Question
If schizophrenia is caused by an overabundance of the neurotransmitters dopamine and serotonin in the synapses of some areas of the brain, which drug action could work in treating the symptoms?
A. Release of cholinesterase into the synaptic cleft
B. Increased re-uptake of dopamine and serotonin by presynaptic neurons
C. Increased permeability of the presynaptic neuron to sodium
D. Blockage of dopamine and serotonin receptors on presynaptic neurons
▶️Answer/Explanation
Ans:B
To determine the most effective drug action for treating schizophrenia symptoms based on the given cause—an overabundance of the neurotransmitters dopamine and serotonin in the synapses of some brain areas—let’s analyze the scenario step by step, focusing on the neurochemical imbalance and how it can be addressed.
### Understanding the Cause
Schizophrenia is characterized by symptoms such as hallucinations, delusions, and disorganized thinking. The question specifies that this condition is caused by an excess of dopamine and serotonin in the synaptic clefts of certain brain regions. The dopamine hypothesis of schizophrenia links elevated dopamine activity, particularly in the mesolimbic pathway, to positive symptoms (e.g., hallucinations), while serotonin dysregulation, especially via 5-HT2A receptors, may contribute to both positive and negative symptoms. An overabundance in the synapse means these neurotransmitters are excessively available to bind to postsynaptic receptors, overstimulating neural circuits. A treatment would need to reduce this excess activity, either by decreasing the amount of neurotransmitter in the synapse or blocking its effects.
### Evaluating Drug Actions
Let’s examine each option in the context of reducing the overabundance of dopamine and serotonin:
– **A. Release of cholinesterase into the synaptic cleft**
Cholinesterase is an enzyme that breaks down acetylcholine into choline and acetate, terminating its action in the synapse. However, acetylcholine is not implicated in the described cause of schizophrenia here; the focus is on dopamine and serotonin. Releasing cholinesterase would only affect acetylcholine levels, which are irrelevant to this scenario. This action would not address the excess dopamine or serotonin and is unlikely to alleviate schizophrenia symptoms.
– **B. Increased re-uptake of dopamine and serotonin by presynaptic neurons**
Re-uptake involves the presynaptic neuron reabsorbing neurotransmitters from the synaptic cleft via transporter proteins (e.g., dopamine transporter [DAT] for dopamine and serotonin transporter [SERT] for serotonin). Increasing re-uptake would enhance the removal of excess dopamine and serotonin from the synapse, reducing their availability to stimulate postsynaptic receptors. This would decrease the overstimulation caused by the overabundance, potentially alleviating symptoms. This mechanism is consistent with treatments that regulate neurotransmitter levels, making it a plausible therapeutic approach.
– **C. Increased permeability of the presynaptic neuron to sodium**
Increasing sodium permeability in the presynaptic neuron would depolarize the membrane, potentially increasing calcium influx and triggering the release of more neurotransmitters (including dopamine and serotonin) from vesicles. This would exacerbate the overabundance in the synapse, worsening the symptoms of schizophrenia rather than treating them. This action is counterproductive and unsuitable.
– **D. Blockage of dopamine and serotonin receptors on presynaptic neurons**
Blocking receptors on presynaptic neurons (autoreceptors) would interfere with negative feedback mechanisms. Dopamine D2 autoreceptors and serotonin 5-HT1A/1B autoreceptors normally inhibit further neurotransmitter release when levels are high. Blocking these receptors would reduce this inhibitory feedback, likely increasing dopamine and serotonin release, which would aggravate the overabundance and symptoms. This approach does not align with the goal of reducing synaptic neurotransmitter levels.
### Relating to Schizophrenia Treatment
Antipsychotic drugs, such as first-generation (e.g., haloperidol) and second-generation (e.g., risperidone) medications, primarily work by blocking postsynaptic dopamine D2 receptors and, in some cases, serotonin 5-HT2A receptors. This reduces the effect of excess neurotransmitters on postsynaptic neurons. However, the question focuses on a drug action addressing the cause (overabundance in the synapse) rather than just symptom management. Option B (increased re-uptake) directly tackles the cause by removing excess neurotransmitters from the synapse, which could complement receptor blockade by lowering the overall neurotransmitter load.
### Conclusion
The most effective drug action to treat schizophrenia caused by an overabundance of dopamine and serotonin in the synapses would be to reduce their levels in the synaptic cleft. **Increased re-uptake of dopamine and serotonin by presynaptic neurons** (Option B) achieves this by enhancing the removal of excess neurotransmitters, thereby decreasing their overstimulation of postsynaptic receptors and potentially alleviating symptoms.
The correct answer is:
**B. Increased re-uptake of dopamine and serotonin by presynaptic neurons**
To determine the most effective drug action for treating schizophrenia based on the given cause—an overabundance of the neurotransmitters dopamine and serotonin in the synapses of some brain areas—let’s analyze the problem step by step, focusing on the role of these neurotransmitters and how their levels can be regulated.
### Understanding Schizophrenia and Neurotransmitters
Schizophrenia is a complex mental disorder with symptoms including hallucinations, delusions, and disorganized thinking. The dopamine hypothesis of schizophrenia suggests that an excess of dopamine activity, particularly in the mesolimbic pathway of the brain, contributes to positive symptoms (e.g., hallucinations). Similarly, an overabundance of serotonin (e.g., in the prefrontal cortex) has been implicated in some symptoms, as serotonin modulates dopamine release and other neural processes. The question specifies that schizophrenia in this scenario is caused by an excess of both dopamine and serotonin in the synapses, meaning their levels are too high in the synaptic cleft (the gap between neurons where neurotransmitters facilitate communication).
To alleviate symptoms, a treatment would need to reduce the excessive activity of these neurotransmitters at the synapse, either by decreasing their release, enhancing their removal, or blocking their effects on postsynaptic neurons.
### Evaluating Drug Actions
Let’s assess each option based on its impact on neurotransmitter levels and activity:
– **A. Release of cholinesterase into the synaptic cleft**
Cholinesterase is an enzyme that breaks down acetylcholine, another neurotransmitter, into inactive components (choline and acetate) to terminate its action in the synaptic cleft. However, this option is irrelevant here because schizophrenia is linked to an overabundance of dopamine and serotonin, not acetylcholine. Releasing cholinesterase would affect acetylcholine levels, which are not mentioned as a factor in this scenario. This action would not address the excess dopamine or serotonin and is unlikely to treat schizophrenia symptoms effectively.
– **B. Increased re-uptake of dopamine and serotonin by presynaptic neurons**
Re-uptake is the process by which presynaptic neurons reabsorb neurotransmitters from the synaptic cleft via transporter proteins (e.g., dopamine transporter [DAT] for dopamine and serotonin transporter [SERT] for serotonin). Increasing re-uptake would remove excess dopamine and serotonin from the synapse, reducing their availability to bind to postsynaptic receptors and thus lowering their overall activity. This mechanism aligns with treatments for conditions involving neurotransmitter excess. For example, some antidepressants (e.g., SSRIs) increase serotonin re-uptake to regulate mood, and enhancing dopamine re-uptake could similarly counteract the overabundance linked to schizophrenia. This is a plausible and targeted approach to reducing synaptic levels of both neurotransmitters.
– **C. Increased permeability of the presynaptic neuron to sodium**
Increasing sodium permeability in the presynaptic neuron would affect membrane potential and could lead to increased neurotransmitter release by promoting depolarization and calcium influx (which triggers vesicle release). This would exacerbate the overabundance of dopamine and serotonin in the synapse, worsening schizophrenia symptoms rather than treating them. This action is counterproductive and unsuitable as a treatment.
– **D. Blockage of dopamine and serotonin receptors on presynaptic neurons**
Blocking receptors on presynaptic neurons (autoreceptors) would typically inhibit negative feedback, potentially increasing neurotransmitter release rather than decreasing it. Presynaptic autoreceptors for dopamine (D2 receptors) and serotonin (5-HT1A/1B receptors) normally reduce release when activated by excess neurotransmitter. Blocking these receptors would disrupt this regulatory mechanism, likely leading to even higher levels of dopamine and serotonin in the synapse, aggravating the condition. This approach is inconsistent with the goal of reducing neurotransmitter activity.
### Linking to Schizophrenia Treatment
Current treatments for schizophrenia, such as antipsychotic medications (e.g., risperidone, olanzapine), often work by blocking postsynaptic dopamine D2 receptors and, in some cases, serotonin 5-HT2A receptors in the brain. This reduces the effect of excess dopamine and serotonin on postsynaptic neurons, alleviating symptoms. However, the question asks specifically about a drug action that could work based on the cause (overabundance in the synapse), not just symptom management. Option B (increased re-uptake) directly addresses the cause by removing excess neurotransmitters from the synapse, which could complement receptor blockade by reducing the total amount of neurotransmitter available.
### Conclusion
The most effective drug action to treat schizophrenia caused by an overabundance of dopamine and serotonin in the synapses would be to reduce their levels in the synaptic cleft. **Increased re-uptake of dopamine and serotonin by presynaptic neurons** (Option B) achieves this by enhancing the removal of excess neurotransmitters, thereby decreasing their overstimulation of postsynaptic receptors. This mechanism could help normalize neural activity and alleviate symptoms.
The correct answer is:
**B. Increased re-uptake of dopamine and serotonin by presynaptic neurons**
Question
Neurons transmit electrical impulses. Which statement describes part of this process?
A. \(\mathrm{K}^{+}\)ions are pumped out of the cell to depolarize the membrane.
\(B\). Ion channels let \(\mathrm{K}^{+}\)diffuse into the cell to depolarize the membrane.
C. \(\mathrm{Na}^{+}\)ions are pumped into the cell to repolarize the membrane.
D. Ion channels let \(\mathrm{Na}^{+}\)diffuse into the cell to depolarize the membrane.
▶️Answer/Explanation
Ans:D
The correct answer is:
**D. Ion channels let \(\mathrm{Na}^{+}\) diffuse into the cell to depolarize the membrane.**
### Explanation:
– Neurons transmit electrical impulses through a process called **action potential**. This involves changes in the permeability of the neuron’s membrane to specific ions, particularly \(\mathrm{Na}^{+}\) (sodium) and \(\mathrm{K}^{+}\) (potassium).
– **Depolarization** occurs when \(\mathrm{Na}^{+}\) ions rush into the neuron through voltage-gated ion channels, causing the membrane potential to become more positive. This is the first step in generating an action potential.
– **Why not the other options?**
– **A.** Incorrect because \(\mathrm{K}^{+}\) ions are pumped **out** of the cell during **repolarization**, not depolarization.
– **B.** Incorrect because \(\mathrm{K}^{+}\) ions diffuse **out** of the cell (not into the cell) during repolarization.
– **C.** Incorrect because \(\mathrm{Na}^{+}\) ions are not pumped into the cell; they diffuse in through ion channels during depolarization.
Thus, **D** is the correct answer, as it accurately describes the role of \(\mathrm{Na}^{+}\) ions in depolarizing the neuron’s membrane.
Question
Atropine drops are used by opticians to dilate the pupil, so that a thorough examination of the retina can be performed. Atropine binds to acetylcholine receptors in synapses.
What is the effect of atropine binding in synapses?
A. Inhibits the binding of acetylcholine at the presynaptic membrane
B. Inhibits the release of acetylcholine from the presynaptic neuron
C. Prevents binding of acetylcholine at the postsynaptic membrane
D. Prevents transport of acetylcholine through the postsynaptic membrane
Answer/Explanation
Ans:C
To determine the effect of atropine binding in synapses, let’s break down the problem by examining the role of atropine, the function of acetylcholine in pupil dilation, and the synaptic mechanisms involved.
### Understanding the Context
The image shows a normal pupil (smaller) and a dilated pupil (larger), illustrating the effect of atropine drops used by opticians. Atropine is applied to dilate the pupil, allowing a better view of the retina during eye examinations. The pupil’s size is controlled by two muscles in the iris:
– **Circular (sphincter) muscle**: Contracts to constrict the pupil (miosis), reducing the amount of light entering the eye. This muscle is innervated by the parasympathetic nervous system, which uses acetylcholine as its neurotransmitter.
– **Radial (dilator) muscle**: Contracts to dilate the pupil (mydriasis), allowing more light in. This muscle is innervated by the sympathetic nervous system, which uses norepinephrine.
Atropine dilates the pupil, so we need to understand how it interacts with the nervous system to achieve this effect. The question states that atropine binds to acetylcholine receptors in synapses, so we’ll focus on its role in the parasympathetic pathway, which controls pupil constriction.
### Role of Acetylcholine and the Parasympathetic System
The parasympathetic nervous system promotes pupil constriction via the oculomotor nerve (cranial nerve III). At the synapse in the ciliary ganglion:
– Preganglionic neurons release acetylcholine, which binds to nicotinic receptors on postganglionic neurons, activating them.
– Postganglionic neurons then release acetylcholine at the neuromuscular junction of the iris, where it binds to muscarinic receptors on the circular muscle, causing it to contract and constrict the pupil.
To dilate the pupil, we need to inhibit this parasympathetic pathway, preventing the circular muscle from contracting. Atropine, as stated, binds to acetylcholine receptors, so let’s explore how this binding affects synaptic transmission.
### Atropine’s Mechanism of Action
Atropine is a well-known muscarinic receptor antagonist. It binds to muscarinic acetylcholine receptors, which are G-protein-coupled receptors found on the postsynaptic membrane of target cells (like the circular muscle of the iris). By binding to these receptors, atropine prevents acetylcholine from binding and activating them. This blocks the parasympathetic signal to the circular muscle, preventing constriction and allowing the radial muscle (via the sympathetic system) to dominate, leading to pupil dilation.
Now, let’s evaluate the options based on synaptic mechanisms:
– **Presynaptic membrane**: This is where acetylcholine is released from the neuron into the synaptic cleft.
– **Postsynaptic membrane**: This is where acetylcholine binds to receptors (e.g., muscarinic receptors on the circular muscle) to produce a response.
– **Synaptic cleft**: The space between the presynaptic and postsynaptic membranes where neurotransmitters diffuse.
### Evaluating the Options
– **A. Inhibits the binding of acetylcholine at the presynaptic membrane**
The presynaptic membrane releases acetylcholine into the synaptic cleft, but acetylcholine does not bind to receptors on the presynaptic membrane to exert its primary effect (though autoreceptors exist, they’re not the main target here). Atropine’s primary action is not on the presynaptic membrane; it targets postsynaptic muscarinic receptors. This option is incorrect.
– **B. Inhibits the release of acetylcholine from the presynaptic neuron**
Atropine does not directly affect the release of acetylcholine from the presynaptic neuron. It acts as a receptor antagonist, binding to muscarinic receptors on the postsynaptic membrane, not by altering presynaptic release mechanisms. Drugs that inhibit release might target calcium channels or vesicle fusion, but atropine’s mechanism is receptor-based. This option is incorrect.
– **C. Prevents binding of acetylcholine at the postsynaptic membrane**
This aligns with atropine’s known mechanism. Atropine is a competitive antagonist at muscarinic acetylcholine receptors on the postsynaptic membrane (e.g., on the circular muscle of the iris). By binding to these receptors, atropine prevents acetylcholine from binding, blocking the parasympathetic signal that causes pupil constriction. This allows the pupil to dilate, as the radial muscle’s action (via the sympathetic system) is unopposed. This option is correct.
– **D. Prevents transport of acetylcholine through the postsynaptic membrane**
Acetylcholine does not get “transported” through the postsynaptic membrane. It binds to receptors on the surface of the postsynaptic membrane, triggering a response (e.g., ion channel opening or second messenger systems). The concept of transport through the membrane doesn’t apply here. Acetylcholine is broken down in the synaptic cleft by acetylcholinesterase, but that’s a different process. This option is incorrect.
### Conclusion
Atropine dilates the pupil by binding to muscarinic acetylcholine receptors on the postsynaptic membrane of the circular muscle in the iris, preventing acetylcholine from binding and activating these receptors. This inhibits the parasympathetic-mediated constriction, allowing the pupil to dilate. The effect of atropine binding in synapses is best described as:
**C. Prevents binding of acetylcholine at the postsynaptic membrane**