Chronic ganglioside treatment (10 mg/kg, i.p.) using the molecular species withonly one neuroaminic acid residue (GM1) given together with haloperidol (0.3 and 5 mg/kg, i.p.) once daily in male rats, counteracted the haloperidol-inducedincrease in the number of [3H]spiperone binding sites in striatal membranes when the low dose of haloperidol, but not the high dose, was administered. The presentresults therefore indicate that chronic GM1 treatment can partially counteractthe increase in the number of dopamine receptors having a high affinity for neuroleptics (D2 type) induced by chronic haloperidol treatment in striatalmembranes, and therefore may also partially counteract the development ofneuroleptic-induced dopamine receptor supersensitivity.
Chronic ganglioside treatment counteracts the biochemical signs of dopamine receptor supersensitivity induced by chronic haloperidol treatment / Agnati, Lf; Fuxe, K; Benfenati, F; Battistini, Nino Carlo; Zini, I; Toffano, G.. - In: NEUROSCIENCE LETTERS. - ISSN 0304-3940. - STAMPA. - 40(3):(1993), pp. 293-297.
Chronic ganglioside treatment counteracts the biochemical signs of dopamine receptor supersensitivity induced by chronic haloperidol treatment.
BATTISTINI, Nino Carlo;
1993
Abstract
Chronic ganglioside treatment (10 mg/kg, i.p.) using the molecular species withonly one neuroaminic acid residue (GM1) given together with haloperidol (0.3 and 5 mg/kg, i.p.) once daily in male rats, counteracted the haloperidol-inducedincrease in the number of [3H]spiperone binding sites in striatal membranes when the low dose of haloperidol, but not the high dose, was administered. The presentresults therefore indicate that chronic GM1 treatment can partially counteractthe increase in the number of dopamine receptors having a high affinity for neuroleptics (D2 type) induced by chronic haloperidol treatment in striatalmembranes, and therefore may also partially counteract the development ofneuroleptic-induced dopamine receptor supersensitivity.Pubblicazioni consigliate
I metadati presenti in IRIS UNIMORE sono rilasciati con licenza Creative Commons CC0 1.0 Universal, mentre i file delle pubblicazioni sono rilasciati con licenza Attribuzione 4.0 Internazionale (CC BY 4.0), salvo diversa indicazione.
In caso di violazione di copyright, contattare Supporto Iris