EEG, Evoked Potential, and Extracellular Single-Unit Recordings In Vivo - Animal Models of Acute Neurological Injuries: Injury and Mechanistic Assessments - page 95

Fig. 5. Systemic exposure to nicotine induced two types of responses in VTA DA neurons. Type-I neurons showed a biphasic
response (initially reduced and then increased, A left, and Ba) while type-II neurons had a monophasic (increase) response
(A right and Bb). Statistical analysis indicates that after injection of nicotine for 1 min type-I and type-II neurons show
opposite responses in fi ring frequency (FR), bursting (BS), and the power of slow oscillation (Pso). However, after a 5-min
injection of nicotine, the FR and BS are increased in both type-I and type-II neurons (Bb and Cb). Since type-I neurons have
a high level of slow oscillation relative to type-II neurons, systemic nicotine reduces Pso in type-I neurons but does not
signifi cantly alter that in type-2 neurons. In these experiments, each neuron was recorded from a single rat (* p < 0.05,
** p < 0.01).
121.6 ± 4.8% ( p < 0.05), 180.3 ± 46.4% ( p > 0.05), and 170.7 ± 42.1%
( p > 0.05), respectively. Five minutes following nicotine adminis-
tration, the altered FR, BF, and SO (baseline as 100%) for type-I
neurons ( n = 17) were 124.2 ± 7.7% ( p < 0.01), 142.2 ± 28.9%
( p < 0.01), and 36.2 ± 8.2% ( p < 0.01), respectively, and for type-II
neurons ( n = 7) they were 115.1 ± 9.1% ( p < 0.05), 204.0 ± 49.2%
( p < 0.05), and 135.5 ± 28.8% ( p < 0.05), respectively (Fig. 5c ).
These results suggest that there are two subtypes of VTA DA
neurons (type I and type II), which exhibit different responses to
systemic exposure to a smoking-relevant concentration of nicotine.