76 



iod (Karras and Kane 1980). In contrast, naloxone has not been shown 

 to be an effective antagonist of nicotine- induced antinociception in 

 rats (Sah!ey et a1. 1977; Tripathi et al. 1982). The present results 

 are consistent with previous findings in rats in that naloxone across a 

 range of doses was ineffective as an antagonist to the positive rein- 

 forcing effects of iv nicotine in rats. 



To sunrarize, previous atteanpts to establish nicotine as ar iv deliv- 

 e'-ed reinforcer for rats have shovirn that only under conditions of 

 reduced body weight ard/or concurrent fixed-tine food presentation c 

 following prograimed nicotine infusions will nicotine self- 

 administratior, occur at rates above vehicle control levels (Lang et al. 

 1977; Hanson et a1 1979; Lang and Smith 1980). The present results 

 show that nicotine can function as an intravenously delivered positive 

 rein'orcer for rats in the abserce of such conditions, and th?t the lev- 

 el of responding can be ir.aintaired across several ratio values. In 

 this study the maintenance of leve-- pressing was uneoui vocally the 

 result of consequent nicotine infusions. The fact that pretreatmert 

 with irecamyl amine (a centrally-active nicotinic antagonist) but not 

 hexatrethonium {a nicotinic antagonist that does not readily penetrate 

 the central nervous system) blocked the positive reinforcing effects of 

 nicotine suggests that this effect is centrally mediated. In addition, 

 the failure of large doses (3.0 ng/kg) of naloxone to alter the rein- 

 'orcing effects of nicct'ne suggests that the erdocerous opioid system 

 may net mediate the effects. Furthenrore, the behavicr was shewn to be 

 sensitive to both dose and response contingency manipulations. 



If 



