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Could a male fertility pill adversely affect inhibition via allopregnanolone levels?

kofi kofi at anon.un
Fri Oct 17 12:19:10 EST 2003


Ok, some more.

Nihon Shinkei Seishin Yakurigaku Zasshi. 2002 Aug;22(4):121-9. Related 
Articles, Links

    [Modifications of several pharmacological actions by diabetes: 
effects on the opioid receptor agonist and benzodiazepines]

    [Article in Japanese]

    Kamei J, Zushida K, Miyata S.

    Department of Pathophysiology and Therapeutics, Hoshi University 
School of Pharmacy and Pharmaceutical Sciences, 2-4-41, Ebara, 
Shinagawa-ku, Tokyo, 142-8501 Japan.

    Diabetic neuropathy is a most-convoluted complication. Diabetic 
gastropathy, ulcers, diarrhea, and bladder dysfunction are the major 
peripheral neuropathies. Peripheral neuropathies have been the primary 
neuroscience focus of diabetes research. In contrast to the periphery, 
the brain is not usually thought to be a target of chronic diabetic 
complications. However, the impact of diabetes mellitus on the central 
nervous system has recently gained attention. It is well known that 
diabetes or hyperglycemia influences the sensitivity of laboratory 
animals to various pharmacological agents. An increased sensitivity of 
hyperglycemic or diabetic animals to barbiturates and a decreased 
sensitivity of D-amphetamine, p-chloroamphetamine, and carbon 
tetrachloride have been demonstrated. Furthermore, it was reported that 
mice and rats with streptozotocin-induced diabetes and spontaneously 
diabetic mice are significantly less sensitive than non-diabetic mice to 
the antinociceptive effect of morphine. However, little information is 
available regarding the mechanism responsible for these changes. It is 
well established that anxiety and depression are common in patients with 
diabetes. Moreover, diabetic animals showed significantly more 
anxiogenic activity than non-diabetic animals did. However, the 
mechanisms through which diabetes may contribute to the development of, 
or be a risk factor for, psychiatric disorders are not clear. We provide 
an overview of our current understanding of the effects of 
streptozotocin-induced diabetes on the opioid receptor and the 
benzodiazepine receptor.

    Publication Types:

        * Review
        * Review, Tutorial


    PMID: 12373865 [PubMed - indexed for MEDLINE]

J Pharmacol Exp Ther. 2002 Jun;301(3):1067-78. Related Articles, Links
    Click here to read 
    SSR180575 
(7-chloro-N,N,5-trimethyl-4-oxo-3-phenyl-3,5-dihydro-4H-pyridazino[4,5-b]
indole-1-acetamide), a peripheral benzodiazepine receptor ligand, 
promotes neuronal survival and repair.

    Ferzaz B, Brault E, Bourliaud G, Robert JP, Poughon G, Claustre Y, 
Marguet F, Liere P, Schumacher M, Nowicki JP, Fournier J, Marabout B, 
Sevrin M, George P, Soubrie P, Benavides J, Scatton B.

    Discovery Research, Central Nervous System Research Department, 
Sanofi-Synthelabo Recherche, 31 avenue P. Vaillant-Couturier, 92225 
Bagneux Cedex, France.

    In the present study, we have investigated the potential 
neuroprotective effects of a novel peripheral benzodiazepine binding 
site (PBR) ligand, 
7-chloro-N,N,5-trimethyl-4-oxo-3-phenyl-3,5-dihydro-4H-pyridazino[4,5-b]i
ndole-1-acetamide (SSR180575), in models of central and peripheral 
neurodegeneration in vivo and its effect on steroid concentrations in 
plasma and nervous tissue. SSR180575 shows high affinity (IC(50), 
2.5-3.5 nM) and selectivity for the rat and human PBR and potently 
inhibits the in vivo binding of [(3)H]alpidem to PBR in the rat brain 
and spleen after oral or i.p. administration (ID(50), 0.1-0.3 mg/kg). In 
an experimental model of motoneuron degeneration induced by facial nerve 
axotomy in the immature rat, SSR180575 given i.p. or orally for 8 days 
rescued facial motoneurons, increasing their survival by 40 to 72% at 6 
and 10 mg/kg p.o. b.i.d. Moreover, in this model, SSR180575 (10 mg/kg 
p.o. b.i.d.) increased by 87% the number of motoneurons immunoreactive 
to peripherin, a type III intermediate filament, whose expression is 
up-regulated during nerve regeneration. SSR180575 also improved 
functional recovery in acrylamide-induced neuropathy in the rat when 
given therapeutically at 2.5 to 10 mg/kg/day p.o. Furthermore, SSR180575 
(3 mg/kg i.p. b.i.d.) accelerated functional recovery of the blink 
reflex after local injury of the facial nerve in the rat. SSR180575 
increased pregnenolone accumulation in the brain and sciatic nerve 
(+100% at 3 mg/kg i.p.), suggesting that its neuroprotective effects are 
steroid-mediated. These results indicate that PBR ligands (e.g., 
SSR180575) promote neuronal survival and repair in axotomy and 
neuropathy models and have potential for the treatment of 
neurodegenerative diseases (e.g., peripheral neuropathies or amyotrophic 
lateral sclerosis).

    PMID: 12023539 [PubMed - indexed for MEDLINE]

 Brain Res Brain Res Rev. 2001 Nov;37(1-3):360-71. Related Articles, 
Links
    Click here to read 
    Neuroactive steroids and peripheral myelin proteins.

    Magnaghi V, Cavarretta I, Galbiati M, Martini L, Melcangi RC.

    Department of Endocrinology and Center of Excellence for 
Neurodegenerative Disorders, University of Milan, Via Balzaretti 9, 
20133, Milan, Italy.

    The present review summarizes observations obtained in our 
laboratories which underline the importance of neuroactive steroids 
(i.e., progesterone (PROG), dihydroprogesterone (5alpha-DH PROG), 
tetrahydroprogesterone (3alpha, 5alpha-TH PROG), testosterone (T), 
dihydrotestosterone (DHT) and 5alpha-androstan-3alpha,17beta-diol 
(3alpha-diol)) in the control of the gene expression of myelin proteins 
(i.e. glycoprotein Po (Po) and the peripheral myelin protein 22 (PMP22)) 
in the peripheral nervous system. Utilizing different in vivo (aged and 
adult male rats) and in vitro (Schwann cell cultures) experimental 
models, we have observed that neuroactive steroids are able to stimulate 
the mRNA levels of Po and PMP22. The effects of these neuroactive 
steroids, which are able to interact with classical (progesterone 
receptor, PR, and androgen receptor, AR) and non-classical (GABA(A) 
receptor) steroid receptors is further supported by our demonstration in 
sciatic nerve and/or Schwann cells of the presence of these receptors. 
On the basis of the observations obtained in the Schwann cells cultures, 
we suggest that the stimulatory effect of neuroactive steroids on Po is 
acting through PR, while that on PMP22 needs the GABA(A) receptor. The 
present findings might be of importance for the utilization of specific 
receptor ligands as new therapeutical approaches for the rebuilding of 
the peripheral myelin, particularly in those situations in which the 
synthesis of Po and PMP22 is altered (i.e. demyelinating diseases like 
Charcot-Marie-Tooth type 1A and type 1B, hereditary neuropathy with 
liability to pressure palsies and the Dejerine-Sottas syndrome, aging, 
and after peripheral injury).

    Publication Types:

        * Review
        * Review, Tutorial


    PMID: 11744100 [PubMed - indexed for MEDLINE]



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