of those multiple intracellular signaling pathways that lead to the establishment of hyperexcitability in dorsal horn neurons [...]. In other words, there are many parallel inputs to dorsal horn neurons that can independently or cooperatively initiate central sensitization.

So that gives numerous potential [malevolent] pharmacological/genetic/physical interventions that could have the same (ultimate) effect of causing central sensitization to pain. And if you care about the practical details, you can read the experimental methods section of the papers cited in that review.