Lack of a high affinity transport system for dopamine in the median eminence and posterior pituitary
Reference (20)
- et al.
Ultrastructural identification of catecholamine neurons in the hypothalamic periventricular-arcuate nucleus-median eminence complex with special reference to quantitative aspects
Brain Research
(1973) - et al.
The organization of tubero-hypophyseal and reticuloinfundibular catecholamine neuron systems in the rat brain
Brain Research
(1973) - et al.
Localization of tritiated dopamine in the median eminence of the rat hypothalamus by electron microscope autoradiography
Brain Research
(1973) - et al.
Effect of 6-hydroxydopamine on hypothalamic norepinephrine and dopamine content, ultrastructure of the median eminence, and plasma corticosterone
Brain Research
(1974) - et al.
The effect of drugs on accumulation of monoamines in tuberoinfundibular dopamine neurons
Europ. J. Pharmacol.
(1967) - et al.
Effects of 6-hydroxydopamine on the uptake and storage of noradrenaline in sympathetic adrenergic neurons
Europ. J. Pharmacol.
(1970) - et al.
Effects of amphetamine, methylphenidate and cocaine on serum prolactin concentrations in the male rat
Life Sci.
(1977) - et al.
Organization and ultrastructural identification of the catecholamine nerve terminals in the neural lobe and para intermedia of the rat pituitary
Z. Zellforsch
(1972) - et al.
Catecholamine uptake by synaptosomes in homogenates of rat brain: stereospecificity in different areas
J. Pharmacol. exp. Ther.
(1969) - et al.
Catecholamines in the median eminence: new evidence for a major noradrenergic input
Nature (Lond.)
(1973)
Cited by (108)
Incomplete concordance of dopamine transporter Cre (DAT <sup>IREScre</sup> )-mediated recombination and tyrosine hydroxylase immunoreactivity in the mouse forebrain
2018, Journal of Chemical NeuroanatomyCitation Excerpt :These neurons secrete dopamine into the hypophyseal portal system to regulate prolactin release at the pituitary, and thus have little functional requirement for dopamine re-uptake. Indeed, earlier work has suggested that these TIDA neurons do not express a high affinity uptake system for dopamine (Annunziato et al., 1980; Demarest and Moore, 1979). It is also possible that these include the L-DOPA producing mono-enzymatic TH neurons, which are thought to act cooperatively with the mono-enzymatic AADC neurons to produce dopamine following up-take of L-DOPA from their TH-expressing counterparts and contributing to the regulation of prolactin secretion (Melnikova et al., 1998; Ugrumov et al., 2002, 2014).
Dopamine Autoreceptor Regulation of a Hypothalamic Dopaminergic Network
2016, Cell ReportsCitation Excerpt :The existence of the DAT in the TIDA system is controversial. Evidence has been presented for both the absence (Demarest and Moore, 1979b; Annunziato et al., 1980) and existence (Demaria et al., 2000; Bossé et al., 1997) of functional dopamine reuptake in these cells. We addressed this issue directly by applying a DAT blocker, either GBR-12783 or methylphenidate, and recorded the electrophysiological response.
TIDAL WAVES: Network mechanisms in the neuroendocrine control of prolactin release
2014, Frontiers in NeuroendocrinologyCitation Excerpt :Unlike dopaminergic neurons of the mesencephalon, however, TIDA cells do not release transmitter onto another neuron within a confined neuropil compartment, but towards the capillaries where transmitter reuptake is difficult to accomplish. Indeed, though the dopamine transporter (DAT) is expressed in arcuate dopamine cells (Meister and Elde, 1993; Demaria et al., 2000) reuptake, while present (Bossé et al., 1997; Demaria et al., 2000), is less efficient than in other central dopamine systems (Demarest and Moore, 1979; Annunziato et al., 1980; Annunziato and Weiner, 1980; Lookingland et al., 1987). Thus, continuous tonic discharge, without the potential relief that quiescent DOWN states may provide, may successively deplete transmitter stores resulting in substantially diminished dopamine release.
Sustained resistance to acute MPTP toxicity by hypothalamic dopamine neurons following chronic neurotoxicant exposure is associated with sustained up-regulation of parkin protein
2013, NeuroToxicologyCitation Excerpt :TIDA neurons originate in the arcuate nucleus (ARC) and terminate adjacent to the hypophysial portal vessels in the median eminence (ME). Reuptake of DA in TIDA neurons is mediated by low affinity, high volume transport as well as by the DA transporter (DAT), albeit to a lesser extent than NSDA neurons (Demarest and Moore, 1979; Revay et al., 1996; DeMaria et al., 2000; Lookingland and Moore, 2005). Despite these differences in DA reuptake mechanisms, the cellular machinery responsible for DA synthesis, storage, release and catabolism are similar in both NSDA and TIDA neurons.
Recovery of hypothalamic tuberoinfundibular dopamine neurons from acute toxicant exposure is dependent upon protein synthesis and associated with an increase in parkin and ubiquitin carboxy-terminal hydrolase-L1 expression
2012, NeuroToxicologyCitation Excerpt :Our previously published data indicated that an intrinsic neuronal mechanism (rather than extrinsic factors such as toxicant distribution or elimination) most likely accounts for the differential susceptibility of TIDA versus NSDA neurons to toxicant-induced degeneration (Behrouz et al., 2007). TIDA neurons have been thought to be resistant to the toxicant MPP+ due to lower expression of the high affinity DAT (Annunziato et al., 1980; Demarest and Moore, 1979; Revay et al., 1996). However, our previous findings and the data presented herein indicate that this is not likely to be the case.
Chapter VIII Functional neuroanatomy of hypothalamic dopaminergic neuroendocrine systems
2005, Handbook of Chemical Neuroanatomy
This work was supported by USPHS Grant NS 09174 and by a NIH postdoctoral fellowship to K.T.D.