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Adult onset-hypothyroidism increases response latency and long-term potentiation (LTP) in rat hippocampus
Citation:
Sanchez-Huerta, K., J. Pacheco-Rosado, AND M. E. GILBERT. Adult onset-hypothyroidism increases response latency and long-term potentiation (LTP) in rat hippocampus. Presented at Society of Toxicology (SOT) Annual Meeting, San Francisco, CA, March 11 - 15, 2012.
Impact/Purpose:
The present study was designed to assess the effects of adult onset TH deficiency on hippocampal physiology and learning.
Description:
Thyroid hormones (TH) influence central nervous system (CNS) function during both development and in adulthood. The hippocampus is critical for some types of learning and memory and is particularly sensitive to thyroid hormone deficiency. Hypothyroidism in adulthood has been associated with cognitive decline, and both morphological and biochemical alterations have been reported in hippocampus following TH deficiency. The impact of the TH deficiency on the hippocampal synaptic function has not been well studied -reports are limited and results inconsistent across laboratories. The present study was designed to assess the effects of adult onset TH deficiency on hippocampal physiology and learning. Adult male rats (PN60-80) were exposed to propylthiouracil (PTU: 0 or 10 ppm), through the drinking water for 1 month to reduce serum TH. Body weight gain was reduced and thyroid gland weight increased by PTU. Learning was assessed using a trace fear conditioning paradigm. Field potentials were recorded in the dentate gyrus under urethane anesthesia. In contrast to TH insufficiency induced during development, trace fear conditioning, amplitudes of excitatory synaptic potentials, and magnitude of inhibitory transmission were not significantly altered by PTU. However, response latencies were increased in hypothyroid animals. LTP of the excitatory postsynaptic potential was slightly increased whereas no effect was observed in LTP of the population spike. The data indicate that only modest changes in hippocampal physiology accompany TH-insufficiencies induced in adulthood. Nongenomic actions of TH or secondary effects of hypothyroidism on temperature regulation may underlie some of these observations. These data are in partial agreement with previous published reports and indicate that in contrast to developmental exposure, hippocampal dysfunction is mild in response adult onset hypothyroidism. (Does not reflect EPA policy)