Thyrotropin Releasing Hormone: Enhancement of Dopa Activity by a Hypothalamic Hormone

Plotnikoff, Nicholas P.; Prange, Arthur J.; Breese, George R.; Anderson, Mary B.; Wilson, Ian C.

doi:10.1126/science.178.4059.417

Cited by 275 publications

(29 citation statements)

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“…Many of these effects appear to share a common dopaminergic mechanism; for example, (a) potentiation of the behavioural effects of l-3,4-dihydroxy phenyl alanine (Plotnikoff et al, 1972), (b) induction of ro ta tional behaviour in apomorphine-treated mice (Rips and Boschi, 1985), and (c) activation of tyrosine hy droxylase (Yokoo et al, 1987). F urtherm ore, it has been found th at inhibition of dopam ine recep tors attenuates T R H effects (Popoli et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

YM-14673, a thyrotropin-releasing hormone analogue, injected into the nucleus accumbens and the striatum produces repetitive jaw movements in rats

Miwa

Koshikawa

Miyata

et al. 1995

European Journal of Pharmacology

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Section: Introductionmentioning

confidence: 99%

YM-14673, a thyrotropin-releasing hormone analogue, injected into the nucleus accumbens and the striatum produces repetitive jaw movements in rats

Miwa

Koshikawa

Miyata

et al. 1995

European Journal of Pharmacology

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“…Enhanced locomotor activity following monoamine oxidase inhibition plus L-DOPA administration is seen if the animals have been pretreated with either of the peptides thyrotropin releasing hormone (TRH) or melanocyte stimulating hormone release inhibitory factor (MIF) (Plotnikoff, Kastin, Anderson & Schally, 1971;Plotnikoff, Prange, Breese, Anderson & Wilson, 1972; Plotnikoff, Prange, Breese & Wilson, 1974;Green & Grahame-Smith, 1974a; Huidobro-Toro, Scotti de Carolis & Longo, 1974).…”

Section: Introductionmentioning

confidence: 99%

EVIDENCE CONCERNING THE INVOLVEMENT OF 5‐HYDROXYTRYPTAMINE IN THE LOCOMOTOR ACTIVITY PRODUCED BY AMPHETAMINE OR TRANYLCYPROMINE PLUS l‐DOPA

Green¹,

Kelly

1976

British J Pharmacology

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I Pretreatment of rats with p-chlorophenylalanine (PCPA; 2 x 200 mg/kg) decreased the concentration of 5-hydroxytryptamine (5-HT) in the brain. It also decreased the locomotor activity produced by tranylcypromine plus L-DOPA administration 24 h after the second dose of PCPA. 2 Pretreatment with p-chloroamphetamine, which produced a similar decrease in brain 5-HT concentrations did not decrease the locomotor response to tranylcypromine and L-DOPA. 3 PCPA pretreatment decreased the rise in the concentration of DOPA and dopamine in the brain following tranylcypromine and L-DOPA, suggesting its effect on the dopamine-induced locomotor activity was the result of this drug diminishing dopamine formation in the brain, probably by inhibiting L-DOPA uptake. 4 The locomotor activity produced by tranylcypromine and L-DOPA was not decreased by pretreatment 6 h earlier with disulfiram (400 mg/kg). This argues against the locomotor activity being due to noradrenergic stimulation. 5PCPA pretreatment did not alter amphetamine-induced stereotypy or the circling behaviour in unilateral nigro-striatal lesioned rats.

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“…These effects often involve interactions with other neurotransmitters. The first report involved the dihydroxyphenylalanine potentiation test (Plotnikoff et al, 1972), in which antidepressant-like effects were noted. Notably, hypophysectomized and/or thyroidectomized animals demonstrated full behavioral responses.…”

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confidence: 99%

The Thyrotropin-Releasing Hormone (TRH) Hypothesis of Homeostatic Regulation: Implications for TRH-Based Therapeutics

Gary¹,

Sevarino²,

Yarbrough³

et al. 2003

J Pharmacol Exp Ther

101

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The functions of thyrotropin-releasing hormone (TRH) in the central nervous system (CNS) can be conceptualized as performed by four anatomically distinct components that together comprise a general TRH homeostatic system. These components are 1) the hypothalamic-hypophysiotropic neuroendocrine system, 2) the brainstem/midbrain/spinal cord system, 3) the limbic/cortical system, and 4) the chronobiological system. We propose that the main neurobiological function of TRH is to promote homeostasis, accomplished through neuronal mechanisms resident in these four integrated systems. This hypothesis offers a unifying basis for understanding the myriad actions of TRH and TRH-related drugs already demonstrated in animals and humans. It is consistent with the traditional role of TRH as a regulator of metabolic homeostasis. An appreciation of the global function of TRH to modulate and normalize CNS activity, along with an appreciation of the inherent limitations of TRH itself as a therapeutic agent, leads to rational expectations of therapeutic benefit from metabolically stable TRH-mimetic drugs in a remarkably broad spectrum of clinical situations, both as monotherapy and as an adjunct to other therapeutic agents. The actions of TRH are numerous and varied. This has been viewed in the past as a conceptual and practical impediment to the development of TRH analogs. Herein, we alternatively propose that these manifold actions should be considered as a rational and positive impetus to the development of TRH-based drugs with the potential for unique and widespread applicability in human illness.Thyrotropin-releasing hormone (pGlu-His-Pro-NH 2 ) was the first hypothalamic releasing factor to be identified. Soon after this seminal event, however, it was clear that the biological functions of TRH extend far beyond regulation of the thyroid axis. Greater than two-thirds of immunoreactive TRH in the CNS is detected outside the thyrotropic zone of the hypothalamus (Winokur and Utiger, 1974). Consistent with this widespread distribution, TRH has been implicated in the regulation of arousal, autonomic function, control of circadian rhythmicity, endotoxic and hemorrhagic shock, mood, pain perception, seizure activity, and spinal motor function (Nillni and Sevarino, 1999). As this new information emerged, clinical trials have proceeded to test TRH as a treatment for various disorders including depression, schizophrenia, amyotrophic lateral sclerosis (ALS), and spinocerebellar degeneration (SCD;Griffiths, 1986). Possibly reflecting the consistent use of a metabolically stable TRH analog, trials in SCD have been generally positive. In other conditions, generally employing TRH, early trials showed promise although later trials produced inconsistent results. This variability may reflect the fact that native TRH is poorly suited as a therapeutic agent. It has low bioavailability, and its half-life in plasma is about 5 min.Herein, we first review data concerning the neurobiological mechanisms of TRH systems, and we suggest a new anat...

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Thyrotropin Releasing Hormone: Enhancement of Dopa Activity by a Hypothalamic Hormone

Cited by 275 publications

References 14 publications

YM-14673, a thyrotropin-releasing hormone analogue, injected into the nucleus accumbens and the striatum produces repetitive jaw movements in rats

YM-14673, a thyrotropin-releasing hormone analogue, injected into the nucleus accumbens and the striatum produces repetitive jaw movements in rats

EVIDENCE CONCERNING THE INVOLVEMENT OF 5‐HYDROXYTRYPTAMINE IN THE LOCOMOTOR ACTIVITY PRODUCED BY AMPHETAMINE OR TRANYLCYPROMINE PLUS l‐DOPA

The Thyrotropin-Releasing Hormone (TRH) Hypothesis of Homeostatic Regulation: Implications for TRH-Based Therapeutics

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