Gambling disorder (GD) as a type of behavioral addictions has different mechanism compared with neuroadaptive addictions caused by substance use disorder (SUD). Wikipedia source on operant conditioning has hinted gambling addiction is caused by its variable ratio schedule of (positive) reinforcement. And indeed dopamine underlying reinforcement plays a key role in general behavioral addictions such as gambling, since prolonged and abnormally high levels of dopamine in the synaptic cleft can induce receptor downregulation in the neural pathway. Downregulation of mesolimbic dopamine receptors can result in a decrease in the sensitivity to natural reinforcers.
Schedules of reinforcement are rules that control the delivery of reinforcement. The rules specify either the time that reinforcement is to be made available, or the number of responses to be made, or both... Variable ratio schedule: Reinforcement occurs after a variable number of responses have been emitted since the previous reinforcement... This schedule typically generates rapid, persistent responding. Slot machines pay off on a variable ratio schedule, and they produce just this sort of persistent lever-pulling behavior in gamblers. The variable ratio payoff from slot machines and other forms of gambling has often been cited as a factor underlying gambling addiction.
A neurochemical process involving dopamine has been suggested to underlie reinforcement. When an organism experiences a reinforcing stimulus, dopamine pathways in the brain are activated. This network of pathways "releases a short pulse of dopamine onto many dendrites, thus broadcasting a global reinforcement signal to postsynaptic neurons."[30] This allows recently activated synapses to increase their sensitivity to efferent (conducting outward) signals, thus increasing the probability of occurrence for the recent responses that preceded the reinforcement. These responses are, statistically, the most likely to have been the behavior responsible for successfully achieving reinforcement.
To further address your concern about failure to detect reduced D2/D3 receptor availability in GD, see Yau et al's 2015 paper Gambling Disorder and Other Behavioral Addictions: Recognition and Treatment.
The precise role for dopamine in gambling disorder continues to be debated,79 but a model based on studies in rats and humans suggests different roles for D2, D3, and D4 dopamine receptors, with D3 receptors in the substantia nigra correlating with problem-gambling severity and impulsivity, and linked to greater dopamine release in the dorsal striatum... These findings, in conjunction with those showing the induction of gambling urges by drugs promoting and blocking D2-like dopamine receptor activity,88,89 have raised questions regarding the centrality of dopamine to disordered gambling.
Dysregulated serotonin functioning may mediate behavioral inhibition and impulsivity in disordered gambling.8,67,69 Disordered gambling has been associated with reduced levels of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in cerebrospinal fluid.90 Low levels of platelet monoamine oxidase (MAO) activity (considered a peripheral marker of serotonin activity) among males with disordered gambling91,92 has provided additional support for serotonergic dysfunction. Striatal binding of a ligand with high affinity for the serotonin 1B receptor correlated with problem-gambling severity among individuals with disordered gambling.93 These findings are consistent with those from challenge studies using meta-chlorophenylpiperazine (m-CPP), a partial agonist with high affinity for the serotonin 1B receptor.
Relatively decreased ventral striatal activation has been reported in disordered gamblers during monetary reward anticipation99,100 and simulated gambling.101 In gambling cue-exposure tasks, disordered gamblers exhibited decreased activation in the ventral113 and dorsal114 striatum compared to healthy controls. Moreover, both ventral striatal and vmPFC activity was inversely correlated with problem-gambling severity in problem-gambling subjects during simulated gambling.101... Unlike findings from patients with SUDs,116 studies involving small samples of disordered gamblers did not display significant volumetric differences in white or gray matter from controls
In summary dopaminergic basis for GD is still not settled, while there're many other possible causes or correlations such as above mentioned reduced levels of the serotonin metabolite, low levels of platelet monoamine oxidase (MAO) activity, decreased ventral striatal activation and vmPFC activity, etc. I believe decreased vmPFC activity is very likely related which includes the orbital frontal cortex (OFC) encoding affective "liking" values of different sensory stimuli. Unlike other more basic level behavioral disorders and SUD, normal gambling obviously involves many advanced executive cognitive functions such as detailed complex planning, rational reasoning of both reward and loss, sustained attentional control and connection with various other types of high-level information. If vmPFC activity is inhibited or decreased, then the subcortical mesolimbic dopamine pathway mainly responsible for the "wanting" incentive salience component of gambling can easily dominate an individual and thus cause addiction by the "wanting" even without abnormal dopamine downregulation or reduction of D2/D3 receptors.
Reference:
Ms. Yvonne H. C. Yau, MSc and Dr. Marc N. Potenza, MD, PhD, "Gambling Disorder and Other Behavioral Addictions: Recognition and Treatment", Harv Rev Psychiatry. 2015 Mar-Apr; 23(2): 134–146.
doi: 10.1097/HRP.0000000000000051.
