Spent the night on youtube searching for educational videos regarding the brain, basal ganglia and dopamine. Here are some of
Functional Areas of the Brain
A series of seven interesting videos of the different functional areas of the brain. #6 covers Basal Ganglia
What is Dopamine?
Disrupted Dopaminergic Neurotransmission in 22q11 Deletion Syndrome
Here is a study on 22q11 micro-deletion and dopamine.
It has been hypothesized that in 22q11DS subjects COMT haploinsufficiency may cause decreased COMT enzyme activity and hence an increase in brain DA levels (Dunham et al, 1992; Graf et al, 2001; Gothelf et al, 2004). Our findings in the peripheral dopaminergic markers are in line with such a ‘hyperdopaminergic state’. High DA levels could explain the increased risk for neuropsychiatric disorders in 22q11DS including psychosis, irritability, and agitation as has been suggested by the inverted U-shaped curve model (Goldman-Rakic et al, 2000). This paradigm emphasizes that DA should vary between optimal levels and that both increased and decreased DA levels may be associated with cognitive and/or psychiatric problems. Further support for excessive DA levels in 22q11DS subjects comes from the fact that three of our study subjects reported subjective improvements following AMPT administration with similar findings reported by Graf et al (2001).
On Huntington’s Chorea and dopamine
Huntington’s chorea is due to slow degeneration in the basal ganglia, which eventually leads to cell death in the brain and the decrease and increase of various neurotransmitters. The symptoms of the disease are caused by a significant reduction (volume and activity) of two principal neurotransmitters (naturally occurring chemicals in the brain) – namely Acetylcholine and GABA, in turn affecting the activity of the neurotransmitter Dopamine, which becomes hyperactive. The disorder is partly characterized by an increase in the availability of dopamine, which can cause symptoms of chorea. HD is a basal ganglia disease; the portions most severely affected are caudate and putamen.
On Valproic acid and neurotransmetter GABA (via wikipedia)
Valproate is believed to affect the function of the neurotransmitter GABA in the human brain, making it an alternative tolithium salts in treatment of bipolar disorder. Its principal mechanism of action is believed to be the inhibition of the transamination of GABA (by inhibiting GABA transaminase). Valproate is also believed to reverse the transamination process to form more GABA.
[Edwin K.] Reading this, I am wondering if the impact of the GABA deficiency induced by “post pump chorea” is not aggravated by Clarisse’s 22q11.2 micro deletion hyperdopaminergic state. Need to get a better understanding of what a neuro transmitter is, how basal ganglia uses DA and GABA and how does two balance each other.