Addiction Balancing Personalities .
Andre Willers .
26 Oct 2012
Unfortunate humans with both short Serotonin transporter genes (depression) and the A1 allele of DRD2 gene (too few dopamine brakes = too much pleasure) develop cycles of downside and upside to form a dynamic way of coping .
The control mechanism evolved from homeostasis . If the system is destabilized by either serotonin or dopamine excesses as set out in Appendices I and II , then the other co-factor is dusted off and resurrected out of the grab-bag of the switching mechanisms in DNA . Epigenetic effects evolve.
“If mummy can’t cope , neither will child.”
Hence the evolutionary advantage of the D2 receptor inhibition (see Appendix II) .
Any hierarchical social system uses serotonin inhibition to structure the society , form armies , maintain discipline , etc .
Learned helplessness is a major part of this . See Sapolsky .
The only way out is Exuberant Pleasure , as the Dopamine Brakes are released . This is expressed as addiction .
Corrollary major :
Addiction is then transferable . Already found experimentally (see Samantha Murphy et al) .
The result :
Individual humans show manic-depressive behaviour . Because the manic-behaviour is associated with transferable addictions , it is the prevalent human behaviour pattern .
“Think Positive !” , “ The horse will learn to sing” , “they can never win” , hobby , work , etc
The manic behaviour is accentuated as meaningless reward systems get driven to extremes . This is independent of the socio-economic system .
Those on top always want more . At a basic neural-reward level .
An interesting aside :
Cocaine is a dopamine re-uptake inhibitor . For normal humans (ie with sufficient D2 receptor sites) , it ends up as a dopamine brake . They simply cannot get excited . The major damage to the USA system as major cocaine importers .
They lost their edge , letting China do the nitty-gritty manufacturing because it was not exciting enough .
And what about the poor sod stuck with a shortage on both neurotransmitters ?
He ends up juggling depression and learned helplessness with a choice of addictions : alcohol , nicotine , over-eating , sex-addiction , politics , religion , internet , love , etc .
The system hunts for “commitment” , ie addictions to counter the emptiness of periodic low serotonin (depression) .
A stable system , but not a very happy one.
It depends whether you remember the good parts or the bad parts .
A random event (the boss shits you out , drought ) causes a depression . (low serotonin) Your homeostatic brain tries to compensate by increasing dopamine rewards and steering towards greater rewards . The positive feedback leads to excess . Crashing against hard reality leads to low serotonin and depression . The cycle repeats , but the society as a whole gains more in the manic episodes . Even individuals do.
Manic-Depression in unhappy families and societies are a duality .
The trick is to be depressed on your own (with a bottle) and happy with others .
Who wants to die bored ?
Length of Serotonin transporter genes
13 Jan 2012
Professor Elaine Fox, who led the study, explained: "Our findings suggest that people with a short serotonin transporter gene are likely to be far more reactive to both very negative situations, such as a car crash, and very positive ones, such as a very supportive relationship. This supports the idea of short serotonin transporter genes as 'adaptability', rather than 'vulnerability', genes. They may not only increase the risk of an individual developing emotional vulnerability in a negative environment but also increase the chances of them benefiting from a supportive environment, compared to people with the long form.
"People with a long serotonin transporter gene are likely to be less influenced by their emotional environment, which may help to protect them from negative events but could also mean that they are less able to benefit from a positive environment."
NewScientist 8 Sep 2012 p37 .
J Neurosci. 2012 Oct 10;32(41):14094-14101.
Braking Dopamine Systems: A New GABA Master Structure for Mesolimbic and Nigrostriatal Functions.
Barrot M, Sesack SR, Georges F, Pistis M, Hong S, Jhou TC.
Institut des Neurosciences Cellulaires et Intégratives, Centre National de la Recherche Scientifique, Université de Strasbourg, 67084 Strasbourg, France, Department of Neuroscience and Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, Université de Bordeaux, Interdisciplinary Institute for Neuroscience, UMR 5297, F-33000 Bordeaux, France, Centre National de la Recherche Scientifique, Interdisciplinary Institute for Neuroscience, UMR 5297, F-33000 Bordeaux, France, Department of Biomedical Sciences, University of Cagliari, 09042 Monserrato, Italy, Laboratory of Sensorimotor Research, National Eye Institute/National Institutes of Health, Bethesda, Maryland 20892, and Medical University of South Carolina, Department of Neurosciences, Charleston, South Carolina 29425.
A new mesopontine structure exerting a strong influence on dopamine systems has recently been defined: the tail of the ventral tegmental area/rostromedial tegmental nucleus (tVTA/RMTg). This review presents a neuroanatomical, physiological, and behavioral overview of some of the recent and ongoing research on this brain region and its relationship with dopamine systems. The tVTA/RMTg sends dense GABA projections to VTA and substantia nigra neurons. The inhibitory influence of tVTA/RMTg on dopamine neurons is supported by both neuroanatomical and electrophysiology data. The latter studies also reveal the tVTA/RMTg as a substrate for morphine and cannabinoid action on dopamine cells. In primates, the tVTA/RMTg has been implicated in reward prediction error signals, through a basal ganglia-lateral habenula-tVTA/RMTg-dopamine-basal ganglia circuit. In rodents, the tVTA/RMTg has been shown to play a critical role in aversive behaviors, particularly those involving behavioral inhibition, such as freezing and avoidance. These findings highlight the functional importance of the tVTA/RMTg as a major GABA brake for dopamine systems.
[PubMed - as supplied by publisher]
This ties in as follows :
D2 receptor-mediated inhibition of GABA release by endogenous dopamine in the rat globus pallidus.
Floran B, Floran L, Sierra A, Aceves J.
Departamento de Fisiología Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Mexico City, Mexico.
Attempting to better understand the role of the dopaminergic innervation in the rat globus pallidus, we examined here whether or not endogenous dopamine modulates the release of [3H]GABA in superfused pallidal slices. The superfusion medium contained elevated (15 mM) potassium. The release of endogenous dopamine was induced by the dopamine releaser drug, methamphetamine. Methamphetamine (100 microM) inhibited by 46% the release of [3H]GABA. Methamphetamine inhibition was completely blocked by reserpinization of the rats. It was also completely blocked by the D2 dopamine receptor antagonist sulpiride (10 microM). Sulpiride alone caused a 105% increase in GABA release. The increase was not observed in slices from reserpinized rats. Quinpirole (10 microM), a D2 dopamine receptor agonist, inhibited (43%) [3H]GABA release. The results suggest that endogenous dopamine exerts an inhibitory effect on GABA release in the rat globus pallidus. The effect is mediated by D2 receptors presumably located on striatopallidal axon terminals.
[PubMed - indexed for MEDLINE]