Recent experimentation in mice leads to suggestion that patterns of chemical ‘caps’ on deoxyribonucleic acid (DNA) may be responsible for preserving memory.
The recollection of a particular event requires a specific succession of neurons to trigger just at the right time. For this to occur, these neurons must be connected in a particular sequence by chemical junctions, referred to as synapses. It remains a mystery how these synapses endure over decades, given the proteins in the brain, including those that form synapses, are destroyed and replaced constantly.
Courtney Miller and David Sweatt of the University of Alabama (Birmingham), suggest that long-term memories may be preserved by a process termed DNA methylation - the addition of chemical ‘caps’ in the form of methyl groups onto our DNA. There are methyl group substituents already present in many of the genes within our genome. At the division of a cell, this alleged “cellular memory” is passed on and tells the new cell what type it is - for example, a kidney cell. Miller and Sweatt argue that in neurons, methyl groups also assist the control of exacting patterns in protein expression required to maintain the synapses that constitute memories.
They started by looking at short-term memories. When caged mice were given a small electric shock, they normally freeze in fear when returned to the cage. However, injecting the mice with either of Hydralazine hydrochloride (1-hydrazinophthalazine monohydrochloride) or Procainamide (4-amino-N-(2-diethylaminoethyl) benzamide to inhibit methylation seemed to erase any memory of the shock. The researchers also showed that in untreated subjects, gene methylation changed rapidly in the hippocampus region of the brain for an hour following the procedure. A day later, it had returned to normal, suggesting that methylation was involved in creating short-term memories in the hippocampus (Neuron, DOI: 10.1016/j.neuron.2007.02.022).
To determine whether methylation is elemental in formation of long-term memories, Miller and Sweatt repeated the experiment, this time observing reaction in the cerebral cortex (centre for memory, perceptual awareness & consciousness). It was found that methyl groups were being removed from a gene called calcineurin and allocated to another gene. As the exacting pattern of methylation eventually stabilised and remained constant, the researchers determined that the methyl alterations may be anchoring memory of the shock into long-term memory, rather than just controlling a process involved in memory formation.
The findings of this experiment were that short-term memories forming in the hippocampus slowly turned into long-term memory in the cerebral cortex. “The cool idea here is that the brain could be borrowing a form of cellular memory from developmental biology to use for what we think of as memory”.
Courtney Miller and David Sweatt of the University of Alabama (Birmingham), suggest that long-term memories may be preserved by a process termed DNA methylation - the addition of chemical ‘caps’ in the form of methyl groups onto our DNA. There are methyl group substituents already present in many of the genes within our genome. At the division of a cell, this alleged “cellular memory” is passed on and tells the new cell what type it is - for example, a kidney cell. Miller and Sweatt argue that in neurons, methyl groups also assist the control of exacting patterns in protein expression required to maintain the synapses that constitute memories.
They started by looking at short-term memories. When caged mice were given a small electric shock, they normally freeze in fear when returned to the cage. However, injecting the mice with either of Hydralazine hydrochloride (1-hydrazinophthalazine monohydrochloride) or Procainamide (4-amino-N-(2-diethylaminoethyl) benzamide to inhibit methylation seemed to erase any memory of the shock. The researchers also showed that in untreated subjects, gene methylation changed rapidly in the hippocampus region of the brain for an hour following the procedure. A day later, it had returned to normal, suggesting that methylation was involved in creating short-term memories in the hippocampus (Neuron, DOI: 10.1016/j.neuron.2007.02.022).
To determine whether methylation is elemental in formation of long-term memories, Miller and Sweatt repeated the experiment, this time observing reaction in the cerebral cortex (centre for memory, perceptual awareness & consciousness). It was found that methyl groups were being removed from a gene called calcineurin and allocated to another gene. As the exacting pattern of methylation eventually stabilised and remained constant, the researchers determined that the methyl alterations may be anchoring memory of the shock into long-term memory, rather than just controlling a process involved in memory formation.
The findings of this experiment were that short-term memories forming in the hippocampus slowly turned into long-term memory in the cerebral cortex. “The cool idea here is that the brain could be borrowing a form of cellular memory from developmental biology to use for what we think of as memory”.
References
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Tomkoya, J, Friedecky, D, Polynkova, A, Adam, T 2009, ‘Capillary electrophoresis determination of thiopurine methyl transferase activity in erythrocytes’, Analytic, Technological & Biomedical Life Science’, viewed 24 May 2009.
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Tomkoya, J, Friedecky, D, Polynkova, A, Adam, T 2009, ‘Capillary electrophoresis determination of thiopurine methyl transferase activity in erythrocytes’, Analytic, Technological & Biomedical Life Science’, viewed 24 May 2009.
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