116 



latencies than observed initially in both groups at all doses tested (Table 1). 

 At .2 -.8 mg/kg the redetermined latencies of the before group were not 

 different from control, while at .8 mg/kg the latency of the after group was 

 substantially lengthened compared to its control. Further, the two groups 

 differed significantly from each other at .8 ng/kg (p<.05). The 1.2 and 1.6 

 mg/kg doses Increased latencies in both groups with greater increases observed 

 in the after group. 



The persistence of tolerance as determined by weekly administration^ o^ .8 

 mg/kg of nicotine follo wing the ce ssation of chronic dosing is slmwn in Figure 

 3. Response rates in the before group were reduced less than h\ the after 

 group by nicotine during weeks 1 and 2. By week 3 response rates were reduced 

 to a similar degree in the two groups by nicotine. Since both groups exhibited 

 a small loss of tolerance each week over weeks 1 to 3, it was necessary for the 

 before group to show a greater loss of tolerance than the after group In order 

 for both groups to respond similarly to nicotine during week 3. Response rates 

 were similarly or slightly less affected by nicotine delivery during week 4 

 compared to week 3, suggesting that a stable level of responding had been 

 achieved with weekly nicotine administrations. Response rates were reduced 

 less by .8 mg/kg of nicotine during weeks 3 and 4 than during the initial dose- 

 effect detersii nations (filled circles), suggesting that some degrea^of toler- 

 ance persisted in each group. ^ 



Following cessation of chronic dosing, latencies to complete the first 

 ratio in the before group were lengthened less by nicotine than were latencies 

 in the after group over all four weeks (Table 3); group differences were sig- 

 nificant for weeks 1 and 2 (p<.05). Latencies increased in each group over 

 weeks 1 to 3, although only the before group showed significant increases from 



