Terma
Member
- Joined
- May 8, 2017
- Messages
- 1,063
Yeah sometimes both those sources come up with good ideas. I won't really have time to comment more right now. The 5-HT2c receptor is particularly related to circadian processes (i.e. its pattern of activation could become inverted, like cortisol, in sick people): Sci-Hub | Serotonin 5-HT2c agonists mimic the effect of light pulses on circadian rhythms. Brain Research, 806(2), 257–270 | 10.1016/s0006-8993(98)00746-x, Dysregulation of Diurnal Rhythms of Serotonin 5-HT2C and Corticosteroid Receptor Gene Expression in the Hippocampus with Food Restriction and Glucocorticoids
I'm interested in the Area1255 guy's idea of post-synaptic 5-HT1a overactivation inhibiting these processes, because that one sometimes seems like a wolf in sheep's clothing, but I would have to read more of his references. (It is one of the things to suspect if someone says they have problems yet low anxiety)
Good luck with the licorice, can't make predictions on that one today (they tend to avoid that here, because of the aldosterone effects iirc... tool for the job). Watch out for some things: Effect of eating liquorice on the renin-angiotensin aldosterone axis in normal subjects.
There's too much material, but he linked one which is particularly interesting to me although it only loosely relates to yours - it combines several topics together:
ACTIVATION OF PPAR GAMMA RECEPTORS REDUCES LEVODOPA-INDUCED DYSKINESIAS IN 6-OHDA-LESIONED RATS
I'm interested in the Area1255 guy's idea of post-synaptic 5-HT1a overactivation inhibiting these processes, because that one sometimes seems like a wolf in sheep's clothing, but I would have to read more of his references. (It is one of the things to suspect if someone says they have problems yet low anxiety)
Good luck with the licorice, can't make predictions on that one today (they tend to avoid that here, because of the aldosterone effects iirc... tool for the job). Watch out for some things: Effect of eating liquorice on the renin-angiotensin aldosterone axis in normal subjects.
There's too much material, but he linked one which is particularly interesting to me although it only loosely relates to yours - it combines several topics together:
ACTIVATION OF PPAR GAMMA RECEPTORS REDUCES LEVODOPA-INDUCED DYSKINESIAS IN 6-OHDA-LESIONED RATS
(Cannabinoids go nuclear: evidence for activation of peroxisome proliferator-activated receptors)Long-term administration of L-3,4-dihydroxyphenylalanine (levodopa), the mainstay treatment for Parkinson’s disease (PD), is accompanied by fluctuations in its duration of action and motor complications (dyskinesia) that dramatically affect the quality of life of patients. Levodopa-induced dyskinesias (LID) can be modeled in rats with unilateral 6-OHDA lesions via chronic administration of levodopa, which causes increasingly severe axial, limb and oro-facial abnormal involuntary movements (AIMs) over time. In previous studies, we showed that direct activation of CB1 cannabinoid receptors alleviated rat AIMs. Interestingly, elevation of the endocannabinoid anandamide by URB597 (URB), an inhibitor of endocannabinoid catabolism, produced an anti-dyskinetic response that was only partially mediated via CB1 receptors and required the concomitant blockade of transient receptor potential vanilloid type-1 (TRPV1) channels by capsazepine (CPZ) [1]. In this study, we showed that stimulation of peroxisome proliferator-activated receptors (PPAR), a family of transcription factors activated by anandamide, contributes to the anti-dyskinetic effects of URB+CPZ, and that direct activation of the PPARγ subtype by rosiglitazone (RGZ) alleviates levodopa-induced AIMs in 6-OHDA rats. AIM reduction was associated with an attenuation of levodopa-induced increase of dynorphin, zif-268 and of ERK phosphorylation in the denervated striatum. RGZ treatment did not decrease striatal levodopa and dopamine bioavailability, nor did it affect levodopa antiparkinsonian activity. Collectively, these data indicate that PPARγ may represent a new pharmacological target for the treatment of LID.
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