Post-traumatic stress disorder (PTSD) is a debilitating psychiatric condition with
a wide range of behavioral disturbances and serious consequences for both patient
and society. One of the main reasons for unsuccessful therapies is insufficient knowledge
about its underlying pathomechanism. In the search for centrally signaling molecules
that might be relevant to the development of PTSD we focus here on arginine vasopressin
(AVP). So far AVP has not been strongly implicated in PTSD, but different lines of
evidence suggest a possible impact of its signaling in all clusters of PTSD symptomatology.
More specifically, in laboratory rodents, AVP agonists affect behavior in a PTSD-like
manner, while significant reduction of AVP signaling in the brain e.g. in AVP-deficient
Brattleboro rats, ameliorated defined behavioral parameters that can be linked to
PTSD symptoms. Different animal models of PTSD also show alterations in the AVP signaling
in distinct brain areas. However, pharmacological treatment targeting central AVP
receptors via systemic routes is hampered by possible side effects that are linked
to the peripheral action of AVP as a hormone. Indeed, the V1a receptor, the most common
receptor subtype in the brain, is implicated in vasoconstriction. Thus, systemic treatment
with V1a receptor antagonists would be implicated in hypotonia. This implies that
novel treatment concepts are needed to target AVP receptors not only at brain level
but also in distinct brain areas, to offer alternative treatments for PTSD.
