PMID- 2864781
OWN - NLM
STAT- MEDLINE
DCOM- 19851114
LR  - 20131121
IS  - 0001-6772 (Print)
IS  - 0001-6772 (Linking)
VI  - 124
IP  - 4
DP  - 1985 Aug
TI  - Effects of lesions and ganglioside GM1 treatment on striatal polyamine levels and 
      nigral DA neurons. A role of putrescine in the neurotropic activity of 
      gangliosides.
PG  - 499-506
AB  - The effects of a partial hemitransection at the meso-diencephalic level, with or 
      without chronic ganglioside GMI treatment, have been evaluated on striatal 
      polyamine levels, 7, 14 and 21 days after lesion, as well as on the ability of 
      the polyamine synthesis inhibitor alpha-difluoromethylornithine (alpha-DFMO) to 
      modulate the protective effects of chronic ganglioside GMI treatment against 
      retrograde degeneration of the nigral dopamine (DA) nerve cell bodies (14 day 
      time interval). The striatal polyamine levels were measured by high pressure 
      liquid chromatography after dansylation of the polyamines. The nigral DA nerve 
      cells were studied by means of tyrosine hydroxylase (TH) immunocytochemistry 
      using the indirect immunoperoxidase technique. Quantitation was performed by 
      means of morphometrical evaluation of the TH immunoreactive area of the 
      substantia nigra. Seven days after partial hemitransection there is a marked 
      increase (above 350%) in striatal putrescine levels, which is not modulated by 
      chronic GMI treatment. This marked increase could, to a large extent, be 
      counteracted by simultaneous treatment with alpha-DFMO, which blocks mainly the 
      synthesis of putrescine. Twenty-one days after lesion chronic GMI treatment could 
      produce an increase in striatal putrescine levels on the intact side and also 
      after this time-interval prevent the reduction of striatal spermine levels. It 
      was also found that simultaneous treatment with alpha-DFMO prevents the 
      development of the protective action of chronic ganglioside GMI treatment against 
      retrograde degeneration of the nigral DA neurons.(ABSTRACT TRUNCATED AT 250 
      WORDS)
FAU - Agnati, L F
AU  - Agnati LF
FAU - Fuxe, K
AU  - Fuxe K
FAU - Zini, I
AU  - Zini I
FAU - Davalli, P
AU  - Davalli P
FAU - Corti, A
AU  - Corti A
FAU - Calza, L
AU  - Calza L
FAU - Toffano, G
AU  - Toffano G
FAU - Zoli, M
AU  - Zoli M
FAU - Piccinini, G
AU  - Piccinini G
FAU - Goldstein, M
AU  - Goldstein M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Acta Physiol Scand
JT  - Acta physiologica Scandinavica
JID - 0370362
RN  - 0 (Polyamines)
RN  - 37758-47-7 (G(M1) Ganglioside)
RN  - E524N2IXA3 (Ornithine)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - V10TVZ52E4 (Putrescine)
RN  - VTD58H1Z2X (Dopamine)
RN  - ZQN1G5V6SR (Eflornithine)
SB  - IM
MH  - Animals
MH  - Corpus Striatum/*metabolism/physiology
MH  - Dopamine/*metabolism
MH  - Eflornithine
MH  - G(M1) Ganglioside/*pharmacology
MH  - Male
MH  - Neurons/*metabolism
MH  - Ornithine/analogs & derivatives/pharmacology
MH  - Polyamines/*metabolism
MH  - Putrescine/*physiology
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Substantia Nigra/*metabolism/physiology
MH  - Tyrosine 3-Monooxygenase/metabolism
EDAT- 1985/08/01 00:00
MHDA- 1985/08/01 00:01
CRDT- 1985/08/01 00:00
PHST- 1985/08/01 00:00 [pubmed]
PHST- 1985/08/01 00:01 [medline]
PHST- 1985/08/01 00:00 [entrez]
AID - 10.1111/j.1748-1716.1985.tb00041.x [doi]
PST - ppublish
SO  - Acta Physiol Scand. 1985 Aug;124(4):499-506. doi: 
      10.1111/j.1748-1716.1985.tb00041.x.