Understanding Neurotransmission and Neurotransmitters

In this video, I will be going over neurotransmission and neurotransmitters. It is a topic that falls under the subunit of brain and behavior in the biological approach. It is important for you to know this topic in detail as there are quite a few specific SAQ questions that can come in your paper one exam. So the SAQ questions that you can be asked are to outline, describe, or explain neurotransmission, the role of one neurotransmitter, agonists, antagonists, excitatory synapses, and inhibitory synapses. It can be an LAQ question as well. However, it would be a more general question on neurotransmission in general. The topic covered before neurotransmission and neurotransmitters is neuroplasticity. While there are links between these two phenomena, for the purpose of IV, we will be treating them as completely separate. So, SAQ questions on the formation of neural networks and neural pruning are completely different and unrelated to the researches used in this current topic of neurotransmitters. I would recommend using Martinez and Kessner's research, Antonova's research, and Privat et al.'s research for the questions under neurotransmission and neurotransmitters. These researches can be used to answer all the specific SAQ questions and also provide a... good balanced argument for an LAQ question. Researches by McGuire and Draginski would be completely irrelevant to this topic so make sure to not use these researchers at any cost. So what is neurotransmission? Neurotransmission is the process of communication within the nervous system. It is an electrochemical process by which different neurons communicate with one another and this is through again electrochemical signals. This is done in order to communicate and for bodily functions that are both psychological and physiological to occur. Neurotransmission starts when an action potential is stimulated and passes down the axon of a presynaptic neuron. Once the action potential travels down the axon, it goes to the axon terminals which have vesicles containing neurotransmitters. Neurotransmitters are chemical messengers found in the nervous system. So once these vesicles are stimulated, the neurotransmitters are released into the synapse. The synapse is the gap between the presynaptic neuron and the postsynaptic neuron. The neurotransmitters then travel through the synapse and bind to the postsynaptic neuron's receptors. Here, they can either cause an excitatory reaction or an inhibitory reaction. An excitatory reaction would mean that the postsynaptic neuron would fire another action potential and the process would continue. And an inhibitory reaction would mean that the postsynaptic neuron would not be able to fire another action potential. So once this is done, the neurotransmitters are released back into the synapse where they are either broken down by enzymes or undergo the process of reuptake by the presynaptic neuron. The body has optimal levels of neurotransmitters and aims to maintain homeostasis. So too much or too little of a neurotransmitter can have both short-term and long-term impacts on behavior. cognition. A little more detail about excitatory and inhibitory neurons. An excitatory neurotransmitter causes the postsynaptic neuron to depolarize which allows it to fire an action potential. Acetylcholine is an excitatory neurotransmitter in the central nervous system and one can use Martinez and Kessner's research or Antenova's research to support ACH as an excitatory neurotransmitter. On the other hand, an inhibitory neurotransmitter hyperpolarizes the postsynaptic neuron and when this happens, an action potential cannot be fired. GABA, which is basically gamma-aminobutyric acid, is an inhibitory neurotransmitter and Privat et al.'s research can be used to support this. Moving on to agonists and antagonists, an agonist is in any chemical that when bound to a receptor site causes a response in the postsynaptic neuron. can either be an inhibitory reaction or an excitatory reaction depending on the agonist. An agonist can either be endogenous or exogenous. An endogenous agonist is a chemical that is found within the body, which is basically naturally occurring within the body, also known as neurotransmitters produced by the nervous system. An exogenous agonist is any chemical that can mimic a neurotransmitter. and cause similar reactions. An exogenous agonist is not produced by the body. It is something that is ingested or taken in that is an artificial chemical or a chemical that is produced outside the body. So drugs, alcohol, and caffeine are examples of exogenous agonists. Martinez and Kessner's research or Antonova's research on acetylcholine can be used in an SAQ on agonists as ACH is an endogenous agonist. Antagonists, on the other hand, are any chemical substance that, when bound to a receptor site, block out the effects of an agonist. It causes the neuron to hyperpolarize and hence not be capable of firing an action potential. This can then prevent the subsequent behavior or cognitive process from occurring. An example of an antagonist is a skull polar mine. that blocks the effects of acetylcholine and has a negative effect on memory. Acetylcholine, as I mentioned before, is one of the neurotransmitters that we will be looking at. In the central nervous system, it is excitatory in nature. It plays a vital role in the neuroplasticity of the hippocampus. and we know that the hippocampus is responsible for memory. ACH is also responsible for attention, motivation, and learning. It is also associated with REM sleep during which people dream. Low levels of ACH have been observed in individuals with Alzheimer's disease and Parkinson's disease which are both neurodegenerative diseases that are observed in the elderly population and these can also result in memory deficits and other cognitive deficits. Martinez and Kessner's research is an animal model research. When using any animal model research, one needs to ensure to link it to human behavior. In an SAQ response, if you use an animal model research and do not explicitly link it to human behavior, your response will earn no more than 4 out of 5 marks. So please make sure to make that link. Martinez and Kessner's research is a lab experiment. First, they had 30 mice run a maze to acclimatize them and control for distress as a possible extraneous variable. Following this, the mice were divided into three groups. Group one was injected with scopolamine, which is an antagonist of acetylcholine and blocks ACH from binding to the postsynaptic neuron. Group 2 was injected with physiostigmine, which blocks the production of cholinesterase, an enzyme that breaks down ACH in the synapse. Note that physiostigmine is not the agonist. ACH is the endoagonist over here. Since the production of the enzyme is blocked out, there would be a surplus or an increased level of ACH available in the synapse in this condition. Group 3 on the other hand was the control group and received no injection and hence would have normal levels of ACH and consequent functioning. Following the injections, the mice were made to run the maze again. Group 1 was found to perform the worst. They ran the maze the slowest and made the most errors. Again, this is the group that had their ACH being blocked out by scopolamine which is the antagonist so there was low levels of ach hence we can conclude that low levels of ach result in deficits in memory okay or at least negative effects on memory group two performed the best they ran the maze the fastest and made the least errors again this is the group that had the most ach so you can say that high levels of ach can have an enhancing effect on memory Group 3 did better than group 1, but not as good as group 2. This research has a lot to convey about neurotransmitters. neurotransmitters. First, ACH is an excitatory neurotransmitter. It is through the passing of an action potential, basically the excitation of that group of neurons, that memory functions effectively. Second, when there are low levels of ACH, or ACH is blocked from binding to the postsynaptic neuron by antagonists such as scopolamine, the memory is negatively impacted. And finally, when ACH is available in high levels such as when physiostatic mind blocks the production of the enzyme that breaks down ACH, memory may be enhanced. When it comes to the link and evaluation of the research, the researchers were able to conduct a lab experiment which involves a highly controlled environment. The researchers are able to manipulate the independent variable and control for possible confounding variables. This basically means that the research has high internal validity and a cause-effect relationship can be established between acetylcholine and memory. But at the same time, when there is high internal validity, the external validity tends to be compromised. This is increased in this research because animal models are used, so the generalizability to human cognitions is questionable. However, Antenova's research used the same procedure They administered scopolamine and a placebo to their participants. Then they made their participants do a virtual reality task. The scopolamine group, just like in Martinez and Kessner's research, performed worse than the control group in the task, which is again indicative of their memory. As mentioned before, low levels of ACH have been observed in patients with Alzheimer's disease. Alzheimer's disease is a neurodegenerative disease and is characterized by episodic memory deficits. If you've watched the movie The Notebook, you'd know that the main character isn't able to remember any of her memories and has small pockets of recollection that she often tends to forget again. This evidence of ACH deficits in individuals with Alzheimer's disease supports the role of ACH functioning and its impact on memory. At the same time, evidence that increasing levels of ACH in Alzheimer's disease patients is only moderately effective in treating their cognitive impairments cannot be ignored. Okay, so there is some contradictory evidence over here. Having said that, it is then too reductionist to assume that only one neurotransmitter is responsible for complex cognitive processes and behaviors such as memory functioning. The next neurotransmitter that we are going to go over is GABA, which stands for gamma aminobutyric acid. It is an inhibitory neurotransmitter that plays a significant role in balancing neural excitability in the nervous system. So it basically controls and maintains the level of excitation and activity of not just its own functioning, but of other neurotransmitters as well. Close to 40% of the synapses in the brain work in relation to GABA and prevent hyperactivity in the nervous system. GABA functioning is complex. Different effects are observed on different cognitions and behaviors when present in varying levels. GABA functioning also changes over one's lifespan. In the initial developmental phases, GABA is seen to be excitatory, but once the brain has matured, it is inhibitory in nature. So a basic rundown of what happens when there are high or low levels of GABA. When there is low levels of GABA in the nervous system, there is an association with lack of control over intrusive thoughts, memories, and rumination. This is a potential cause of various mental health disorders including anxiety, depression, schizophrenia, and PTSD. High levels on the other hand can inhibit memory consolidation which can be observed in Alzheimer's disease and also in people who have blackouts due to alcohol. Alcohol is an agonist of GABA, so if a person has been drinking a lot, the alcohol mimics GABA in the brain and increases the level of what these receptor sites assume to be GABA in the body. This can then have negative effects on memory. Basically, it is possible that a person is not able to have any recollection of the night that they were out drinking and partying or they might have fragmented memories of that night. A research that investigated the role of GABA on memory is Privet et al.'s research that was conducted on mice. The mice had memory impairment either due to chronic stress or aging and were compared to healthy mice controls. This research is based on the assumption that the mice that have the memory impairment would have some kind of GABA deficit. So they hypothesized that by using agonists of GABA, in this case benzodiazepines, that bind and activate GABA receptor sites in the hippocampus, they would increase the inhibition of neural activity and reduce the hyperactivity. This would then at least it was assumed that this would then improve memory functioning. The mice had to run a y-shaped maze and for healthy mice it is expected that when placed in the y-shaped maze they would first explore one arm and then they would and then if they were placed again into the Y-shaped maze, they would explore the other arm. On the other hand, those with memory deficits would have lesser aim and may not remember having explored the first arm in the first trial itself, and hence when placed back into the Y-shaped maze, they might explore the same arm again and again. The mice were divided into three groups. Group 1 included the mice that had memory impairment and were administered benzodiazepines. Group 2 included memory impairment mice as well but were given no treatment at all. And group 3 consisted of the healthy mice controls that received no treatment as well. On the Y-shaped maze test, group 1 performed almost as well as group 3 with the healthy controls and group 2 with no treatment and memory impairment. performed the worst when compared to group 1 and group 3. The benzodiazepines in group 1 were able to mimic GABA and inhibit the neural activity in the mice, hence enhancing their spatial working memory. After this procedure, the mice were sacrificed and it was found that the mice from the drug treatment group had new hippocampal self-growth, which is indicative of the reversing effects of stress and aging. Again, this is a highly controlled research. The researchers were also blinded to the conditions, so they did not know if the mice were healthy controls or memory impairment mice, or whether they had received benzodiazepines or no treatment at all. This increases the internal validity and the reliability of the research, and a cause-effect relationship between GABA and memory can be drawn. One of the main drawbacks of this research is that the researchers assumed that the sample of mice with memory impairment would have lower levels of GABA to begin with in comparison to the healthy mice. There were no pre-test or pre-treatment measurements which may have resulted in biased findings. This, in addition to the use of animal models, decreases the potential of generalizability to human participants. However, the research is supported by human research. Low levels of GABA have been found in individuals with Alzheimer's disease and is associated to the hyperactivity in the hippocampus, which causes episodic memory failures. This relationship, however, is complex and hence not always clear. Alcohol, an agonist, mimics GABA and inhibits other neurotransmitters, which impairs memory functioning and causes blackouts. In this case, high levels of GABA and its agonists can result in memory impairment as well. So from the evidence that we have, both high and low levels of GABA seem to have significant impacts on memory. This basically suggests that maintaining optimal levels of GABA is essential for memory functioning among other behaviors and cognitive processes. So in this video, I've gone over two different neurotransmitters, acetylcholine and GABA. along with research for each of them and evaluation for those researches. If you found this video helpful, hit the thumbs up button and subscribe to my channel for more IB psychology content.

It can be an LAQ question as well. However, it would be a more general question on neurotransmission in general. The topic covered before neurotransmission and neurotransmitters is neuroplasticity. While there are links between these two phenomena, for the purpose of IV, we will be treating them as completely separate.

So, SAQ questions on the formation of neural networks and neural pruning are completely different and unrelated to the researches used in this current topic of neurotransmitters. I would recommend using Martinez and Kessner's research, Antonova's research, and Privat et al.'s research for the questions under neurotransmission and neurotransmitters. These researches can be used to answer all the specific SAQ questions and also provide a... good balanced argument for an LAQ question. Researches by McGuire and Draginski would be completely irrelevant to this topic so make sure to not use these researchers at any cost.

So what is neurotransmission? Neurotransmission is the process of communication within the nervous system. It is an electrochemical process by which different neurons communicate with one another and this is through again electrochemical signals.

This is done in order to communicate and for bodily functions that are both psychological and physiological to occur. Neurotransmission starts when an action potential is stimulated and passes down the axon of a presynaptic neuron. Once the action potential travels down the axon, it goes to the axon terminals which have vesicles containing neurotransmitters.

Neurotransmitters are chemical messengers found in the nervous system. So once these vesicles are stimulated, the neurotransmitters are released into the synapse. The synapse is the gap between the presynaptic neuron and the postsynaptic neuron. The neurotransmitters then travel through the synapse and bind to the postsynaptic neuron's receptors.

Here, they can either cause an excitatory reaction or an inhibitory reaction. An excitatory reaction would mean that the postsynaptic neuron would fire another action potential and the process would continue. And an inhibitory reaction would mean that the postsynaptic neuron would not be able to fire another action potential. So once this is done, the neurotransmitters are released back into the synapse where they are either broken down by enzymes or undergo the process of reuptake by the presynaptic neuron. The body has optimal levels of neurotransmitters and aims to maintain homeostasis.

So too much or too little of a neurotransmitter can have both short-term and long-term impacts on behavior. cognition. A little more detail about excitatory and inhibitory neurons.

An excitatory neurotransmitter causes the postsynaptic neuron to depolarize which allows it to fire an action potential. Acetylcholine is an excitatory neurotransmitter in the central nervous system and one can use Martinez and Kessner's research or Antenova's research to support ACH as an excitatory neurotransmitter. On the other hand, an inhibitory neurotransmitter hyperpolarizes the postsynaptic neuron and when this happens, an action potential cannot be fired. GABA, which is basically gamma-aminobutyric acid, is an inhibitory neurotransmitter and Privat et al.'s research can be used to support this.

Moving on to agonists and antagonists, an agonist is in any chemical that when bound to a receptor site causes a response in the postsynaptic neuron. can either be an inhibitory reaction or an excitatory reaction depending on the agonist. An agonist can either be endogenous or exogenous.

An endogenous agonist is a chemical that is found within the body, which is basically naturally occurring within the body, also known as neurotransmitters produced by the nervous system. An exogenous agonist is any chemical that can mimic a neurotransmitter. and cause similar reactions. An exogenous agonist is not produced by the body.

It is something that is ingested or taken in that is an artificial chemical or a chemical that is produced outside the body. So drugs, alcohol, and caffeine are examples of exogenous agonists. Martinez and Kessner's research or Antonova's research on acetylcholine can be used in an SAQ on agonists as ACH is an endogenous agonist.

Antagonists, on the other hand, are any chemical substance that, when bound to a receptor site, block out the effects of an agonist. It causes the neuron to hyperpolarize and hence not be capable of firing an action potential. This can then prevent the subsequent behavior or cognitive process from occurring. An example of an antagonist is a skull polar mine. that blocks the effects of acetylcholine and has a negative effect on memory.

Acetylcholine, as I mentioned before, is one of the neurotransmitters that we will be looking at. In the central nervous system, it is excitatory in nature. It plays a vital role in the neuroplasticity of the hippocampus.

and we know that the hippocampus is responsible for memory. ACH is also responsible for attention, motivation, and learning. It is also associated with REM sleep during which people dream.

Low levels of ACH have been observed in individuals with Alzheimer's disease and Parkinson's disease which are both neurodegenerative diseases that are observed in the elderly population and these can also result in memory deficits and other cognitive deficits. Martinez and Kessner's research is an animal model research. When using any animal model research, one needs to ensure to link it to human behavior.

In an SAQ response, if you use an animal model research and do not explicitly link it to human behavior, your response will earn no more than 4 out of 5 marks. So please make sure to make that link. Martinez and Kessner's research is a lab experiment. First, they had 30 mice run a maze to acclimatize them and control for distress as a possible extraneous variable.

Following this, the mice were divided into three groups. Group one was injected with scopolamine, which is an antagonist of acetylcholine and blocks ACH from binding to the postsynaptic neuron. Group 2 was injected with physiostigmine, which blocks the production of cholinesterase, an enzyme that breaks down ACH in the synapse.

Note that physiostigmine is not the agonist. ACH is the endoagonist over here. Since the production of the enzyme is blocked out, there would be a surplus or an increased level of ACH available in the synapse in this condition.

Group 3 on the other hand was the control group and received no injection and hence would have normal levels of ACH and consequent functioning. Following the injections, the mice were made to run the maze again. Group 1 was found to perform the worst. They ran the maze the slowest and made the most errors.

Again, this is the group that had their ACH being blocked out by scopolamine which is the antagonist so there was low levels of ach hence we can conclude that low levels of ach result in deficits in memory okay or at least negative effects on memory group two performed the best they ran the maze the fastest and made the least errors again this is the group that had the most ach so you can say that high levels of ach can have an enhancing effect on memory Group 3 did better than group 1, but not as good as group 2. This research has a lot to convey about neurotransmitters. neurotransmitters. First, ACH is an excitatory neurotransmitter.

It is through the passing of an action potential, basically the excitation of that group of neurons, that memory functions effectively. Second, when there are low levels of ACH, or ACH is blocked from binding to the postsynaptic neuron by antagonists such as scopolamine, the memory is negatively impacted. And finally, when ACH is available in high levels such as when physiostatic mind blocks the production of the enzyme that breaks down ACH, memory may be enhanced. When it comes to the link and evaluation of the research, the researchers were able to conduct a lab experiment which involves a highly controlled environment. The researchers are able to manipulate the independent variable and control for possible confounding variables.

This basically means that the research has high internal validity and a cause-effect relationship can be established between acetylcholine and memory. But at the same time, when there is high internal validity, the external validity tends to be compromised. This is increased in this research because animal models are used, so the generalizability to human cognitions is questionable.

However, Antenova's research used the same procedure They administered scopolamine and a placebo to their participants. Then they made their participants do a virtual reality task. The scopolamine group, just like in Martinez and Kessner's research, performed worse than the control group in the task, which is again indicative of their memory. As mentioned before, low levels of ACH have been observed in patients with Alzheimer's disease. Alzheimer's disease is a neurodegenerative disease and is characterized by episodic memory deficits.

If you've watched the movie The Notebook, you'd know that the main character isn't able to remember any of her memories and has small pockets of recollection that she often tends to forget again. This evidence of ACH deficits in individuals with Alzheimer's disease supports the role of ACH functioning and its impact on memory. At the same time, evidence that increasing levels of ACH in Alzheimer's disease patients is only moderately effective in treating their cognitive impairments cannot be ignored.

Okay, so there is some contradictory evidence over here. Having said that, it is then too reductionist to assume that only one neurotransmitter is responsible for complex cognitive processes and behaviors such as memory functioning. The next neurotransmitter that we are going to go over is GABA, which stands for gamma aminobutyric acid.

It is an inhibitory neurotransmitter that plays a significant role in balancing neural excitability in the nervous system. So it basically controls and maintains the level of excitation and activity of not just its own functioning, but of other neurotransmitters as well. Close to 40% of the synapses in the brain work in relation to GABA and prevent hyperactivity in the nervous system.

GABA functioning is complex. Different effects are observed on different cognitions and behaviors when present in varying levels. GABA functioning also changes over one's lifespan. In the initial developmental phases, GABA is seen to be excitatory, but once the brain has matured, it is inhibitory in nature.

So a basic rundown of what happens when there are high or low levels of GABA. When there is low levels of GABA in the nervous system, there is an association with lack of control over intrusive thoughts, memories, and rumination. This is a potential cause of various mental health disorders including anxiety, depression, schizophrenia, and PTSD.

High levels on the other hand can inhibit memory consolidation which can be observed in Alzheimer's disease and also in people who have blackouts due to alcohol. Alcohol is an agonist of GABA, so if a person has been drinking a lot, the alcohol mimics GABA in the brain and increases the level of what these receptor sites assume to be GABA in the body. This can then have negative effects on memory.

Basically, it is possible that a person is not able to have any recollection of the night that they were out drinking and partying or they might have fragmented memories of that night. A research that investigated the role of GABA on memory is Privet et al.'s research that was conducted on mice. The mice had memory impairment either due to chronic stress or aging and were compared to healthy mice controls.

This research is based on the assumption that the mice that have the memory impairment would have some kind of GABA deficit. So they hypothesized that by using agonists of GABA, in this case benzodiazepines, that bind and activate GABA receptor sites in the hippocampus, they would increase the inhibition of neural activity and reduce the hyperactivity. This would then at least it was assumed that this would then improve memory functioning. The mice had to run a y-shaped maze and for healthy mice it is expected that when placed in the y-shaped maze they would first explore one arm and then they would and then if they were placed again into the Y-shaped maze, they would explore the other arm.

On the other hand, those with memory deficits would have lesser aim and may not remember having explored the first arm in the first trial itself, and hence when placed back into the Y-shaped maze, they might explore the same arm again and again. The mice were divided into three groups. Group 1 included the mice that had memory impairment and were administered benzodiazepines.

Group 2 included memory impairment mice as well but were given no treatment at all. And group 3 consisted of the healthy mice controls that received no treatment as well. On the Y-shaped maze test, group 1 performed almost as well as group 3 with the healthy controls and group 2 with no treatment and memory impairment.

performed the worst when compared to group 1 and group 3. The benzodiazepines in group 1 were able to mimic GABA and inhibit the neural activity in the mice, hence enhancing their spatial working memory. After this procedure, the mice were sacrificed and it was found that the mice from the drug treatment group had new hippocampal self-growth, which is indicative of the reversing effects of stress and aging. Again, this is a highly controlled research. The researchers were also blinded to the conditions, so they did not know if the mice were healthy controls or memory impairment mice, or whether they had received benzodiazepines or no treatment at all. This increases the internal validity and the reliability of the research, and a cause-effect relationship between GABA and memory can be drawn.

One of the main drawbacks of this research is that the researchers assumed that the sample of mice with memory impairment would have lower levels of GABA to begin with in comparison to the healthy mice. There were no pre-test or pre-treatment measurements which may have resulted in biased findings. This, in addition to the use of animal models, decreases the potential of generalizability to human participants.

However, the research is supported by human research. Low levels of GABA have been found in individuals with Alzheimer's disease and is associated to the hyperactivity in the hippocampus, which causes episodic memory failures. This relationship, however, is complex and hence not always clear. Alcohol, an agonist, mimics GABA and inhibits other neurotransmitters, which impairs memory functioning and causes blackouts. In this case, high levels of GABA and its agonists can result in memory impairment as well.

So from the evidence that we have, both high and low levels of GABA seem to have significant impacts on memory. This basically suggests that maintaining optimal levels of GABA is essential for memory functioning among other behaviors and cognitive processes. So in this video, I've gone over two different neurotransmitters, acetylcholine and GABA.

along with research for each of them and evaluation for those researches. If you found this video helpful, hit the thumbs up button and subscribe to my channel for more IB psychology content.

Transcript for:Understanding Neurotransmission and Neurotransmitters

Transcript for:
Understanding Neurotransmission and Neurotransmitters