soundphaRm
Bluelighter
Here's a study that was done that I have access to the info (from the New England Journal of Medicine) on, that I thought the ADD community would be interested in...
"The Molecular Mechanisms of Fear: An Animal Model
Although the neural circuitry of fear and anxiety (i.e., the role of the amygdala and related subcortical structures) is now better understood, we know little about the molecular and cellular mechanisms involved in these circuits. This series of studies examined the role of stathmin, an inhibitor of microtubule formation, in both conditioned and unconditioned fear models in mice. The stathmin gene and protein are highly expressed in the amygdala and in anatomic areas known to process conditioned and unconditioned stimuli before they reach the amygdala.
Mice that had stathmin knocked out had more microtubules in the amygdala than did wild-type mice, but no abnormalities in amygdala-related neurons, neuronal synaptic strength, or glutamate- or GABA-facilitated neurotransmission. However, stathmin-knockout mice had a deficit in long-term potentiation and decreases in both conditioned fear and innate (unconditioned) fear.
Comment: These studies show that stathmin is required for the expression of innate fear and the formation of memory for learned fear. It is most intriguing that intracellular events in addition to communication between cells are crucial to, and underlie abnormalities in, behavior and emotion. Thus, some cellular events crucial to fear formation may depend on proper functioning of microtubules (i.e., transport of protein and RNA to synapses helps to increase synaptic strength, which is required to create memories underlying conditioned fear). The increased number of microtubules could indicate greater stability and a decrease in plasticity needed for synaptic regulation and change in response to new stimuli. Studies such as these open a new window on what might be going awry in the brains of individuals with pathologic anxiety states."
"The Molecular Mechanisms of Fear: An Animal Model
Although the neural circuitry of fear and anxiety (i.e., the role of the amygdala and related subcortical structures) is now better understood, we know little about the molecular and cellular mechanisms involved in these circuits. This series of studies examined the role of stathmin, an inhibitor of microtubule formation, in both conditioned and unconditioned fear models in mice. The stathmin gene and protein are highly expressed in the amygdala and in anatomic areas known to process conditioned and unconditioned stimuli before they reach the amygdala.
Mice that had stathmin knocked out had more microtubules in the amygdala than did wild-type mice, but no abnormalities in amygdala-related neurons, neuronal synaptic strength, or glutamate- or GABA-facilitated neurotransmission. However, stathmin-knockout mice had a deficit in long-term potentiation and decreases in both conditioned fear and innate (unconditioned) fear.
Comment: These studies show that stathmin is required for the expression of innate fear and the formation of memory for learned fear. It is most intriguing that intracellular events in addition to communication between cells are crucial to, and underlie abnormalities in, behavior and emotion. Thus, some cellular events crucial to fear formation may depend on proper functioning of microtubules (i.e., transport of protein and RNA to synapses helps to increase synaptic strength, which is required to create memories underlying conditioned fear). The increased number of microtubules could indicate greater stability and a decrease in plasticity needed for synaptic regulation and change in response to new stimuli. Studies such as these open a new window on what might be going awry in the brains of individuals with pathologic anxiety states."
![:\](https://bluelight.org/xf/BL_Images/Orig_Emoji/wrygrin.gif "wry grin :\")
