Mother Nature has solutions for us. Some of them grow invasively, many in fact, of the medicinal herbs/foods are easy to grow plants that are invasive in many areas.
What are the potential long-term consequences of chronic benzodiazepine use on glutamate receptor function and synaptic plasticity?
Based on the search results, here are the potential long-term consequences of chronic benzodiazepine use on glutamate receptor function and synaptic plasticity:
Downregulation of BZD receptors: Chronic administration of benzodiazepines induces downregulation of BZD receptors, which may lead to:
Reduced inhibitory function of GABA, potentially desensitizing GABAergic synapses
Increased excitatory tone, as glutamate receptors (NMDA and AMPA) become more sensitive
Neuroadaptive changes: Chronic benzodiazepine use may induce neuroadaptive changes, including:
Hyperpolarization of neuron cell membranes, potentially compromising synaptic plasticity and memory formation
Reduction in synaptic plasticity, making it more difficult to form new memories
Metaplasticity: Chronic drug use, including benzodiazepines, can hijack glutamate receptor activity and long-term synaptic plasticity processes, leading to:
Long-lasting effects on neurotransmission and synaptic strength
Maladaptive changes in synaptic plasticity, contributing to durable drug memory and increased risk of relapse
Specific findings:
Chronic benzodiazepine administration alters hippocampal CA1 neuron excitability, with changes in NMDA receptor function and expression (Van Sickle et al., 2002)
Long-term potentiation and depression of glutamatergic synapses on dopamine neurons in the ventral tegmental area (VTA) are modulated by benzodiazepine agonists (Long-lasting Modulation of Glutamatergic Transmission in VTA Dopamine Neurons after a Single Dose of Benzodiazepine Agonists)
Metaplasticity-based modulation of synaptic plasticity contributes to durable neurotransmission changes in mesocorticolimbic pathways, including the ventral tegmental area and the nucleus accumbens (Glutamate receptors and metaplasticity in addiction)
In summary, chronic benzodiazepine use can lead to:
Downregulation of BZD receptors and altered GABAergic function
Neuroadaptive changes, including hyperpolarization and reduced synaptic plasticity
Metaplasticity, resulting in long-lasting effects on neurotransmission and synaptic strength
Maladaptive changes in synaptic plasticity, contributing to durable drug memory and increased risk of relapse
These findings suggest that chronic benzodiazepine use can have significant and lasting impacts on glutamate receptor function and synaptic plasticity, potentially contributing to cognitive impairment, memory deficits, and increased risk of addiction.
Thank you so much for this outstanding piece of research and analysis, Doc. Amazing how much you have produced in <24 HRS !!
I have been looking at a few supplements for overcoming/attentuating Benzo withdrawal symptoms as well as rewiring the brain. Some of them appear very promising and I am still working on ranking them based on their effectiveness. Two that have particularly caught my attention:
PEA is an endocannabinoid found helpful for a variety of conditions I think.
++ Choline and Inositol - support methylation cycles and inositol is calming. People with seizure risk benefit from taking higher dose Inositol throughout the day.
++ Lithium Orotate - 5 mg (or micrograms, not sure) per day as a preventative was in the BDNF series - Michael Nehls interview I think.
++ L-Tryptophan - supports niacin and serotonin which is supportive of calm and lower inflammation.
Thanks for this.
What are the potential long-term consequences of chronic benzodiazepine use on glutamate receptor function and synaptic plasticity?
Based on the search results, here are the potential long-term consequences of chronic benzodiazepine use on glutamate receptor function and synaptic plasticity:
Downregulation of BZD receptors: Chronic administration of benzodiazepines induces downregulation of BZD receptors, which may lead to:
Reduced inhibitory function of GABA, potentially desensitizing GABAergic synapses
Increased excitatory tone, as glutamate receptors (NMDA and AMPA) become more sensitive
Neuroadaptive changes: Chronic benzodiazepine use may induce neuroadaptive changes, including:
Hyperpolarization of neuron cell membranes, potentially compromising synaptic plasticity and memory formation
Reduction in synaptic plasticity, making it more difficult to form new memories
Metaplasticity: Chronic drug use, including benzodiazepines, can hijack glutamate receptor activity and long-term synaptic plasticity processes, leading to:
Long-lasting effects on neurotransmission and synaptic strength
Maladaptive changes in synaptic plasticity, contributing to durable drug memory and increased risk of relapse
Specific findings:
Chronic benzodiazepine administration alters hippocampal CA1 neuron excitability, with changes in NMDA receptor function and expression (Van Sickle et al., 2002)
Long-term potentiation and depression of glutamatergic synapses on dopamine neurons in the ventral tegmental area (VTA) are modulated by benzodiazepine agonists (Long-lasting Modulation of Glutamatergic Transmission in VTA Dopamine Neurons after a Single Dose of Benzodiazepine Agonists)
Metaplasticity-based modulation of synaptic plasticity contributes to durable neurotransmission changes in mesocorticolimbic pathways, including the ventral tegmental area and the nucleus accumbens (Glutamate receptors and metaplasticity in addiction)
In summary, chronic benzodiazepine use can lead to:
Downregulation of BZD receptors and altered GABAergic function
Neuroadaptive changes, including hyperpolarization and reduced synaptic plasticity
Metaplasticity, resulting in long-lasting effects on neurotransmission and synaptic strength
Maladaptive changes in synaptic plasticity, contributing to durable drug memory and increased risk of relapse
These findings suggest that chronic benzodiazepine use can have significant and lasting impacts on glutamate receptor function and synaptic plasticity, potentially contributing to cognitive impairment, memory deficits, and increased risk of addiction.
AI-generated answer. Please verify critical facts.
Elsevier
Neuropharmacology
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Follow up
What specific subtypes of glutamate receptors are most affected by chronic benzodiazepine use?
Can chronic benzodiazepine use lead to long-term alterations in glutamate receptor trafficking and synaptic localization?
How do benzodiazepines influence the activity of other neurotransmitters, such as dopamine and serotonin, in relation to glutamate receptor function?
Context
🌐
sciencedirect.com
Chronic clonazepam administration induced benzodiazepine receptor subsensitivity - ScienceDirect
🌐
mdpi.com
Neurology International |
Very welcome 🙏
It needs a rewrite and tge Kudzu made into a Kudzu article but I got tired of it.
Love your Kudzu retreat idea! If I had any business sense....
We have plenty of Kudzu in VA.
And you have horses - petting zoo and harvesting kudzu retreats. - Day events, simpler.
Thank you so much for this outstanding piece of research and analysis, Doc. Amazing how much you have produced in <24 HRS !!
I have been looking at a few supplements for overcoming/attentuating Benzo withdrawal symptoms as well as rewiring the brain. Some of them appear very promising and I am still working on ranking them based on their effectiveness. Two that have particularly caught my attention:
++ Agmatine - NMDA receptor antagonist
https://www.proquest.com/openview/9b8f0feec313f15a422110cf797f2981/1
++ Palmitoylethanolamide (PEA) - Precursor to Allopregnanolone if access to Allopregnanolone is unavailable
https://pubmed.ncbi.nlm.nih.gov/9385589/
And did you have any thoughts on the following (I am still studying these):
++ Choline and Inositol
++ Lithium Orotate
++ L-Tryptophan and L-Taurine
You're welcome and thanks. I learned quite a bit. It was helpful.
An NMDA receptor agonist would likely help.
PEA is an endocannabinoid found helpful for a variety of conditions I think.
++ Choline and Inositol - support methylation cycles and inositol is calming. People with seizure risk benefit from taking higher dose Inositol throughout the day.
++ Lithium Orotate - 5 mg (or micrograms, not sure) per day as a preventative was in the BDNF series - Michael Nehls interview I think.
++ L-Tryptophan - supports niacin and serotonin which is supportive of calm and lower inflammation.
and L-Taurine - can be helpful, can also become an excess thing - like, assess individually. - Brave AI summary re taurine's protective actions https://search.brave.com/search?q=How+does+taurine%27s+antioxidant+and+membrane-stabilizing+activity+compare+to+other+compounds+in+mitigating+excitotoxicity-induced+neural+damage%3F&summary=%7B%22query%22%3A%22taurine+benefits+and+risks+for+mood+symptoms%22%2C%22country%22%3A%22us%22%2C%22language%22%3A%22en%22%2C%22safesearch%22%3A%22moderate%22%2C%22results_hash%22%3A%2261edbb8292b93f5ee82801a8ae990d0edf83b46838a1fb88ce63a8b6817a38a9%22%7D&source=summarizer&summary_og=3f279480e8e8b575656bf2