To sum up, this animal model is able to resemble various behavioral aspects of human BD mania (Cassidy et al. 1998; van Enkhuizen et al. 2015a).
The drug response profile demonstrated by lithium and VPA in just attenuating but not completely abolishing manic-like behaviors resembles the efficacy of these medications in treating humans with mania (Greil et al. [1997]; Hartong et al. [2003]).
It's funny, too, both in its observations about the lovelorn mania of human behaviour and its deadpan poking at Nance's tortured soul.
This involvement of the dopaminergic system supports the dopamine hypothesis (Berk et al. 2007) that hyper-dopaminergic transmission might be responsible for mania in humans and therefore also for mania-like behavior in animals.
In summary, the ClockΔ19 mutant mice resemble various but not all behavioral aspects of BD mania in humans to its full extent.
Mania in humans can involve a lack of modulation of brain activity in nucleus accumbens with reward [34] and it would be interesting if a key contributor to neglect was an inability of neglectful mice to modulate dopamine levels in nucleus accumbens in response to pups.
Could genes that make human mood regulation systems vulnerable to mania have become fixed because they give selective advantages, separate from mania, that more than counter-balance the disadvantages of illness experienced by some people?
We've had investment manias before and, human nature being what it is, we'll have them again.
A passion enacted is not necessarily a passion communicated, and at no point do we really move beyond the mania to glimpse the human being possessed by it.
Mania is a complicated human state that involves a whole cluster of different symptoms.
