Exogenous growth hormone administration during total sleep deprivation changed the microRNA-9 and dopamine D2 receptor expressions followed by improvement in the hippocampal synaptic potential, spatial cognition, and inflammation in rats.

Rationale: Disorders caused by total sleep deprivation can be modulated by the administration of growth hormone, which could affect the expression of microRNA-9 and dopamine D2 receptor expressions followed by improvement in the hippocampal synaptic potential, spatial cognition, and inflammation in rats.

Objectives: The present study aimed to elucidate the putative effects of exogenous growth hormone (GH) against total sleep deprivation (TSD)-induced learning and memory dysfunctions and possible involved mechanisms.

Methods: To induce TSD, rats were housed in homemade special cages equipped with stainless steel wire conductors to induce general and inconsistent TSD.

Administration of growth hormone ameliorates adverse effects of total sleep deprivation.

Total sleep deprivation (TSD) causes several harmful changes including anxiety, inflammation, and increased expression of extracellular signal-regulated kinase (ERK) and tropomyosin receptor kinase B (TrkB) genes in the hippocampus. The current study was conducted to explain the possible effects of exogenous GH against the above parameters caused by TSD and the possible mechanisms involved. Male Wistar rats were divided into 1) control, 2) TSD and 3) TSD + GH groups.

Therapeutic effects of growth hormone in a rat model of total sleep deprivation: Evaluating behavioral, hormonal, biochemical and electrophysiological parameters.

Objective: Total sleep deprivation (TSD) causes several harmful changes in the brain, including memory impairment, increased stress and depression levels, as well as reduced antioxidant activity. Growth hormone (GH) has been shown to boost antioxidant levels while improving memory and depression. The present study was conducted to explain the possible effects of exogenous GH against behavioral and biochemical disorders caused by TSD and the possible mechanisms involved.