Neurologists help!
Hi, First off, I'm a paranoid schizophrenic. Secondly, I have come to realise that the drugs, haloperidol, in my case... works. However, I am an expert in the science behind antipsychotics, having written a book about it, but not exactly an expert. The chemical imbalance theory is sketchy and yet to be proved but I was wondering if anybody had ever studied the dopamine receptor itself (dopamine being the responsible neurotransmitter in schizophrenia). I know of studies in which dopamine receptor densities increase due to the introduction of drugs and also of reduction and stability of receptor densities. I'm just wondering if perhaps the ability to respond to drugs is caused by the introduction of newly formed dopamine receptors. There is a lot of evidence to suggest that antipsychotics can worsen outcome and this would tie in neatly with a reduction in density. Can anyone help?
Ill explain a bit more... The chemical imbalance theory goes like this... if you have schizophrenia youre treated as though you have excess dopamine in your brain. Antipsychotics are antagonists, that is, they block the receptors (dopamine) and therefore reduce the transmission of dopamine through the brain. However, this theory has yet to be supported. What im asking is this... what if the receptor itself was responsible for the symptoms of schizophrenia and the introduction of drugs (in most cases) increased receptor density (which it does) and therefore you have new receptors that are doing their jobs properly and reducing symptoms.
Hi the right er...,
Really interesting question and I'm glad you're finding treatment useful.
A little bit about myself, as I have some knowledge in this area, I've got an Msc in clinical neuroscience and am a medical student; I've also read most of the literature out there on schizophrenia and neuroleptics.
Anyway, first off the dopamine hypothesis is far from proven, and its claims are based upon the so called effectiveness of drug actions, which I'll come to in a moment. You need to be careful when putting a lot of faith in it as a pathogenesis of schizophrenia. There is lots of work with glutamate and serotonin receptors in schizophrenia these days (not to mention all the psychological explanations), and to be frank the dopamine hypothesis is old news. It is a theory that largely became accepted belief without ever really getting strong evidence behind it.
On to the drugs themselves. Typical first generation antipsychotics e.g. chlorpromazine were discovered originally as anaesthetic drugs and were first labelled as major sedative hypnotics i.e. tranquilisers. If you give anyone a D2 receptor antagonist they will calm down; this effect is obviously just more pronounced in schizophrenic patients. They are general sedatives and are far from a targeted cure for schizophrenia that they are often portrayed as. D2 receptors are in large quantities in the basal ganglia (a group of nuclei involved in movement) and are involved in movement pathways, which is why their modulation often leads to movement disorders seen in antipsychotic treatment (tardive dyskinesia) and why their loss in Parkinson's disease has such profound effects on movement.
On the receptor issue you are very right that receptor density changes in response to transmitter supply, hence why they increase when you deprive the brain of dopamine.For this one you need to think about genetics though. Receptors are just proteins implanted in a cell membrane and encoded for by a gene. If the fault does lie within the receptor it is because you have a genetic abnormality, so all subsequent receptors of that particular type would be translated as defective.
The only way you would suddenly get healthy receptors being produced is if there was an activation/inactivation of genes through some means e.g. epigenetic mechanisms (an explanation best left for someone who knows far more about genetics than I!). So it is unlikely that you would get widespread mixing of healthy and defective receptors. Effectively the receptors would either all be abnormal or all be normal, unless something altered the gene e.g. radiation or epigenetic effects etc etc.
Interesting question!
Really interesting question and I'm glad you're finding treatment useful.
A little bit about myself, as I have some knowledge in this area, I've got an Msc in clinical neuroscience and am a medical student; I've also read most of the literature out there on schizophrenia and neuroleptics.
Anyway, first off the dopamine hypothesis is far from proven, and its claims are based upon the so called effectiveness of drug actions, which I'll come to in a moment. You need to be careful when putting a lot of faith in it as a pathogenesis of schizophrenia. There is lots of work with glutamate and serotonin receptors in schizophrenia these days (not to mention all the psychological explanations), and to be frank the dopamine hypothesis is old news. It is a theory that largely became accepted belief without ever really getting strong evidence behind it.
On to the drugs themselves. Typical first generation antipsychotics e.g. chlorpromazine were discovered originally as anaesthetic drugs and were first labelled as major sedative hypnotics i.e. tranquilisers. If you give anyone a D2 receptor antagonist they will calm down; this effect is obviously just more pronounced in schizophrenic patients. They are general sedatives and are far from a targeted cure for schizophrenia that they are often portrayed as. D2 receptors are in large quantities in the basal ganglia (a group of nuclei involved in movement) and are involved in movement pathways, which is why their modulation often leads to movement disorders seen in antipsychotic treatment (tardive dyskinesia) and why their loss in Parkinson's disease has such profound effects on movement.
On the receptor issue you are very right that receptor density changes in response to transmitter supply, hence why they increase when you deprive the brain of dopamine.For this one you need to think about genetics though. Receptors are just proteins implanted in a cell membrane and encoded for by a gene. If the fault does lie within the receptor it is because you have a genetic abnormality, so all subsequent receptors of that particular type would be translated as defective.
The only way you would suddenly get healthy receptors being produced is if there was an activation/inactivation of genes through some means e.g. epigenetic mechanisms (an explanation best left for someone who knows far more about genetics than I!). So it is unlikely that you would get widespread mixing of healthy and defective receptors. Effectively the receptors would either all be abnormal or all be normal, unless something altered the gene e.g. radiation or epigenetic effects etc etc.
Interesting question!
(edited 10 years ago)
Erm, I'm confused. I take this too, for Tourette's Syndrome! It works like a. Charm, had no idea it was for Schizophrenia. :/
Posted from TSR Mobile
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Original post by Sinatrafan
Hi the right er...,
Really interesting question and I'm glad you're finding treatment useful.
A little bit about myself, as I have some knowledge in this area, I've got an Msc in clinical neuroscience and am a medical student; I've also read most of the literature out there on schizophrenia and neuroleptics.
Anyway, first off the dopamine hypothesis is far from proven, and its claims are based upon the so called effectiveness of drug actions, which I'll come to in a moment. You need to be careful when putting a lot of faith in it as a pathogenesis of schizophrenia. There is lots of work with glutamate and serotonin receptors in schizophrenia these days (not to mention all the psychological explanations), and to be frank the dopamine hypothesis is old news. It is a theory that largely became accepted belief without ever really getting strong evidence behind it.
On to the drugs themselves. Typical first generation antipsychotics e.g. chlorpromazine were discovered originally as anaesthetic drugs and were first labelled as major sedative hypnotics i.e. tranquilisers. If you give anyone a D2 receptor antagonist they will calm down; this effect is obviously just more pronounced in schizophrenic patients. They are general sedatives and are far from a targeted cure for schizophrenia that they are often portrayed as. D2 receptors are in large quantities in the basal ganglia (a group of nuclei involved in movement) and are involved in movement pathways, which is why their modulation often leads to movement disorders seen in antipsychotic treatment (tardive dyskinesia) and why their loss in Parkinson's disease has such profound effects on movement.
On the receptor issue you are very right that receptor density changes in response to transmitter supply, hence why they increase when you deprive the brain of dopamine.For this one you need to think about genetics though. Receptors are just proteins implanted in a cell membrane and encoded for by a gene. If the fault does lie within the receptor it is because you have a genetic abnormality, so all subsequent receptors of that particular type would be translated as defective.
The only way you would suddenly get healthy receptors being produced is if there was an activation/inactivation of genes through some means e.g. epigenetic mechanisms (an explanation best left for someone who knows far more about genetics than I!). So it is unlikely that you would get widespread mixing of healthy and defective receptors. Effectively the receptors would either all be abnormal or all be normal, unless something altered the gene e.g. radiation or epigenetic effects etc etc.
Interesting question!
Really interesting question and I'm glad you're finding treatment useful.
A little bit about myself, as I have some knowledge in this area, I've got an Msc in clinical neuroscience and am a medical student; I've also read most of the literature out there on schizophrenia and neuroleptics.
Anyway, first off the dopamine hypothesis is far from proven, and its claims are based upon the so called effectiveness of drug actions, which I'll come to in a moment. You need to be careful when putting a lot of faith in it as a pathogenesis of schizophrenia. There is lots of work with glutamate and serotonin receptors in schizophrenia these days (not to mention all the psychological explanations), and to be frank the dopamine hypothesis is old news. It is a theory that largely became accepted belief without ever really getting strong evidence behind it.
On to the drugs themselves. Typical first generation antipsychotics e.g. chlorpromazine were discovered originally as anaesthetic drugs and were first labelled as major sedative hypnotics i.e. tranquilisers. If you give anyone a D2 receptor antagonist they will calm down; this effect is obviously just more pronounced in schizophrenic patients. They are general sedatives and are far from a targeted cure for schizophrenia that they are often portrayed as. D2 receptors are in large quantities in the basal ganglia (a group of nuclei involved in movement) and are involved in movement pathways, which is why their modulation often leads to movement disorders seen in antipsychotic treatment (tardive dyskinesia) and why their loss in Parkinson's disease has such profound effects on movement.
On the receptor issue you are very right that receptor density changes in response to transmitter supply, hence why they increase when you deprive the brain of dopamine.For this one you need to think about genetics though. Receptors are just proteins implanted in a cell membrane and encoded for by a gene. If the fault does lie within the receptor it is because you have a genetic abnormality, so all subsequent receptors of that particular type would be translated as defective.
The only way you would suddenly get healthy receptors being produced is if there was an activation/inactivation of genes through some means e.g. epigenetic mechanisms (an explanation best left for someone who knows far more about genetics than I!). So it is unlikely that you would get widespread mixing of healthy and defective receptors. Effectively the receptors would either all be abnormal or all be normal, unless something altered the gene e.g. radiation or epigenetic effects etc etc.
Interesting question!
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