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Estrogen/ CCK sulfated/unsulfated..dopamine .. » KaraS

Posted by tealady on November 22, 2004, at 17:49:12

In reply to Re: CCK sulfated/unsulfated..dopamine/CCK autoreceptor » raybakes, posted by KaraS on November 18, 2004, at 21:00:35

Hi Kara,

Just occurred to me that estrogen levels play a part in this picture(probably when considered together with hahsimotos and maybe evn previous SSRI use)
..with low estrogen levels maybe causing part of the auto receptor sensitivity problem?...I really get lost, not sure but from clicking on links I posted at the start of this thread and links within these you get to the first one..then following thru
http://www.acnp.org/g4/GN401000056/Default.htm

The ability to visualize CCK mRNA has provided much additional information about the location of CCK cell bodies.

CCK mRNA levels in rat brain are altered by estrogens (medial preoptic area, amygdala, bed nucleus stria terminalis) [97], caffeine (striatum) [143], N-methyl-D-aspartate [NMDA] (striatum) [47], opiates (spinal cord and hypothalamus) [46] and cocaine and benzotript (striatum) [48].

CCK cells are abundant in three sexually dimorphic nuclei in the rat forebrain (the central part of the medial preoptic nucleus, the encapsulated part of the bed nucleus of the stria terminalis, and the posterodorsal part of the media nucleus of the amygdala) [148]. CCK mRNA levels are altered by estrogen in these areas (97).


In the trans-Golgi, three out of four of the tyrosine residues of pro-CCK are sulfated by a specific membrane-bound tyrosine sulfotransferase (109). The sulfation of one of the tyrosine residues (in CCK 8) is important for its biological activity at CCK A receptors. Recent evidence suggests that sulfation of the tyrosines in pro-CCK allows for correct sorting and/or processing of pro-CCK in an endocrine cell in culture (9). This is probably also true for gastrin.
In the trans-Golgi network, sulfated pro-CCK is sorted into secretory granules with other material destined for the regulated secretory pathway.

It is important to remember that CCK release requires a stronger stimulus than dopamine release, so it may be more pronounced when animals are stressed or activated.

A large body of evidence indicates that CCK is an excitatory neurotransmitter or neuromodulator, usually activating specific cells directly. In some cases, the action of CCK can be blocked by antagonists of other neurotransmitter systems like DA, 5-HT , GABA or endogenous opiates, suggesting that CCK is releasing other agents which are excitatory or, in some cases, inhibitory (2). CCK excites neurons in the periaqueductal gray (86), dorsal raphe (15), nucleus accumbens (174), hippocampus (18,38,71), ventral medial hypothalamus (15), substantia nigra (130), thalamus (33), and spinal cord (72). It depolarizes oxytocin-containing neurons in the supraoptic nucleus of the hypothalamus (88) and serotonin-containing neurons in the dorsal raphe nucleus.

CCK increases excitatory amino acid release in the hippocampus (100). Most studies indicate that CCK increases GABA release (128) while it decreases dopamine release (54).

97. Micevych PE, Eckersell CB, Holland K, Smith A. Induction of CCK mRNA levels in the limbic-hypothalamic circuit: time course and site-specific effects of estrogen. J Neurobiol 1996;30:465-479.

Micevych PE estrogen enter ito pubmed

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8814910
Regulation of cholecystokinin receptors in the ventromedial nucleus of the hypothalamus: sex steroid hormone effects.

In the caudal VMH, in both gonadectomized male and female rats, the levels of CCK-R binding were decreased 24 h after injection of 50 micrograms of estrogen benzoate but were not changed after injection of 300 micrograms of testosterone propionate. We hypothesize that these changes in CCK-R binding in the VMH reflect ligand-induced down-regulation that result from an estrogen-facilitation of stimulated CCK release in the VMH.
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Estrogen interacts with the IGF-1 system to protect nigrostriatal dopamine and maintain motoric behavior after 6-hydroxdopamine lesions.

Quesada A, Micevych PE.

Department of Neurobiology, Laboratory of Neuroendocrinology, Brain Research Institute, David Geffen School of Medicine UCLA, Los Angeles, California 90095-1763, USA. aquesada@mednet.ucla.edu

The most prominent neurochemical hallmark of Parkinson's disease (PD) is the loss of nigrostriatal dopamine (DA). Animal models of PD have concentrated on depleting DA and therapies have focused on maintaining or restoring DA. Within this context estrogen protects against 6-hydroxdopamine (6-OHDA) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) lesions of the nigrostriatal DA pathway. Present studies tested the hypothesis that neuroprotective estrogen actions involve activation of the insulin-like growth factor-1 (IGF-1) system. Ovariectomized rats were treated with either a single subcutaneous injection of 17beta-estradiol benzoate or centrally or peripherally IGF-1. All rats were infused unilaterally with 6-OHDA into the medial forebrain bundle (MFB) to lesion the nigrostriatal DA pathway. Tyrosine hydroxylase (TH) immunocytochemistry confirmed that rats injected with 6-OHDA had a massive loss of TH immunoreactivity in both the ipsilateral substantia nigra compacta (60% loss) and the striatum (>95% loss) compared to the contralateral side. Loss of TH immunoreactivity was correlated with loss of asymmetric forelimb movements, a behavioral assay for motor deficits. Pretreatment with estrogen or IGF-1 significantly prevented 6-OHDA-induced loss of substantia nigra compacta neurons (20% loss) and TH immunoreactivity in DA fibers in the striatum (<20% loss) and prevented the loss of asymmetric forelimb use. Blockage of IGF-1 receptors by intracerebroventricular JB-1, an IGF-1 receptor antagonist, attenuated both estrogen and IGF-1 neuroprotection of nigrostriatal DA neurons and motor behavior. These findings suggest that IGF-1 and estrogen acting through the IGF-1 system may be critical for neuroprotective effects of estrogen on nigrostriatal DA neurons in this model of PD. Copyright 2003 Wiley-Liss, Inc.

PMID: 14689453 [PubMed - indexed for MEDLINE]
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Just something else to maybe consider <g>
Jan


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