Involvement of dopamine D2 receptor in the diurnal changes of tuberoinfundibular dopaminergic neuron activity and prolactin secretion in female rats

Liang, Sophie Hsin-Yi; Hsu, Sheng-Chieh; Pan, Jenn-Tser

doi:10.1186/1423-0127-21-37

Cited by 7 publications

(8 citation statements)

References 33 publications

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“…Recent work has suggested that local release of dopamine around the cell body and dendrites of TIDA neurons may serve as a critical component of an ultrashort feedback loop that tunes the electrical activity of these neurons to their recent transmitter secretion history (Belousov and van den Pol, 1997;Durham et al, 1998;Liang and Pan, 2012;Liang et al, 2014;Stagkourakis et al, 2016). Yet to date, no direct evidence exists that dopamine can indeed be released in the somatodendritic compartment in the dmArc.…”

Section: Capacity For Dopamine Release At the Somatodendritic Compartmentioning

confidence: 99%

Dopamine Release Dynamics in the Tuberoinfundibular Dopamine System

et al. 2019

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The relationship between neuronal impulse activity and neurotransmitter release remains elusive. This issue is especially poorly understood in the neuroendocrine system, with its particular demands on periodically voluminous release of neurohormones at the interface of axon terminals and vasculature. A shortage of techniques with sufficient temporal resolution has hindered real-time monitoring of the secretion of the peptides that dominate among the neurohormones. The lactotropic axis provides an important exception in neurochemical identity, however, as pituitary prolactin secretion is primarily under monoaminergic control, via tuberoinfundibular dopamine (TIDA) neurons projecting to the median eminence (ME). Here, we combined electrical or optogenetic stimulation and fast-scan cyclic voltammetry to address dopamine release dynamics in the male mouse TIDA system. Imposing different discharge frequencies during brief (3 s) stimulation of TIDA terminals in the ME revealed that dopamine output is maximal at 10 Hz, which was found to parallel the TIDA neuron action potential frequency distribution during phasic discharge. Over more sustained stimulation periods (150 s), maximal output occurred at 5 Hz, similar to the average action potential firing frequency of tonically active TIDA neurons. Application of the dopamine transporter blocker, methylphenidate, significantly increased dopamine levels in the ME, supporting a functional role of the transporter at the neurons' terminals. Lastly, TIDA neuron stimulation at the cell body yielded perisomatic release of dopamine, which may contribute to an ultrafast negative feedback mechanism to constrain TIDA electrical activity. Together, these data shed light on how spiking patterns in the neuroendocrine system translate to vesicular release toward the pituitary and identify how dopamine dynamics are controlled in the TIDA system at different cellular compartments.A central question in neuroscience is the complex relationship between neuronal discharge activity and transmitter release. By combining optogenetic stimulation and voltammetry, we address this issue in dopamine neurons of the neuroendocrine system, which faces particular spatiotemporal demands on exocytotic release; large amounts of neurohormone need to be secreted into the portal capillaries with precise timing to adapt to physiological requirements. Our data show that release is maximal around the neurons' default firing frequency. We further provide support for functional dopamine transport at the neurovascular terminals, shedding light on a long-standing controversy about the existence of neuroendocrine transmitter reuptake. Finally, we show that dopamine release occurs also at the somatodendritic level, providing a substrate for an ultrashort autoregulatory feedback loop.

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Section: Capacity For Dopamine Release At the Somatodendritic Compartmentioning

confidence: 99%

Dopamine Release Dynamics in the Tuberoinfundibular Dopamine System

et al. 2019

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“…Daily 24‐h rhythms in 5‐Htr2a , 5‐Htr2b , and 5‐Htr2c mRNA have been reported in the VC and PVN regions of the baboon (Mure et al., ). Drd1 and Drd3 mRNA expression shows diurnal oscillations in the mouse NAc and ventral striatum, respectively (Ikeda et al., ; Ozburn et al., ), while Drd2 rhythmic expression has been found in the mouse striatum and rat CPu, medial basal hypothalamus, substantia nigra (SN), and VTA (Liang, Hsu, & Pan, ; Viyoch, Ohdo, Yukawa, & Higuchi, ; Weber et al., ). Regarding glutamate receptors, a 24‐h rhythmic expression of Glur1 and Glur3 has been seen in the rat olfactory bulb (OB) and baboon putamen and VC, as well as for mGlur5 in the baboon ventromedial hypothalamus (VMH) (Corthell, Fadool, & Trombley, ; Mure et al., ).…”

Section: Receptors Transporters and Channelsmentioning

confidence: 99%

Transcriptional control of synaptic components by the clock machinery

Hannou

Roy

Roig

et al. 2019

Eur J of Neuroscience

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Circadian rhythms are generated in mammals by a central clock located in the suprachiasmatic nucleus of the hypothalamus, which regulates the homeostasis of many biological processes. At the molecular level, the regulation of circadian rhythms is under the control of transcriptional‐translational feedback loops composed of clock factors, including transcription factors. In the brain, synaptic plasticity has been shown to vary with a 24‐h rhythm. Also, when measured at a given time‐of‐day, synaptic plasticity has been observed to be disrupted by dysregulation of clock factors. This could suggest a regulation of synaptic functions by the clock machinery. Interestingly, many studies provide support for direct and indirect transcriptional regulation by core clock factors, including rhythmic gene expression, for a variety of synaptic components. Indeed, the gene of several neuropeptides, neurotransmitter regulators, receptors and transporters, ion channels, vesicle proteins, and adhesion and scaffolding molecules present evidence to be clock‐controlled. We here present, while considering different regions of the mammalian brain, an overview of the extent of the transcriptional control of synaptic components by the clock machinery.

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“…Since, in our studies, the CRH antagonist attenuated the haloperidol-evoked response it seems that this effect, to some extent, is independent of the direct action of dopaminergic neurons of the arcuate nucleus on POMC-positive cells of the pituitary. Further, not completely excluding the potential influence of some regions of the mesolimbic system, such as the nucleus accumbens [49], we propose that it is the dopaminergic and peptidergic inputs from the arcuate nucleus [54] that may play significant roles in the central processing of ether-induced HPA activation [28,29]. This way, our experiments provided in vivo, functional evidence for D 2 mediated disinhibition of CRH and ACTH secretion.…”

Section: Discussionmentioning

confidence: 64%

“…Our findings somewhat correspond to those of Zhou but unlike cocaine-binge [23] ether stress appears to rely on CRH, not POMC, transcription. Taking into account the effectiveness of haloperidol and, that the tuberoinfundibular system mainly expresses D 2 and D 3 receptors [46][47][48][49] it appears that the D 2 -like family exerts tonic inhibitory control over HPA activation in the hypothalamus. Earlier studies clearly demonstrated that ether stimulates directly the hypothalamic CRH secretion [28,29], because it proved effective despite complete hypothalamic deafferentation [50][51][52] or olfactory bulbectomy [53].…”

Section: Discussionmentioning

confidence: 99%

Evidence of the dopamine-2 receptor mediated inhibition of the hypothalamic-pituitary-adrenal system; a rodent model of hypercortisolism in chronic neuropsychiatric disorders

Thurzó¹,

Jászberényi²,

Bagosi³

et al. 2017

Transl Brain Rhythmicity

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The purpose of this study was to examine the role of dopaminergic mediation in the hypothalamic-pituitary-adrenal (HPA) response challenged by ether stress. First the effects of the D1 selective (SCH-23390) and the D2 selective (haloperidol) dopamine antagonists on ether stress evoked corticosterone responses were tested. The activation of the HPA axis was assessed by measuring plasma corticosterone levels. Low doses of haloperidol (25 nmol/kg, intraperitoneally) failed to affect either basal or stimulated corticosterone secretion, while SCH-23390 elicited moderate inhibition of stimulated release. However, to our surprise higher doses of haloperidol (250 nmol/kg) raised basal secretion and even potentiated the HPA response evoked by ether stress. Therefore to elucidate the role of D 2 mediation, the intrinsic activity of the D 2 antagonist was tested in further experiments. Haloperidol (from 25 nmol/kg to 2.5 mmol/kg) alone elicited a dose-dependent activation of the HPA system reflected by both corticosterone and ACTH serum levels. This D 2 -antagonist-evoked HPA activation could be prevented by pre-administration of the CRH antagonist, α-helical CRH 9-41 . These findings provide unequivocal evidence that D 2 receptor can exert inhibitory control over the HPA axis.

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Involvement of dopamine D2 receptor in the diurnal changes of tuberoinfundibular dopaminergic neuron activity and prolactin secretion in female rats

Cited by 7 publications

References 33 publications

Dopamine Release Dynamics in the Tuberoinfundibular Dopamine System

Dopamine Release Dynamics in the Tuberoinfundibular Dopamine System

Transcriptional control of synaptic components by the clock machinery

Evidence of the dopamine-2 receptor mediated inhibition of the hypothalamic-pituitary-adrenal system; a rodent model of hypercortisolism in chronic neuropsychiatric disorders

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