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Caron has also been studying the dopamine transporter molecules—with some surprising results. He is a biochemist who has spent a quarter century studying a class of cellular receptors known as G protein-coupled receptors. "They are one of the most important families of molecules that mediate cellular communication, and they are the receptors that define the specificity of signals," says Caron. "For example, signal transduction through G protein-coupled receptors is how we perceive light, how we perceive odors, how we perceive tastes, how our heart basically beats and how essentially many of the cells in our body function." As it turns out, the receptors for catecholamines, and specifically dopamine, are also G protein-coupled receptors, which is why Caron and his colleagues found themselves studying first neurotransmitters and then addiction. After Amara and her colleagues cloned the norepinephrine transporter gene, they followed it up, as did Caron and his colleagues, by cloning the dopamine transporter. Caron has been studying the molecule ever since. His primary tool has been "knockout" mice that are bred without the gene for the dopamine transporter molecule, which makes them unable to produce the transporter. "The absence of the transporter," says Caron, "created havoc in the brain dopamine system. It changed just about every parameter we ever looked at. The receptors were down-regulated and the storage of dopamine was almost abolished. Yet the small amount of dopamine left in the cell was more active than the big load that was there before."
Physically, the mice were smaller than average, and they seemed to stay small because they were so hyperactive that they rarely stopped to eat. Indeed, they seemed to show many of the symptoms of attention deficit hyperactivity disorder (ADHD), illustrating just how complicated these systems can be. When Caron and his colleagues gave cocaine or amphetamines to these mice, doing so actually calmed them, mimicking the effect of the stimulant Ritalin on children with ADHD. To Caron, this suggests that cocaine and amphetamines must also interact with the re-uptake of serotonin. In other words, when the dopamine transporter molecule is removed, stimulants may work just like Prozac. "This is a pretty controversial area," says Caron, "but we hope that we can start looking at these brain pathways and understand how serotonin interacts with the dopamine system to produce a calming effect."
In other words what I gather is that you guys receptors are burnt out. Now its causing the calming effect as described above.
Physically, the mice were smaller than average, and they seemed to stay small because they were so hyperactive that they rarely stopped to eat. Indeed, they seemed to show many of the symptoms of attention deficit hyperactivity disorder (ADHD), illustrating just how complicated these systems can be. When Caron and his colleagues gave cocaine or amphetamines to these mice, doing so actually calmed them, mimicking the effect of the stimulant Ritalin on children with ADHD. To Caron, this suggests that cocaine and amphetamines must also interact with the re-uptake of serotonin. In other words, when the dopamine transporter molecule is removed, stimulants may work just like Prozac. "This is a pretty controversial area," says Caron, "but we hope that we can start looking at these brain pathways and understand how serotonin interacts with the dopamine system to produce a calming effect."
In other words what I gather is that you guys receptors are burnt out. Now its causing the calming effect as described above.
