TRH protection against memory retrieval deficits is independent of endocrine effects

Abstract An electrobrainshock (EBS)-induced memory retrieval deficit was produced in normal and hypophysectomized mice. In normal mice, thyrotropin-releasing hormone (TRH) (0.1 to 30 mg/kg) protected against this EBS disruption of memory after intraperitoneal but not oral (1.0 to 100 mg/kg) administration. In hypophysectomized mice, TRH (0.3 and 3.0 mg/kg) also protected against the retrieval deficit induced by EBS. The memory protection afforded by TRH was unrelated to its ability to elevate plasma levels of triiodothyronine (T 3 ) and thyroxine (T 4 ), nor was TRH's memory protection mediated through an anticonvulsive mechanism. These results support the notion that TRH may play an important role in memory modulation and may have therapeutic value in certain disease states in humans.