Acute and Long-Term Suppression of Stress-Induced ACTH Secretion by a Rat Monoclonal Antibody to Corticotropin Releasing Factor

Abstract

Stress-induced secretion of ACTH from the anterior pituitary appears to be under the control of several humoral and neural factors, including corticotropin releasing factor (CRF), vasopressin, oxytocin and angiotensin II (1,2). Our present knowledge of the physiological role of CRF in the control of pituitary and other functions is largely based on passive immunization studies with antibodies directed against CRF. The passive immunization approach is based on the generally accepted, but poorly evaluated, idea of competition of receptors and antibodies for the same peptide. Dependent on the antibody’s affinity, local concentration and recognition site complexes appear to be formed, preventing the peptide from stimulating its receptor and, thereby, blocking its biological effects. The use of heterologous polyclonal antibodies is hampered by batch-to-batch variation in affinity and specificity. To overcome these drawbacks and to avoid induction of immune responses in long-term studies, we produced a rat monoclonal antibody (MoAb) directed to rat/human-CRF(rCRF).