Effects of tyrosine/phenylalanine depletion on electrophysiological correlates of memory in healthy volunteers
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Summary
This study investigated the impact of acute dopamine depletion on memory function and its electrophysiological correlates in healthy volunteers. Dopamine is known to influence frontal lobe functions, including attention and memory, yet previous research on the cognitive effects of tyrosine/phenylalanine depletion (TPD)—a method to lower dopamine synthesis—has yielded inconsistent results. This research aimed to clarify these discrepancies by simultaneously assessing behavioral performance and event-related potentials (ERPs) during working and episodic memory tasks. The study employed a double-blind, placebo-controlled, three-way crossover design involving 17 healthy volunteers aged 18–25. Participants underwent TPD, a placebo condition, and a histidine depletion condition. Working memory was assessed using the Sternberg memory scanning task (SMS), while episodic memory was evaluated using the Visual Verbal Learning Test (VVLT). Electroencephalography (EEG) was recorded during both tasks to measure ERP components, specifically P150, N200, P3a, and P3b. Blood samples confirmed that TPD significantly reduced plasma tyrosine and phenylalanine levels by 57% and the tyrosine/phenylalanine-to-neutral amino acid ratio by 62%, verifying successful depletion. Behavioral results indicated that TPD did not impair working memory performance; reaction times, accuracy, and scanning slopes remained unchanged. Similarly, episodic memory performance, measured by hit rates in immediate and delayed recall, was not significantly affected by TPD. In fact, TPD reduced false alarms and repeated word mentions during immediate recall, suggesting no behavioral deficit. However, ERP analyses revealed significant alterations in neural processing. During the working memory task, TPD delayed N200 latency, decreased P3a amplitude, and increased P3b latency. During episodic memory encoding, TPD increased P150 and P3b latencies, while during recognition, it decreased P3a latency. These electrophysiological changes indicated impaired stimulus processing and altered memory-related neural activity despite preserved behavioral output. The findings suggest that dopamine plays a critical role in the neural processing underlying both working and episodic memory, even when behavioral performance remains intact. The study concludes that TPD induces subtle deficits in memory-related processing that are detectable via ERPs but too small to manifest in standard behavioral measures. This highlights the sensitivity of electrophysiological methods in detecting dopaminergic influences on cognition and suggests that previous inconsistencies in the literature may stem from relying solely on behavioral outcomes.
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| Stage | Outcome | Tool | Model | Prompt | Attempts | Completed |
|---|---|---|---|---|---|---|
| discover | success | Crossref | — | — | 1 | 2026-06-19 |
| archive | success | semantic_scholar | — | — | 6 | 2026-06-25 |
| extract | success | cached | — | — | 2 | 2026-06-26 |
| clean | success | clean | — | — | 1 | 2026-06-19 |
| chunk | success | chunk | — | — | 1 | 2026-06-19 |
| embed | success | embed | Qwen/Qwen3-Embedding-8B | — | 1 | 2026-06-19 |
| promote | success | — | — | — | 1 | 2026-06-19 |
| summarize | success | llm | qwen3.6-27b-prismaquant | summ-v5 | 1 | 2026-06-26 |
| tag | success | vector_similarity | — | — | 6 | 2026-06-19 |
| verify | success | — | — | — | 1 | 2026-06-26 |
Summary generated by qwen3.6-27b-prismaquant on 2026-06-26; verification: verified.
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