Secret ingredient in stachybotrys: cyclosporin, an immune system suppressant.

[Guest guest]

I was just looking at some pages from Straus's book " Sick

Building Syndrome " and I saw this on page 242 in the text of a paper

by Yike and Dearborn:

" S. Chartarum is also capable of producing cyclosporin, an immune

suppressant targeting T-lymphocytes (Sakamato, et al, 1993) "

Does anyone know what the implications of having cyclosporin in your

home or workplace might be? Cyclosporin's effects seems as if they

might be better documented than satratoxin H, etc.

[Guest guest]

Hmm..

I just saw this.. I *think* that a possible translation may be that

stachybotrys mycotoxin relative cyclosporin (A) disregulates an important

process of reducing neuronal excitability.

I also think that this system is intimately involved in LONG TERM

POTENTIATION (or 'LTP' as its abbreviated) of MEMORY...

Could someone who knows more about this look into this?

------------------------------------

J Neurochem. 2007 Nov 6; [Epub ahead of print]

AMPA and kainate receptors mediate mutually exclusive effects on GABA(A)

receptor expression in cultured mouse cerebellar granule neurones.

Payne HL, Ives JH, Sieghart W, CL.

Centre for Integrative Neurosciences, School of Biological and Biomedical

Sciences, University of Durham, Durham, UK.

Studies on animal models of epilepsy and cerebellar ataxia, e.g.,

stargazer mice (stg) have identified changes in the GABAergic properties of

neurones associated with the affected brain loci. Whether these changes

contribute to or constitute homeostatic adaptations to a state of altered

neuronal excitability is as yet unknown. Using cultured cerebellar granule

neurones from control [+/+;

alpha-amino-3-hydroxyl-5-methyl-4-isoxazolepropionate receptor

(AMPAR)-competent, Kainate receptor (KAR)-competent] and stg

(AMPAR-incompetent, KAR-competent), we investigated whether non-NMDA

receptor (NMDAR) activity regulates GABA(A) receptor (GABAR) expression.

Neurones were maintained in 5 mmol/L KCl-containing basal media or

depolarizing media containing either 25 mmol/L KCl or the non-NMDAR agonist

kainic acid (KA) (100 mumol/L). KCl- and KA-mediated depolarization

down-regulated GABAR alpha1, alpha6 and beta2, but up-regulated alpha4,

beta3 and delta subunits in +/+ neurones. The KCl-evoked but not KA-evoked

effects were reciprocated in stg neurones compatible with AMPAR-regulation

of GABAR expression. Conversely, GABAR gamma2 expression was insensitive to

KCl-mediated depolarization, but was down-regulated by KA-treatment in a

6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)-reversible manner in +/+ and stg

neurones compatible with a KAR-mediated response. KA-mediated up-regulation

of GABAR alpha4, beta3 and delta was inhibited by L-type voltage-gated

calcium channel (L-VGCC) blockers and the Ca(2+)/calmodulin-dependent

protein kinase inhibitor,

4-[(2S)-2-[(5-isoquinolinylsulfonyl)methylamino]-3-oxo-3-(4-phenyl-1-piperazinyl\

)propyl]

phenyl isoquinoline sulfonic acid ester (KN-62). *Up-regulation of GABAR

alpha4 and beta3 was also prevented by calcineurin (CaN) inhibitors, FK506

and cyclosporin A.* Down-regulation of GABAR alpha1, alpha6 and beta2 was

independent of L-VGCC activity, but was prevented by inhibitors of CaN.

Thus, we provide evidence that a KAR-mediated and at least three mutually

exclusive AMPAR-mediated signalling mechanisms regulate neuronal GABAR

expression.

On Nov 12, 2007 11:45 PM, LiveSimply <quackadillian@...> wrote:

> I was just looking at some pages from Straus's book " Sick

> Building Syndrome " and I saw this on page 242 in the text of a paper

> by Yike and Dearborn:

>

> " S. Chartarum is also capable of producing cyclosporin, an immune

> suppressant targeting T-lymphocytes (Sakamato, et al, 1993) "

>

> Does anyone know what the implications of having cyclosporin in your

> home or workplace might be? Cyclosporin's effects seems as if they

> might be better documented than satratoxin H, etc.

>