Could genetics be the answer to all the human race's disorders and problems? We were telling you a few days back that loneliness might be hereditary, and in an article posted today, the researchers announced that schizophrenia was the result of the two genes.
Rutgers geneticist Gleb Shumyatsky has discovered a gene that controls both innate and learned forms of fear.
The gene, known as Stathmin or Oncoprotein 18, is highly concentrated in the amygdala, a key region of the brain that deals with fear and anxiety.
Stathmin knockout mice, or mutants bred to be deficient in this gene, showed an increase in the amount of microtubules. These are the building blocks of the dendrite skeleton and also serve as paths for certain proteins to follow, proteins that govern the strength of the connections between neurons (synapses).
In the absence of Stathmin, microtubule dynamics (meaning the speed and flexibility of building these paths) are likely to be decreased and may lead to the weakening of the synaptic connections.
This is consistent with a significant reduction in long-term potentiation or LTP, the lasting, strengthened electrical connections between neurons that are regarded as a molecular model for memory. The reduction was specifically observed in pathways incoming to the amygdala in the knockout mice.
The microtubule increase, and the LTP decrease, may be at the root of the noted failure in the mice to remember the lessons of learned fear, such as avoiding places that gave electric shocks.
They noted that the knockout mice showed no fear and consistently explored more open areas than normal mice.
"This study provides genetic evidence that amygdala-enriched Stathmin is required for the expression of innate fear and the formation of memory for learned fear," the authors concluded.