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Stepping on a strongly electrified grid is highly aversive. A desperately hungry rat - even a rat who hasn't eaten for 10 days - won't run across an electrified cage-floor to reach a food-source: the shocks are too painful. But a rat with electrodes implanted in its neural reward circuitry will cross the grid, repeatedly, to gain the chance to self-stimulate its pleasure centres. Direct electrical stimulation of the mesolimbic dopamine system is so overpoweringly delightful that the anticipated reward eclipses the immediate pain.
The brain's dopamine system has a dual psychological role: it regulates not just pleasure, but cue-induced craving. Cues such as seeing, smelling or tasting something potentially enjoyable - and the prospect of pressing a magic lever - heighten the desire for an anticipated reward without necessarily increasing the pleasure of the reward itself. An experienced rat with electrodes in its pleasure centers is very highly motivated. A mother will abandon her unweaned pups in order to self-stimulate indefinitely.
Euphoriant drugs such as cocaine and amphetamines activate the mesolimbic reward circuitry too. But they also activate the homeostatic mechanisms of the brain. These are control mechanisms that regulate our level of well-being (or commonly ill-being) analogous to the inhibitory feedback loops of, say, the thermoregulatory system. Psychostimulants activate not just the reward pathways, but neural "stress chemicals" such as corticotrophin-releasing factor(CRF); CRF-1 antagonists now in the pharmaceutical product-pipeline are promising anti-anxiety agents and antidepressants.
Our endogenous stress system serves to minimise, or act as a brake on, the amount of pleasure we can "naturally" obtain in a lifetime. This design-limitation is quietly satisfying to pharmacological Calvinists and religious fundamentalists. It is also the cause of immense suffering and malaise. Stress-induced overactivity of hypothalamic CRF/CRH neurons contributes to hyperactivity of the hypothalamic-pituitary-adrenocortical (HPA) system. Chronic HPA overactivity eventually demotivates and depresses its victims. HPA hyperdrive can lead to a spectrum of learned helplessness and behavioural despair characteristic of some forms of clinical depression.
By contrast, direct intracranial self-stimulation subverts these homeostatic mechanisms. Wireheading never ceases to feel sublime, regardless of how many times the subject self-stimulates the neural reward centres. Possibly - though this is controversial - tolerance to its hedonic effects is absent because electrical stimulation of the mesolimbic dopamine system activates the final common pathway of pleasure.
Experiments with electrified grids for self-stimulating humans to navigate are neither imminent nor ethical. So we can't prove just how powerfully motivating would be the implantation of optimally-located microelectrodes in normal human subjects. Even uncomplicated wireheading is currently considered unethical by medical orthodoxy. Thus the pioneering human experiments of controversial Tulane psychiatrist Robert Heath have not been repeated or refined - even to treat victims of refractory depression unresponsive to conventional antidepressants. Instead, repetitive transcranial magnetic stimulation (rTMS), ECT, and even (rarely) psychosurgery are medically sanctioned in extremis for "treatment-resistant" depressives. Their long-term clinical efficacy is uncertain.
Better drug-design is one option. Another is rewriting our own genetic code. Our genetically-enriched descendants may enjoy levels of incentive-motivation that are analogous to - and possibly far greater than - whatever drives a rat to cross an electrified grid as an ingredient of lifelong mental health. Decoding the human genome - and soon the proteome - opens up technical possibilities it would be unethical to ignore in an viciously pain-ridden world. For we can potentially amplify, modulate and redesign the architecture of our own neural reward mechanisms. Unlike our bodily thermostat, which can operate only within a narrow temperature range, the homeostatic mechanisms that govern human emotion and motivation can be radically recalibrated. Recalibrating the pleasure-pain axis may endow us with a far higher emotional "set-point" around which to oscillate than the dismal Darwinian norm.
Uniform happiness is no more educative or illuminating than uniform despair. A wholly emotionally stable subject - and in theory an entire civilisation - could get "stuck in a rut", whether that "rut" is a slough of despond or a sub-optimal plateau of bliss. But learning and personal development based on gradients of well-being can be both educative and powerfully motivating. A life animated by gradients of well-being is also personally more soul-enriching than learning based on gradients of pain.
On this scenario, bad hair days in any future post-Darwinian era of paradise-engineering may be merely wonderful rather than sublime. Centuries hence, the computational-functional analogs of traditional "painful lessons" will survive, but not their cruel Darwinian textures. Indeed the homeostatic baseline of even our own (un)happiness could potentially be reset at a level of sustainable well-being orders of magnitude higher than the norm adaptive for small social groups of naked apes on the African savannah.
What's the theoretical maximum? We don't know. Should the empirical methodology of science be used to find out? No research proposal with that aim has yet gained funding. How accurately can pleasure and pain be quantified on a single unidimensional scale? This is disputable, albeit more as a complication than a fundamental obstacle to the abolitionist project. What fail-safe genetic mechanisms can prevent - or today sometimes fail to prevent - extreme happiness spiralling off instead into psychotic mania? We're still not sure. This challenge must be met before we can safely explore germline therapy for hereditary mental superhealth.
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