1 tment with the 5-HT synthesis inhibitor para-chlorophenylalanine.

2 , where 2Nal is 2-naphthylalanine, 4Cpa is 4-chlorophenylalanine, 3Pal is 3-pyridylalanine, Aph is 4-

3                                            p-Chlorophenylalanine, a 5-HT synthesis inhibitor, but not

4 sequence [PhAc-Tyr1,D-Arg2, Phe(4-Cl)6 (para-chlorophenylalanine), Abu15 (alpha-aminobutyric acid), N

5 inhibitor of phenylalanine hydroxylase, DL-p-chlorophenylalanine, and L-phenylalanine in the diet.

6  mice, reduction of 5-HT synthesis with para-chlorophenylalanine increased MES-induced seizure severi

7 selective tryptophan hydroxylase inhibitor p-chlorophenylalanine on postnatal days 0 and 1 restored t

8                               The compound p-chlorophenylalanine (p-CPA) blocks the enzymatic synthes

9 mined the effect of 5-HT depletion with para-chlorophenylalanine (p-CPA) on the cardiac vagal baroref

10 tion of tryptophan hydroxylase (Tph) using p-chlorophenylalanine (pCPA) or genetic knockout of the ne

11 d either with the serotonin depleting drug p-chlorophenylalanine (PCPA) or with the serotonin reuptak

12 macological depletion of 5-HT stores using p-chlorophenylalanine (PCPA), a 5-HT-synthesis inhibitor,

13  injection of the 5-HT synthesis inhibitor p-chlorophenylalanine (pCPA), which increases feeding, inc

14 s were treated systemically with saline or p-chlorophenylalanine (pCPA, 350 mg/kg) to block 5-HT synt

15 ale rats were treated systemically with para-chlorophenylalanine (pCPA; 350 mg/kg single i.p. injecti

16 p-tyrosine (AMPT, catecholamine depletor), p-chlorophenylalanine (serotonin depletor), prazosin (PRAZ

17                  With or without postnatal p-chlorophenylalanine treatment, 5-HTT(-/-) mice exhibited

18 (3) = 3-(3-pyridyl)alanine, and Phe(4CI) = 4-chlorophenylalanine] was followed by the removal of the