both of which can produce incentive salience. The LHb sends glutaminergic
projections, the majority of which synapse on GABAergic RMTg neurons that in
turn drive inhibition of dopaminergic VTA neurons, although some LHb
projections terminate on VTA interneurons. These LHb projections are activated
both by aversive stimuli and by the absence of an expected reward, and
excitation of the LHb can induce aversion.  [22]  [23]  [24]

Most of the  dopamine pathways 
(i.e., neurons that use the  neurotransmitter   dopamine  to communicate
with other neurons) that project out of the ventral tegmental area are part of
the reward system;  [13]  in these pathways, dopamine acts on  D1-like
receptors  or  D2-like receptors
 to either stimulate (D1-like) or
inhibit (D2-like) the production of  cAMP  .
[25]  The  GABAergic   medium spiny neurons
 of the  striatum
 are components of the reward system as well.
[13]  The glutamatergic projection nuclei in the subthalamic nucleus,
prefrontal cortex, hippocampus, thalamus, and amygdala connect to other parts
of the reward system via glutamate pathways.  [13]  The  medial forebrain
bundle  , which is a
set of many neural pathways that mediate  brain stimulation reward
 (i.e., reward
derived from direct electrochemical stimulation of the  lateral hypothalamus
 ), is also a component of
the reward system.  [26]

Two theories exist with regard to the activity of the nucleus accumbens and
the generation liking and wanting. The inhibition (or hyper­polar­ization)
hypothesis proposes that the nucleus accumbens exerts tonic inhibitory effects
on downstream structures such as the ventral pallidum, hypothalamus or ventral
tegmental area, and that in inhibiting  MSNs  in the nucleus accumbens (NAcc),
these structures are excited, "releasing" reward related behavior. While 
GABA receptor   agonists
 are capable of eliciting both "liking" and
"wanting" reactions in the nucleus accumbens, glutaminergic inputs from the 
basolateral amygdala  ,
ventral hippocampus, and medial prefrontal cortex can drive incentive
salience. Furthermore, while most studies find that NAcc neurons reduce firing
in response to reward, a number of studies find the opposite response. This
had led to the proposal of the disinhibition (or depolarization) hypothesis,
that proposes that excitation or NAcc neurons, or at least certain subsets,
drives reward related behavior.  [2]  [27]  [28]

After nearly 50 years of research on brain-stimulation reward, experts have
certified that dozens of sites in the brain will maintain  intracranial self-
stimulation  . Regions include the lateral hypothalamus and medial forebrain
bundles, which are especially effective. Stimulation there activates fibers
that form the ascending pathways; the ascending pathways include the 
mesolimbic dopamine pathway  , which projects from the ventral tegmental area to the 
nucleus accumbens  . There are
several explanations as to why the mesolimbic dopamine pathway is central to
circuits mediating reward. First, there is a marked increase in dopamine
release from the mesolimbic pathway when animals engage in intracranial self-
stimulation.  [8]  Second, experiments consistently indicate that brain-
stimulation reward stimulates the reinforcement of pathways that are normally
activated by  natural rewards  ,