In The Making of Memory Steven Rose recounts his search for the physical changes that occur when anything is committed to memory – a quest that has dominated neuroscience for twenty years.
He settled for new-born chicks, who peck naturally at small round objects. If a coloured bead is dipped in a bitter solution, the chick rejects the bead as soon as it has pecked it, shaking its head in disgust. More important, after one such experience, it will never peck a bead of the same colour again. Here is learning with a vengeance. What changes in the chick’s brain mediate it?
Rose found that in chicks which had learned to avoid a coloured bead, there was an increase in the type of protein needed to make new receptor cells in the areas already identified as being connected with learning, and when he and his colleagues looked through a microscope they found that there was indeed a large increase in one type of receptor site (a spine) in these two areas. This structural change, which they measured 24 hours after the chicks’ training, could well be the basis of memory.
The situation is very different from that confronting a schoolboy who has to learn the dates of kings – an unnatural task if ever there was one.
To understand memory we need to know the whole circuit in which the memory is embodied, not what and where the physical change is that underlies it. Without such knowledge we cannot begin to answer questions about the way memories are retrieved or how they become distorted by later memories. This is one of several psychological issues over which Rose goes astray. He distinguishes procedural memory (how to ride a bicycle) from declarative memory (remembering that something is the case), and states correctly that procedural memory is not usually forgotten as readily as declarative. But it is likely that these are not two distinct kinds of memory: if you are a tennis-player and then learn squash it will almost certainly interfere with your tennis-playing. The reason we do not forget how to cycle is that, having learned this skill, we do not subsequently engage in similar activities that would interfere with our memory for it. The way in which old memories are distorted by – and to some extent protected from – new ones is an important problem. Except possibly in very young chicks, new memories are always laid down on top of existing ones
It has been established that mental illness can result from too much or too little activity of particular transmitters. Thus, schizophrenia is thought to be caused by too much dopamine activity and can be alleviated, though not cured, by giving drugs that reduce it. Reduced levels of the same substance produce Parkinsonism, which can be ameliorated by drugs that increase dopamine activity. Again, depression is thought to be caused by too little activity in other transmitters, especially serotonin and epinephrine. It can be relieved by drugs (for example, the tricyclics that increase the activity of these two neurotransmitters). Although many details remain to be worked out, all these findings are exciting, comparatively new, reasonably secure and of practical value.
Despite the brain biochemists’ successes, there remains a huge gap in our knowledge. We haven’t the remotest idea why overactivity in the dopamine system should produce the observed symptoms of schizophrenia, such as hearing imaginary voices, believing that one’s thoughts are controlled by outside agencies, or paranoia in all its forms. Nor do we know how fluctuation in the activity of serotonin gives rise to depression and mania, and probably even to normal changes of mood. We know the sites of action in the brain on which opiates operate, but once again there is a huge hiatus between brain and mind. Why do they reduce pain? The gap between the functioning of neurotransmitter systems and the mental illnesses and thought processes and feelings to which they give rise is as wide as ever and nobody has any inkling of how to reduce it.
Extracts are from Stuart Sutherland's reveiw of The Making of Memory: From Molecules to Mind by Steven Rose
Bantam, 355 pp, £6.99, October 1993, ISBN 0 553 40748 1
He settled for new-born chicks, who peck naturally at small round objects. If a coloured bead is dipped in a bitter solution, the chick rejects the bead as soon as it has pecked it, shaking its head in disgust. More important, after one such experience, it will never peck a bead of the same colour again. Here is learning with a vengeance. What changes in the chick’s brain mediate it?
Rose found that in chicks which had learned to avoid a coloured bead, there was an increase in the type of protein needed to make new receptor cells in the areas already identified as being connected with learning, and when he and his colleagues looked through a microscope they found that there was indeed a large increase in one type of receptor site (a spine) in these two areas. This structural change, which they measured 24 hours after the chicks’ training, could well be the basis of memory.
The situation is very different from that confronting a schoolboy who has to learn the dates of kings – an unnatural task if ever there was one.
To understand memory we need to know the whole circuit in which the memory is embodied, not what and where the physical change is that underlies it. Without such knowledge we cannot begin to answer questions about the way memories are retrieved or how they become distorted by later memories. This is one of several psychological issues over which Rose goes astray. He distinguishes procedural memory (how to ride a bicycle) from declarative memory (remembering that something is the case), and states correctly that procedural memory is not usually forgotten as readily as declarative. But it is likely that these are not two distinct kinds of memory: if you are a tennis-player and then learn squash it will almost certainly interfere with your tennis-playing. The reason we do not forget how to cycle is that, having learned this skill, we do not subsequently engage in similar activities that would interfere with our memory for it. The way in which old memories are distorted by – and to some extent protected from – new ones is an important problem. Except possibly in very young chicks, new memories are always laid down on top of existing ones
It has been established that mental illness can result from too much or too little activity of particular transmitters. Thus, schizophrenia is thought to be caused by too much dopamine activity and can be alleviated, though not cured, by giving drugs that reduce it. Reduced levels of the same substance produce Parkinsonism, which can be ameliorated by drugs that increase dopamine activity. Again, depression is thought to be caused by too little activity in other transmitters, especially serotonin and epinephrine. It can be relieved by drugs (for example, the tricyclics that increase the activity of these two neurotransmitters). Although many details remain to be worked out, all these findings are exciting, comparatively new, reasonably secure and of practical value.
Despite the brain biochemists’ successes, there remains a huge gap in our knowledge. We haven’t the remotest idea why overactivity in the dopamine system should produce the observed symptoms of schizophrenia, such as hearing imaginary voices, believing that one’s thoughts are controlled by outside agencies, or paranoia in all its forms. Nor do we know how fluctuation in the activity of serotonin gives rise to depression and mania, and probably even to normal changes of mood. We know the sites of action in the brain on which opiates operate, but once again there is a huge hiatus between brain and mind. Why do they reduce pain? The gap between the functioning of neurotransmitter systems and the mental illnesses and thought processes and feelings to which they give rise is as wide as ever and nobody has any inkling of how to reduce it.
Extracts are from Stuart Sutherland's reveiw of The Making of Memory: From Molecules to Mind by Steven Rose
Bantam, 355 pp, £6.99, October 1993, ISBN 0 553 40748 1
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