In a
study that evaluated two rodent models of OCD, a disruption of the dopaminergic
system, more specifically a decrease in the dopamine signaling mediated by
dopamine neurons reflected and supported the theory that OCD affects
dopaminergic systems. In this experiment, investigators repeated injection of
dopamine D2 agonist quinpirole and injection of the tricyclic antidepressant
agent clomipramine in combination with a behavioral paradigm designed to
produce compulsive lever pressing. The results
were then compared with their relative impact on the state of activity of the
mesolimbic dopaminergic system in the ventral tegmental area. The clomipramine
model did not caused an increase in compulsive level pressing. In contrast,
quinpirole treated animals did in fact showed significant increases in
compulsive level pressing. Therefore, it was concluded that VTA dopamine
activity correlated with the behavioral responses in these models and confirmed
other experiments that concluded that the disorder impacted the dopaminergic
system.
Obsessive compulsive disorder is a multifactorial condition that, as
demonstrated in twin studies, it’s related to polygenetic and environmental
factors. It has been observed in neuroimaging studies with patients that have
the condition that the cortico-striato-thalamo- cortical circuit or corticostriatal
system plays a role in OCD. This circuit is part of
one of the feedback loops between the basal ganglia and the motor cortex/
premotor cortex. In OCD, genes affecting the dopaminergic, serotonergic and
glutaminergic systems as well as the interaction within them have been
identified as causes of the disorder. Also, external circumstances like
prenatal events, psychological and neurological trauma may modify the
expression of risk genes and, hence, trigger the manifestation of
obsessive–compulsive behaviors. Since the late 1980s, a rapid growth in the
number of imaging studies of individuals with OCD and improvements in imaging
technology and methods have led to considerable advancement in the understanding
of the neural indicators of OCD pathophysiology. As said earlier, the
corticostriatal system has been the prevailing model regarding the neural and pathophysiological
foundations of OCD. It has been explained that the corticostriatal system performs
an excitatory and inhibitory pathway. In healthy individuals, the excitatory
pathway is modulated by the inhibitory function and based on convergent findings from animal and human
research, the prevailing model postulates that a lower threshold for activation
of this system results in excessive activity in the excitatory pathway over the
inhibitory one. This leads to hyperactivation of the orbitofrontal–subcortical
pathway. As a result, exaggerated concerns about danger, hygiene or harm may
result in persistent conscious attention to the perceived threat (obsessions)
and, subsequently, to compulsions aimed at neutralizing the perceived threat.
The temporary relief that results from performing compulsions leads to
reinforcement and repetitive or ritualistic behavior when obsessions reappear.
Finally, it’s important to mention that some functional imaging studies
have found distinct neural correlates of specific OCD symptom dimensions. In
other words, variations in neuronal systems may be partially different
depending of the kind of symptom that the person has like washing, hoarding and
checking.