It has been suggested that
cholecystokinin (CCK), a gut-brain
peptide found in high concentrations in the mammalian brain, might be implicated in the neurobiology of anxiety and
panic disorder. The administration of CCK tetrapeptide induced
panic attacks analogous to spontaneous ones in patients suffering from
panic disorder and to a lesser degree in healthy volunteers. In animal models of anxiety, the pretreatment with CCK agonists and antagonists produced, respectively, anxiogenic- and
anxiolytic-like action on the exploratory paradigms. On the other hand, CCK could also play a role in the pathophysiology of
schizophrenia. The administration of CCK agonists (caerulein, CCK-8s) to rodents results in behavioural effects analogous to those of
antipsychotic drugs. However, CCK agonists lack any activity in rodent behavioural models to reveal
antipsychotic drugs. A significant reduction of CCK concentration and
CCK receptors has been shown in cortical and limbic structures of patients suffering from
schizophrenia. Nevertheless, administration of CCK agonists to these patients does not effect their symptoms. Two major conclusions should be drawn: first, CCK is involved in the neurobiology of anxiety; second, changes in the CCK system in
schizophrenia could be linked to a cortical neurodegeneration related to this disease.