REMEMBER your first kiss? Experiments in mice suggest that patterns of chemical "caps" on our DNA may be responsible for preserving such memories.

To remember a particular event, a specific sequence of neurons must fire at just the right time. For this to happen, neurons must be connected in a certain way by chemical junctions called synapses. But how they last over decades, given that proteins in the brain, including those that form synapses, are destroyed and replaced constantly, is a mystery.

Now Courtney Miller and David Sweatt of the University of Alabama in Birmingham say that long-term memories may be preserved by a process called DNA methylation - the addition of chemical caps called methyl groups onto our DNA.

Many genes are already coated with methyl groups. When a cell divides, this "cellular memory" is passed on and tells the new cell what type it is - a kidney cell, for example. Miller and Sweatt argue that in neurons, methyl groups also help to control the exact pattern of protein expression needed to maintain the synapses that make up memories.

They started by looking at short-term memories. When caged mice are given a small electric shock, they normally freeze in fear when returned to the cage. However, then injecting them with a drug to inhibit methylation seemed to erase any memory of the shock. The researchers also showed that in untreated mice, gene methylation changed rapidly in the hippocampus region of the brain for an hour following the shock. But 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 see whether methylation plays a part in the formation of long-term memories, Miller and Sweatt repeated the experiment, this time looking at the uppermost layers of the brain, called the cortex.

They found that a day after the shock, methyl groups were being removed from a gene called calcineurin and added to another gene. Because the exact pattern of methylation eventually stabilised and then stayed constant for seven days, when the experiment ended, the researchers say the methyl changes may be anchoring the memory of the shock into long-term memory, not just controlling a process involved in memory formation.

"We think we're seeing short-term memories forming in the hippocampus and slowly turning into long-term memories in the cortex," says Miller, who presented the results last week at the Society for Neuroscience meeting in Washington DC.

"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," says Marcelo Wood, who researches long-term memory at the University of California, Irvine.

还记得你的初吻吗？通过老鼠身上的实验，我们发现DNA中的化学“磁带”或许能为你记录下这段记忆。

为了记起某件事情，一系列特定的神经细胞会在适当的时间作出反应。为了做到这点，神经细胞必须通过叫做“神经突触”的化学接口以某种方式联接起来。然而构成神经突触的脑内蛋白质不断地在更新换代，那又是如何做到将记忆保存几十年的呢？这是一个谜。

最近伯明翰阿拉巴马大学的考特尼·米勒和大卫·斯威特认为，长期记忆有可能是通过一个称为DNA甲基化作用的过程而得到保存的，即是指在我们的DNA中加入甲基群来起到化学磁带的作用。

许多基因外部都包有甲基群。当细胞分裂的时候，它的“细胞记忆”就被传递给新生的细胞，好让它记住自己是哪种类型的细胞——比如说肾细胞。米勒和斯威特称，在神经细胞中，甲基群也能够控制蛋白质对信息的传递，从而使得构成记忆的神经突触得以保存。

一开始他们从短期记忆着手进行研究。对笼中的老鼠施加微小的电击后，它们往往会对再次进入笼中感到十分的恐慌。然而，在给它们注射了抑制甲基化作用的药物后，它们对于电击的记忆似乎就完全被消去了。此外研究者们证明，没有注射过药物的老鼠在遭到电击后的一小时内，它们大脑中海马状突起区域内的基因中甲基发生着剧烈的变化，但经过一天之后就恢复正常了。这说明甲基化作用与海马状突起区域内短期记忆的形成是有关连的。

为了探明甲基化作用对于长期记忆的形成是否也有影响，米勒和斯威特重复了上面的实验。这次他们关注的是大脑活动的最高级部位——大脑皮层。

他们发现老鼠在遭受电击一天之后，神经钙蛋白基因中的甲基群就被转移到了其它的基因中去。由于甲基化作用最终稳定下来并且在接下来的七天内都保持如此，实验结束后研究者们认为甲基变化的作用可能在于将对于电击的记忆转化成长期记忆固定下来，而不半单单是控制记忆形成的过程。

“我想我们所看到的，是海马状突起区域内所形成的短期记忆逐渐转化为大脑皮层中长期记忆的过程”，米勒说。在上周神经系统科学学会在华盛顿举行的会议上，他们公布了这一研究结果。

尔湾加利福尼亚大学的马塞洛·伍德从事长期记忆的研究。他认为：“大脑有可能是采用了发生学中细胞记忆的形式，从而构成我们所说的记忆。这是一个十分有趣的想法。”