Spontaneous Nocturnal Plasma Prolactin and Growth Hormone Secretion in Patients with Parkinson’s Disease and Huntington’s Chorea

Murri, Luigi; Iudice, Alfonso; Muratorio, A; Polleri, A; Barreca, T; Murialdo, Giovanni

doi:10.1159/000115147

Cited by 27 publications

(13 citation statements)

References 21 publications

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“…DA from other brain regions may exert feedback effects in the SCN via actions at D 1 and D 5 receptors (Rivkees and Lachowicz, 1997; Mendoza and Challet, 2014). Patients with PD have altered levels of PRL (Murri et al, 1980; Bellomo et al, 1991; Winkler et al, 2002), suggesting disruptions in PRL cycling involving TIDA neurons (Freeman et al, 2000; Bertram et al, 2010). …”

Section: Discussionmentioning

confidence: 99%

“…For example, plasma PRL levels of patients with early stages of idiopathic PD were not significantly different from the levels of the age-matched controls (Aziz et al, 2011), implicating proper function of DA from TIDA neurons. Conversely (and strange when considering that DA reduction should increase PRL levels), other patients with PD have shown significantly lower levels of plasma PRL (Murri et al, 1980; Winkler et al, 2002). Yet again, other PD patients have shown an increase in nocturnal PRL (Bellomo et al, 1991).…”

Section: Hypothalamusmentioning

confidence: 98%

“…Among classes of DA receptors, D 1 and D 2 receptors play a central role in the pathogenesis of PD (Videnovic and Golombek, 2013). Dysfunction of dopaminergic populations in brain regions including the midbrain, striatum, retina, OB, and hypothalamus also may lead to other circadian symptoms of PD such as altered locomotor activity (Fifel and Cooper, 2014), sleep disturbances (Turjanski et al, 1999; Eisensehr et al, 2003; Lima et al, 2007; Chaudhuri and Schapira, 2009; Lima, 2013; Videnovic and Golombek, 2013), visual dysfunction (see Archibald et al, 2009; Chaudhuri and Schapira, 2009; Popova, 2014), olfactory dysfunction/hyposmia (Doty et al, 1988; Huisman et al, 2004; Ross et al, 2008; Lelan et al, 2011; Doty, 2012), and disruptions to cyclic PRL release (Murri et al, 1980; Bellomo et al, 1991; Winkler et al, 2002). Recent evidence suggests that PD may affect circadian rhythms and their cellular mechanisms differently in the peripheral hypothalamus than in the SCN (Gravotta et al, 2011; Kudo et al, 2011; Hayashi et al, 2013; Mattam and Jagota, 2015).…”

Section: Introductionmentioning

confidence: 99%

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Dopamine: A Modulator of Circadian Rhythms in the Central Nervous System

Korshunov

Blakemore

Trombley

2017

Front. Cell. Neurosci.

124

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Circadian rhythms are daily rhythms that regulate many biological processes – from gene transcription to behavior – and a disruption of these rhythms can lead to a myriad of health risks. Circadian rhythms are entrained by light, and their 24-h oscillation is maintained by a core molecular feedback loop composed of canonical circadian (“clock”) genes and proteins. Different modulators help to maintain the proper rhythmicity of these genes and proteins, and one emerging modulator is dopamine. Dopamine has been shown to have circadian-like activities in the retina, olfactory bulb, striatum, midbrain, and hypothalamus, where it regulates, and is regulated by, clock genes in some of these areas. Thus, it is likely that dopamine is essential to mechanisms that maintain proper rhythmicity of these five brain areas. This review discusses studies that showcase different dopaminergic mechanisms that may be involved with the regulation of these brain areas’ circadian rhythms. Mechanisms include how dopamine and dopamine receptor activity directly and indirectly influence clock genes and proteins, how dopamine’s interactions with gap junctions influence daily neuronal excitability, and how dopamine’s release and effects are gated by low- and high-pass filters. Because the dopamine neurons described in this review also release the inhibitory neurotransmitter GABA which influences clock protein expression in the retina, we discuss articles that explore how GABA may contribute to the actions of dopamine neurons on circadian rhythms. Finally, to understand how the loss of function of dopamine neurons could influence circadian rhythms, we review studies linking the neurodegenerative disease Parkinson’s Disease to disruptions of circadian rhythms in these five brain areas. The purpose of this review is to summarize growing evidence that dopamine is involved in regulating circadian rhythms, either directly or indirectly, in the brain areas discussed here. An appreciation of the growing evidence of dopamine’s influence on circadian rhythms may lead to new treatments including pharmacological agents directed at alleviating the various symptoms of circadian rhythm disruption.

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Section: Discussionmentioning

confidence: 99%

Section: Hypothalamusmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Dopamine: A Modulator of Circadian Rhythms in the Central Nervous System

Korshunov

Blakemore

Trombley

2017

Front. Cell. Neurosci.

124

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“…2 In vivo neuroendocrine studies have provided insight into dysfunction of these pathways in neurologic disease. In idiopathic Parkinson's disease (IPD), both GH and PRL responses to levodopa have been reported to be reduced, 3,4 within the normal range, 5,6 or even increased, 7,8 and may reflect pathologic changes affecting the hypothalamic (tuberoinfundibular and incerto-hypothalamic) dopaminergic pathways. 9,10 However, confounding factors include the effects of long-term antiparkinsonian pharmacotherapy and, importantly, inclusion of patients with alternative diagnoses, 11 such as multiple system atrophy (MSA).…”

Section: Discussionmentioning

confidence: 99%

Neuroendocrine responses to levodopa in multiple system atrophy (MSA)

Kimber

Watson

1999

Mov. Disord.

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Hypothalamic dopaminergic pathways are involved in the regulation of growth hormone and prolactin release from the anterior pituitary. Neuroendocrine studies in patients with multiple system atrophy (MSA), in whom there is a reported loss of hypothalamic dopamine, are few and contradictory. We therefore studied the neuroendocrine responses to 250 mg levodopa (plus 25 mg carbidopa) in subjects with MSA (n = 15), and compared them with age‐ and sex‐matched healthy control subjects (n = 8). There were no significant differences in basal or post‐levodopa levels of growth hormone (GH), growth hormone‐releasing hormone (GHRH), glucose, insulin‐like growth factor (IGF‐1), or thyroid‐stimulating hormone (TSH) between the groups. In patients with MSA, basal levels of prolactin were elevated (21.1 ± 5.2 ng/mL [mean ± standard error]) compared with control subjects (12.1 ± 1.7, p <0.05), and after l‐dopa there was increased variability in prolactin response with less suppression compared with control subjects. In conclusion, in patients with MSA, the GHRH and GH responses to l‐dopa were preserved and were similar to responses in age‐matched control subjects. In contrast, there was impaired dopaminergic suppression of prolactin secretion. In patients with MSA this may represent a selective dysfunction, rather than generalized loss, of tubero‐infundibular dopaminergic neurones.

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“…In fact, stress per se is a releasing factor for the secretion of ACTH/cortisol and GH. Previous studies in the literature showed a normal circadian rhythm of ACTH/cortisol (Wiesen et al, 1982;Pique et al, 1985) and a normal unstimulated GH secretory pattern over many hours including overnight (Malarkey et al, 1974;Murri et al, 1980) in parkinsonian patients. Furthermore, both ACTH/cortisol (Pfeiffer et al, 1986;Conte-Devoix et al, 1987) and GH (Martinez-Campos et al, 1981;Vogel et al, 1986) secretory systems showed normal responses to specific challanging stimuli in Parkinson's disease.…”

Section: Resultsmentioning

confidence: 83%

Lack of ACTH/cortisol and GH responses to intravenously-infused substance P in Parkinson's disease

Volpi

Caffarra

Scaglioni³

et al. 1993

J Neural Transm Gen Sect

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In order to test possible changes in the stimulating effect of intravenously-infused substance P (SP) on ACTH/cortisol and GH secretion in Parkinson's disease, 10 male parkinsonian patients and 10 age-matched normal controls were infused intravenously for 60 min with SP (1.0 or 1.5 pmol/kg-1/min-1 SP) or normal saline. The circulating levels of ACTH, cortisol and GH were measured during and for 20 min after SP or saline infusion. No untoward side effects or changes in blood pressure were observed during SP infusion in any subjects. In basal conditions and during saline infusion, plasma ACTH and cortisol levels were similar in normal and parkinsonian patients. During SP infusions, ACTH/cortisol concentrations in normal controls rose significantly vs baseline and saline test in a dose-dependent fashion. In contrast, at both SP infused amounts, parkinsonian patients showed ACTH/cortisol levels similar to those observed in the saline test. All subjects showed similar basal concentrations of GH. GH levels rose significantly in the normal controls when the higher dose of SP was infused, but they were not modified by the infusion of the lower dose of SP or saline. At both tested amounts of SP and during saline infusion, GH levels remained unchanged in the parkinsonian subjects. In agreement with previous observations in the literature showing SP abnormalities in the parkinsonian brain, these data fail to show significant effects of plasma SP on the ACTH/cortisol and GH secretory systems in Parkinson's disease.

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Spontaneous Nocturnal Plasma Prolactin and Growth Hormone Secretion in Patients with Parkinson’s Disease and Huntington’s Chorea

Cited by 27 publications

References 21 publications

Dopamine: A Modulator of Circadian Rhythms in the Central Nervous System

Dopamine: A Modulator of Circadian Rhythms in the Central Nervous System

Neuroendocrine responses to levodopa in multiple system atrophy (MSA)

Lack of ACTH/cortisol and GH responses to intravenously-infused substance P in Parkinson's disease

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