492 v. AFFECTI vE PROCESSES
effort to obtain reward when the probabil -
ity of obtaining reward was relatively low 
(Geaney, Treadway, & Smillie, 2015). This 
suggests that these personality traits may 
help predict motivation in contexts in which 
those with low reward sensitivity would not 
feel that the benefits of potential rewards 
outweigh the costs.
Much research examining physiologi -
cal correlates of behavioral activation has 
focused on frontal cortical asymmetry 
(Harmon-  Jones, Gable, & Peterson, 2010). 
Relative left frontal activity has been associ -
ated with approach motivation as measured 
by the BIS/BAS scales (Amodio, Master, 
Yee, & Taylor, 2008; Sutton & Davidson, 
1997), but some studies have not found this 
relationship (Pizzagalli, Shackman, & Da -
vidson, 2003; P. Gable, Mechin, Hicks, & 
Adams, 2015). Results from a recent meta- 
analysis taking into account unpublished 
dissertations suggest that midline posterior 
versus frontal theta activity may be a more 
robust marker of BAS activity than relative 
left frontal alpha activity (Wacker, Cha -
vanon, & Stemmler, 2010).
Neuroimaging studies have found cor -
respondence between blood-  oxygen- level 
dependent (BOLD) response to potential 
rewards in areas of the reward circuit and 
self- reported levels of approach motivation. 
As one example, in a functional magnetic 
resonance imaging (fMRI) study in which 
participants were presented with images of 
types of food as they lay in the scanner, self- 
reported BAS Drive scores predicted great -
er neural activation in the frontostriatal– 
amygdala–  midbrain network in response to 
appetizing food images (Beaver et al., 2006). 
Greater Anticipatory Pleasure (TEPS), but 
not Consummatory Pleasure, has been 
found to correspond with a stronger con -
nection between key regions in the neural 
reward circuit during anticipation of mon -
etary reward (Z. Li et al., 2015).
Heritability and  Genetic Polymorphisms 
Relevant to  BAS  Research
In a two-wave longitudinal twin study, re -
searchers estimated that genetics accounted 
for 28–35% of the variability in BAS scores 
(Takahashi et al., 2007). Participants were 
retested on the BIS/BAS scales an average of 2.25 years after the first administration, and 
stability in BAS scores appeared to be driven 
predominantly by genetic factors (heritabil -
ity estimates above .5), whereas nonshared 
environmental factors contributed to both 
the stability and change in BAS scores over 
time (Takahashi et al., 2007).
Many studies of the neurological basis of 
reward sensitivity suggest links to specific 
genetic polymorphisms (Bogdan & Pizza -
galli, 2009). Ogden and colleagues (2004) 
integrated findings of a pharmacogenomic 
study of mice with then-  recent human stud -
ies of related phenomena and concluded that 
reward sensitivity is most affected by path -
ways involving dopamine- and cyclic ad -
enosine monophosphate (cAMP)-regulated 
phosphoprotein, DARPP-32, a major target 
for dopamine in the striatum.
Most neuroimaging studies in humans 
that consider genetic influences on neural re -
sponses to reward have identified significant 
effects of genes relevant to dopamine func -
tion, including D2, D3, and D4 receptors 
and dopamine transporter ( DAT ). Research 
on neural responses to reward have found 
significant differences in the following genes 
associated with dopamine: ANKK1,  re-
lated to dopamine synthesis (Felsted, Ren, 
Chouinard-  Decorte, & Small, 2010), 141C 
Ins/Del  polymorphism related to D2 recep -
tors (Forbes et al., 2009), D4 receptor gene 
(DRD4;  Marco-  Pallarés et al., 2009), and 
DAT1  (Dreher, Kohn, Kolachana, Wein -
berger, & Berman, 2009). Individuals car -
rying the 9-repeat allele of the DAT1  poly -
morphism have been shown to take more 
risks in pursuit of rewards during decision- 
making tasks (Zhong et al., 2009) and to 
have increased striatal activity in response 
to reward cues (Zhong, Chark, Ebstein, & 
Chew, 2012).
Beyond the studies of genes that are direct -
ly linked to dopaminergic function, studies 
of genes with indirect links to dopaminergic 
functioning also appear related to neural re -
sponses to rewards, including the catechol-
O-methyltransferase ( COMT ) and brain- 
derived neurotrophic factor ( BDNF ) genes. 
The COMT  gene facilitates the production 
of COMT, an enzyme involved in catalyzing 
dopamine and other catecholamines (Chen 
et al., 2004). The BDNF  gene has neurobio -
logical effects on the mesolimbic dopamine 