5-HT1C/5-HT2 receptor blockade prevents 1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane-, but not stress-induced increases in brain tryptophan

Chaouloff, Francis; Layeillon, Claire; Baudrie, Véronique

doi:10.1016/0014-2999(93)90686-c

Cited by 2 publications

(1 citation statement)

References 39 publications

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“…Again, hypothyroid rats do not show the same level of response as euthyroid rats in this condition, probably due to the low activity of the renin-angiotensin system. The absence of a response to L-tryptophan administration in acute and chronic studies carried out on euthyroid and hypothyroid rats possibly results from the lower neuronal uptake of this amino acid in these conditions, in contrast to other conditions such as stress and fasting (Fernstrom, 1988;Chaouloff et al 1993).…”

Section: Figurementioning

confidence: 99%

Effect of Brain Serotoninergic Stimulation on Sodium Appetite of Euthyroid and Hypothyroid Rats

Badauê‐Passos¹,

Ventura²,

Silva³

et al. 2003

Experimental Physiology

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The aim of the present work was to investigate the role of the serotoninergic system in the control of sodium appetite of hypothyroid rats (HTR) by administering drugs that affect the serotoninergic activity, and to compare the same homeostatic behaviour in euthyroid rats (ETR) also given these drugs. Fenfluramine (FEN; 5.0 mg kg _1 , I.P.), which releases serotonin in the brain, significantly reduced the intake of 1.8 % NaCl in HTR subjected to water and sodium depletion (depleted) or water, sodium and food deprivation (deprived) by 31 and 45 %, respectively, 120 min after FEN injection, compared to HTR that received vehicle alone. Similarly, administration of FEN to ETR reduced 1.8 % NaCl intake in depleted and deprived rats by 64 and 46 %, respectively. The presynaptic serotonin reuptake inhibitor fluoxetine (20.0 mg kg _1 , I.P.) led to the inhibition of sodium appetite in HTR during the initial 30 min in depleted rats and for up to 60 min post-injection in deprived rats, while sodium appetite inhibition persisted for longer periods in ETR. The 5HT2C receptor agonist mCPP (5.0 mg kg _1 , I.P.) caused a drastic reduction in sodium appetite in HTR and ETR in depleted and deprived rats, respectively, after 120 min. Prior administration of the 5HT2C receptor antagonist LY53857 (5.0 mg kg _1 , I.P.) completely blocked the inhibitory action of mCPP on sodium appetite in both HTR and ETR. In summary, our results suggest that the recruitment of serotoninergic neurons involved in the modulation of sodium appetite seems to be decreased in hypothyroidism due to a probable deficiency in the cerebral signalling pathway.

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Section: Figurementioning

confidence: 99%