Depressant action of TRH, LH-RH and somatostatin on activity of central neurones.

Abstract

THREE structurally identified hypothalamic-adenohypophy-seal regulatory peptides—thyrotropin-releasing hormone (TRH)1,2 luteinising hormone releasing hormone (LH–RH)3,4 and growth hormone-release inhibiting hormone (somato statin or SRIF)5 have now been localised both in extra-hypothalamic regions of the central nervous system (CNS)6–9 and in certain extraneural regions such as the pineal gland10. There is increasing evidence that these peptides may affect behaviour by direct action on the brain. Systemic admini stration of TRH to rats induces behavioural effects inde pendent of the pituitary–thyroid axis11; LH–RH can induce mating behaviour in hypophysectomised female rats12 and somatostatin potentiates the behavioural effects of d 1-dopa13. These findings together with evidence of high affinity binding sites for TRH in extrahypothalamic tissues14 identification of LH–RH in synaptosome fractions of brain15 and localisation of LH-RH16,17 and somatostatin18,19 in nerve terminals suggest a role for these peptides in neuronal function. Applying TRH, LH–RH and somatostatin directly to central neurones microiontophoretioally we have found that these peptides have a potent depressant action on the activity of neurones at several levels (cerebral and cerebellar cortex brain stem and hypothalamus) of the neural axis.