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Retrograde neurotransmission: Retrograde signaling occurs when the postsynaptic neuron releases messengers that travel back to the presynaptic neuron to modulate activity. Since the process here moves in the normal presynaptic-to-postsynaptic direction, it does not represent retrograde transmission.

Volume neurotransmission: Volume transmission involves neurotransmitters diffusing through extracellular fluid to affect multiple nearby neurons. The described transmission involves a confined synaptic cleft and specific receptor activation, indicating a localized rather than widespread neurotransmission process.

Signal transduction cascade: A signal transduction cascade refers to intracellular processes initiated after receptor activation that lead to cellular responses. While a cascade is involved in the overall event, it is the mechanism within the cell, not the type of communication between the cells across the synapse.

Presynaptic transporter: Presynaptic transporters are responsible for the reuptake of neurotransmitters from the synaptic cleft back into the presynaptic neuron. They function mainly to terminate neurotransmitter signaling rather than initiate it, and they do not undergo conformational changes in response to ligand binding like receptors do.

Sodium-charged ion channel: Sodium-charged or sodium-dependent channels open primarily in response to voltage changes across the membrane, not ligand binding. They facilitate depolarization in neurons but are not directly activated by neurotransmitters such as GABA.

Voltage-sensitive ion channel: Voltage-sensitive channels open or close based on electrical potential differences across the neuronal membrane. GABA binding triggers a chemical rather than an electrical response, so this process does not involve voltage-sensitive gating.

Norepinephrine: Norepinephrine primarily regulates arousal, alertness, and attention through its effects on the sympathetic nervous system. Although it plays a role in wakefulness, it is not the key neurotransmitter directly influencing the circadian rhythm of the suprachiasmatic nucleus

Acetylcholine: Acetylcholine is involved in learning, memory, and REM sleep modulation. It contributes to sleep-wake transitions but has limited direct influence on the SCN’s regulation of circadian rhythms.

Melatonin: Melatonin is a hormone secreted by the pineal gland that signals darkness and promotes sleep. It acts on receptors in the SCN but is not a neurotransmitter; rather, it modulates circadian rhythm indirectly through hormonal feedback.

Upregulation of serotonin 2A receptors: Serotonin 2A receptor changes are more commonly associated with atypical antipsychotics or serotonergic drugs, not with the movement disorders caused by dopamine receptor blockade. They do not play a primary role in tardive dyskinesia.

Downregulation of serotonin 2A receptors: Decreased serotonin receptor activity may affect mood and cognition but is not directly linked to extrapyramidal side effects. Tardive dyskinesia stems from dopaminergic rather than serotonergic receptor changes.

Downregulation of dopamine 2 receptors: Downregulation would reduce dopaminergic signaling and potentially lessen movement-related symptoms. However, in chronic haloperidol therapy, the opposite occurs—dopamine receptors become hypersensitive and increase in number, producing the abnormal movements seen in tardive dyskinesia.

Serotonin B agonist: Activation of serotonin receptors influences mood and anxiety regulation but does not significantly impact prolactin secretion. Serotonergic effects are more commonly associated with appetite, mood, and sleep, not hormonal changes related to prolactin.

Histamine 1 antagonism: Blocking histamine H1 receptors primarily causes sedation and weight gain due to effects on appetite and arousal pathways. It has little to no direct influence on prolactin secretion, making it an unlikely cause of the breast secretions seen here.

Norepinephrine 1 antagonist: Alpha-1 adrenergic blockade leads to vasodilation and orthostatic hypotension. It does not alter dopaminergic control of prolactin release, so it is not associated with elevated prolactin levels in patients taking antipsychotic medications.

Haloperidol: Haloperidol is a first-generation antipsychotic primarily used to treat schizophrenia and acute psychosis. It is effective for controlling positive symptoms but lacks efficacy in treating depressive symptoms associated with bipolar or unipolar depression.

Chlorpromazine: Chlorpromazine is an older antipsychotic effective for psychosis and agitation but not indicated for bipolar or unipolar depression. Its strong sedative and anticholinergic effects limit its use in depressive conditions.

Thiothixene: Thiothixene is a typical antipsychotic mainly used for schizophrenia management. It does not possess the serotonergic or mood-stabilizing actions required for efficacy in bipolar depression or as augmentation for unipolar depressive disorders.

Olanzapine: Olanzapine has a high risk of metabolic disturbances, including significant weight gain, hyperglycemia, and dyslipidemia, along with moderate motor side effects in some patients. Its potent H1 and 5HT2C antagonism contribute to these effects.

Clozapine: Clozapine also has minimal motor side effects and prolactin elevation but carries a high metabolic risk. It is associated with significant weight gain, insulin resistance, and dyslipidemia, requiring close metabolic monitoring.

Risperidone: Risperidone has a higher propensity for prolactin elevation and can cause motor side effects such as extrapyramidal symptoms, especially at higher doses. Its metabolic risk is moderate, but the endocrine effects limit its “minimal side effect” profile.

Retinal detachment: Retinal detachment is unrelated to alpha-1 adrenergic receptor blockade. It is typically associated with trauma, high myopia, or age-related changes in the vitreous, not with antipsychotic pharmacology.

Gum recession: Gum or periodontal issues are not linked to alpha-1 antagonism. They are more commonly associated with poor oral hygiene, certain medications like phenytoin, or systemic conditions, rather than antipsychotic side effects.

Hyperprolactinemia: Hyperprolactinemia occurs primarily due to D2 receptor blockade in the pituitary, not alpha-1 adrenergic antagonism. While iloperidone may elevate prolactin minimally, this is independent of its alpha-1 effects.