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ECPB 2014, 67(3): 19–24
Experimental physiology and biochemistry

The role of thyroid hormones in the formation of cognitive function in rats

Demchenko Е.
Abstract

Thyroid hormones (TH) have an exceptional role in the formation of cognitive function. In particular, there is enough data on the reduction of the long-term potentiation (LTP) in the hippocampus of rats with hypothyroidism, impairment of attention, learning and memory in the experiment, and in patients with thyroid dysfunction. The violation of thyroid status was accompanied by emotional deficits, mental disorders – from depression to psychosis, and, in general, by reduced intellectual abilities.

But despite the numerous data on the effects of TH on the cognitive function of the brain, the mechanism of their action on the CNS remains unclear. As for this issue, it is known that these hormones directly affect the brain activity through the activation of energy and plastic metabolism by enhancing the cerebral blood flow, glucose uptake, increase in synthesis of enzymes of cellular respiration. In addition, TH indirectly influences the functioning of the central nervous system by modulating neurotransmitter mechanisms, and in the first order – serotoninadrenergic activating system of the brain.

There is no less famous version that the activating effect of TH on the CNS is supported by the increase in the glutamate content in specific brain structures. According to recent reports, the effect of TH on the central nervous system is provided through the regulation of GABA- ergic neurotransmitter system. Equally well-known mechanism of action of TH on cognitive function, accepted nowadays, is participation of hormones in regulation of the activity of NO-synthase (NOS) of the brain. This molecule can act as a possible mediator of synaptic plasticity, LTP and consolidation of LTP. In addition, there is enough known data indicating a link between NMDA- receptors and NO- system in the processes of learning and memory, in particular, in several studies it was shown that NOS inhibitors caused infringement in memory consolidation and blockage of induction of LTP. However, in the literature the opposite data was found. Thus, the reduction in concentration of L-arginine, the precursor of NO, was also accompanied by improvings in memory and changes in the effect of NOS blocking. NO donors reduced LTP and caused synaptic depression. Overall, the given above results allow us to predict the NO participation in learning and memory. Therefore, the study on the role of TH in the implementation of cognitive function through the regulation of nitric oxide system, which was the aim of our research, is relevant and controversial issue.

In this issue, the activity of the hippocampus and spatial memory of animals were proven to be the most studied points. In particular, the experimental hypothyroidism caused infringement of acquired behavior when searching the protective platform in Morris maze that is the hippocampus-dependent learning, by the time spent in the target sector and the duration of the swimming. These changes in the formation of protective behavior were accompanied by the accumulation of NO in the hippocampus. Treatment of rats with L-thyroxine under the hypothyroidism leads to improvement in memory and LTP of the hippocampal CA1 area, and the activity of Ca-calmodulin-dependent NOS.

Study of spatial memory formation process in rats revealed increase of food-getting reactions by 60% in 8-radial maze in conditions of experimental hyperthyroidism and, conversely, decrease of this index by 21% in conditions of experimental hypothyroidism. Improved cognitive function in hyperthyroidism occurred on the base of increased of neuronal NO-synthase activity (by 59.7%, p<0.05) and decreased L-arginine and precursor of NO (17.5%) content in the cortex of experimental animals. Perhaps the formation of spatial memory of young rats is corrected by influence of thyroid hormones by the way of modulation of NO-system of neocortex.

Keywords: thyroid hormones (TH), spatial memory, NO-synthase (NOS), neocortex

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