Monosialoganglioside effects following transitory global cerebral ischemia in rodents

Pharmacological Research Communications, Vol. 20, Supplement II, 1988 MONOSIALOGANGLIOSIDE EFFECTS

355

FOLLOWING TRANSITORY GLOBAL CEREBRAL ISCHEMIA

IN RODENTS M.S. Seren,

R. Rubiml,

A. Lazzaro,

R. Zanoni,

A. Za~otti,

M.G.

Fiori,

G.

Toffano, and A. Leon Fidia Research Laboratories,

Abano Terme, Italy

Hippocampus, Neuronal death

Key words: Ischemla, Gmnglloside,

The systemic administration

of GM1 has been reported to facilitate the re-

covery of the adult CNS following traumatic, tally-induced

brain damage

(Tettamantl

been shown that gangliosides, inhibit

glutamate-induced

ton et al.

to

neurotoxicity

(1988); Faccl et al.,

investigate

whether

monosialoganglloslde

et al. (1986)). In addition,

including monosialoganglioside,

(EAA) have also been implicated begun

in cultured neuronal

this meeting). in post-ischemic

antagonism

of

EAA

As

are

toxicity

able

cells

excitatory

neuronal

it has to

(Fava-

aminoaclds

damage,

we have

underlines

the

effects observed in vlvo following cerebral ~schemia.

In particular we have assessed the effects the post-ischemie

toxic or ischemic experimen-

neuropathologlcal

of the ganglieslde

treatment on

damage of the hippocampus known to re-

ceive prominent EAA transmitter inputs. A transitory global cerebral

isch-

emic insult was induced in adult Wistar rats (four-vessel occlusion model: Pulsinelli and Brierley (1979)). out the occlusion period,

Animals,

of monosialoganglioside

up

days.

21

Our

preliminary

(20 mg/kg) results

and were allowed to

indicate

treatment not only improves EEG recovery during the lowing the ischemic episode creases

the percentage

duced damage addition,

showing

first

the

ganglioside

two weeks

fol-

less

severe

post

ischemic-in-

neurons of the CA1 region of the hippocampus.

to further validate whether

ganglioside-lnduced

that

survive

(see Rubini et al., this meeting) but also in-

of animals

to pyramidal

through-

were post-treated with saline or the inner ester

deri~,ative to

showing ECoG flattening

oecrease

In

such an effect is due to monoslalo-

of glutamate-related

post-ischemic

neuronal cell loss, we are now also assesaing ganglieside

selective

effects

in ger-

bils followlng transitory bilateral common carotid artery occlusion.

REFERENCES: Facci L., Milani D., Leon A., Shaper S.D., this meeting. Favaron M., Alho H., Manev H., Guidotti A., Costa E. (1988) FASEB J. 2:A824 Pulsinelli W.A. and Brierley J.B. (1979) Stroke 10:267-272 Rublni R., Fogarolo F., Biaslolo F., Fiori M.G., Seren M.S., Lazzaro A., Leon A., this meeting Tettamanti G., Ledeen R.W., Sandhoff K., Nagai Y., Toffano G. eds. (1986) Gangliosides and Neuronal Plasticity, Liviana P:ess, Padova