We explain how is motivational state controled by dopamine and serotonin in D1 loop of ventral striatum (VS). It is known that dopamine enforces the impulsivity, motivation and drive via stimulating the D1 loop of VS. We propose that serotonin suppresses wanting (and deprivations), impulsivity and movement by inhibiting dopamine release in VS - to make us slow down and rest (when full, and after the valuable resources were gained and serotonin levels rose up).
https://www.scienceopen.com/document/vid/13e62385-1fb0-4a49-9a5d-e435baa5b95e
Our laboratory has shown how serotonergic activity in, and to, the ventral tegmental area (including projections from raphe nuclei and local 5HT3 receptors locally) modulates DA-efflux in the accumbens. So, it stands to reason that serotonin would be modulating reward-seeking behavior mediated by the mesolimbic DA system. However, the role of the long- vs short-feedback loops is not as clear.
What is the role of the dopamine D1r via the hyperpolarization of paracapsular cells surrounding the amygdala, leading to the prevention of cortex inhibitory feedback to the amygdala? Increased amygdala activity can over-ride the influence of the hippocampus and cortex inputs to the VTA-N.Accumbens junction, suggesting that the D1r may have an important role in the regulation of the affective influence on motivated outputs in co-ordination with altered cortex-amygdala interactions. Serotonin may be having interactions with the D1r both in the N.Accumbens and amygdala,
Also wondered about the role of serotonin conversion to N-acetylserotonin and melatonin, including the idea that increased serotonin will increase N-acetylserotonin from astroyctes, leading to TrkB activation that mimics the BDNF associated plasticity, allowing serotonin to be linked to the plasticity underlying reward attainment following motivated outputs.
Probably elated more to activation of 5HT2 receptors in the medial hypothalamus or PAG (or reduction of 5HT1a receptor activation in the same regions). The prefrontal cortex may contribute as well in the same manner as described for the medial hypothalamus and PAG.
reply to Prof. Richard L. Bell:
Thank you very much for reply. By serotonergic modulation of VTA neurons, do you mean that serotonin decreases dopamine release ?
reply to Prof. George Anderson:
I agree that serotonin attenuates output of amygdala. So it calms the active avoidance, self-defence and aggression. I am curious if the BDNF-associated plasticity caused by serotonin that you suggested occurs in the ventral ACC (anterior cingulate cortex) ? or where in the brain ? Thank you.
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