Sex steroids are neuromodulators that play a crucial role in learning, memory, and synaptic plasticity, providing circuit flexibility and dynamic functional connectivity in mammals. Previous studies indicate that testosterone is crucial for neuronal functions and required further investigation on various frontiers. However, it is surprising to note that studies on testosterone-induced NT-4 expression and its influence on synaptic plasticity and learning and memory moderation are scanty. The present study is focused on analyzing the localized influence of neurotrophin-4 (NT4) on hippocampal synaptic plasticity and associated moderation in learning and memory under testosterone deprivation. Adult Wistar albino rats were randomly divided into various groups, control (Cont), orchidectomy (ORX), orchidectomy + testosterone supplementation (ORX+T) and control + testosterone (Cont+T). After two weeks, the serum testosterone level was undetectable in ORX rats. The behavioural assessment showed a decline in the learning ability of ORX rats with increased working and reference memory errors in the behavioural assessment in the 8-arm radial maze. The mRNA and protein expressions of NT-4 and androgen receptors were significantly reduced in the ORX group. In addition, there was a decrease in the number of neuronal dendrites in Golgi-Cox staining. These changes were not seen in ORX+T rats with improved learning behaviour. Indicating that testosterone exerts its protective effect on hippocampal synaptic plasticity through androgen receptor-dependent neurotrophin-4 regulation in learning and memory upgrade.
The thorny protrusions or spines increase the neuronal surface area, facilitate synaptic interconnections among neurons, and play an essential role in the hippocampus. Increasing evidence suggests that testosterone, the gonadal hormone plays an important role in neurogenesis and synaptic plasticity. The role of testosterone on microtubule-associated proteins on dendritic neurite stability in the hippocampus and its impact on learning disability not elucidated. Adult male Wistar albino rats were randomly selected for the control, castrated, castrated + testosterone, and control + testosterone groups. Bilateral orchidectomy was done, and the testosterone propionate was administered during the entire trial period, i.e., 14d. The learning assessments were done using working/reference memory versions of the 8-arm radial maze and hippocampal tissues processed for histological and protein expressions. There were reduced expressions of microtubule-associated protein2 (MAP2), postsynaptic density protein 95 (PSD95), and androgen receptor (AR) and increased expression of pTau in the castrated group. Conversely, the expression of MAP2, PSD95 and AR were increased, and the pTau expression was reduced in the hippocampus of the castrated rat administrated with testosterone. Androgen-depleted rat showed impaired synaptic plasticity in hippocampus associated with contracted microtubule dynamics. Accompanying learning disability, with an increased number of reference memory errors (RME) and working memory errors (WME) in castrated rats. Observations suggest that androgen regulates expression of neural tissue-specific MAPs and play a vital role in hippocampus synaptic plasticity, and a similar mechanism may underlie neurological disorders in aging and hypogonadal men
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