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Effects of acute tryptophan depletion on prepulse inhibition of the acoustic startle (eyeblink) response and the N1/P2 auditory evoked response in man

E. K. Oxtoby

R. W. Langley

Division of Psychiatry, University of Nottingham, Nottingham, UK

C. M. Bradshaw

Psychopharmachology Section, Division of Psychiatry, University of Nottingham, Room B 109, Medical School, Queen's Medical Centre, Nottingham NG7 2UH, UK

E. Szabadi

Division of Psychiatry, University of Nottingham, Nottingham, UK

Contraction of the orbicularis oculi muscle in response to a sudden loud sound (acoustic startle response) and the N1/P2 component of the auditory evoked potential are both attenuated when a brief low-intensity stimulus is presented 30–500 ms before the ‘startle-eliciting’ stimulus (prepulse inhibition). Here, we report the effect of acute tryptophan depletion on prepulse inhibition of these responses. Thirteen males (21–52 years) participated in two sessions separated by 7 days, in which they ingested a drink containing a mixture of amino-acids, which either included (+ TP) or did not include (– TP) tryptophan, according to a balanced double-blind design. Electromyographic (EMG) responses of the orbicularis oculi muscle and N1/P2 auditory evoked potentials were recorded in a 20-min session, 6 h after ingestion of the mixture. Subjects received 40 trials in which 1-kHz sounds were presented: (i) 40 ms, 115 dB (‘pulse alone’ trials) and (ii) 40 ms, 85 dB, followed after 120 ms by 40 ms, 115 dB (‘prepulse/pulse’ trials). Mean amplitudes of the EMG response and the N1/P2 potential were derived from the pulse-alone trials and, in each case, percentage prepulse inhibition was calculated. Plasma tryptophan levels were measured from blood samples taken before and 7 h after each treatment. Under the + TP condition, both the EMG response and the N1/P2 complex showed > 60% prepulse inhibition. The – TP condition was associated with (i) significant suppression of prepulse inhibition of the EMG response, with no significant change in response amplitude and (ii) reduction of the amplitude of the N1/P2 potential, with no significant change in prepulse inhibition of this response. Tryptophan levels rose by 90 ± 15% under the + TP condition and fell by 81 ± 3% under the – TP condition. The suppression of prepulse inhibition of the acoustic startle response under the – TP condition suggests that central 5-hydroxytryptaminergic mechanisms may be involved in regulating prepulse inhibition of this response. The lack of effect of tryptophan depletion on prepulse inhibition of the N1/P2 potential suggests that different mechanisms are involved in prepulse inhibition of the startle response and the N1/P2 complex.

Key Words: acoustic startle response • acute tryptophan depletion • auditory evoked potential • eyeblink • N1/P2 complex • prepulse inhibition

Journal of Psychopharmacology, Vol. 14, No. 3, 258-265 (2000)
DOI: 10.1177/026988110001400308


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