MD Bodybuilding
Well-known member
Member
- Joined
- Aug 6, 2021
- Messages
- 517
- Points
- 28
Nandrolone belongs to the anabolic androgenic steroid (AAS) class II, which is made up of 19-nor-testosterone-derivates. AAS is a large and fast expanding class of synthetic androgens used both therapeutically and illegally. AAS in general, and nandrolone decanoate (ND) in particular, have been linked to a number of behavioral issues. The goal of this review is to describe the research on ND exposure investigations on animal models, mostly rats that mirror human misuse systems (i.e. supraphysiological doses). We focused on studies that looked at how ND affects the function and expression of neural signaling molecules, which underpin behavior, anxiety, aggressiveness, learning and memory, reproductive activities, locomotion, and reward.
Stress, Anxiety, and Fear
Nandrolone has been linked to anxiogenic and anxiolytic effects. Chronic administration with large doses of ND, according to Kouvelas et colleagues, promotes anxiolytic-type behavior, reduced social memory, potential spatial learning, and recall performance through activation of the central androgenic receptors (ARs), although information acquisition remains unaffected. Anxiety reduction was reversed in rats given ND (15 mg/kg subcutaneously) plus flutamide (FL), an AR antagonist. In contrast, when FL was given to the hippocampus in a previous investigation, enhanced anxiety-like behavior was seen, probably as a consequence of interaction between the medication and targets other than ARs. Interaction of ND and FL with ARs in brain areas such as the hypothalamus, basal ganglia, amygdala, septum, hippocampus, motor nuclei in the brain stem, cerebellum, spinal cord, and cerebral cortex is known to contribute to anxiety-related behavior by interfering with serotonergic, glutamatergic, and dopaminergic pathways, which may lead to anxiety reduction and memory impairment.
Minkin et al., on the other hand, discovered that after ND administration (10 or 50 mg/week for 8 weeks), Long-Evans rats (gonadally intact or gonadectomized) spent more time in the open-field edges (i.e. thigmotaxis), indicating an elevated degree of anxiety. Minkin and Meyer observed similar findings because anxiogenic responses were elicited in rats treated with ND during the open field test.
Nandrolone increases synaptic currents mediated by the GABAA receptor in the hypothalamic ventromedial nucleus but decreases them in the preoptic region. These effects are determined by the GABAA receptor's subunit makeup. Blockade and augmentation of GABAA-mediated currents in the dorsomedial hypothalamus are linked with anxiogenic and anxiolytic responses, respectively [48, 49].
Stress, Anxiety, and Fear
Nandrolone has been linked to anxiogenic and anxiolytic effects. Chronic administration with large doses of ND, according to Kouvelas et colleagues, promotes anxiolytic-type behavior, reduced social memory, potential spatial learning, and recall performance through activation of the central androgenic receptors (ARs), although information acquisition remains unaffected. Anxiety reduction was reversed in rats given ND (15 mg/kg subcutaneously) plus flutamide (FL), an AR antagonist. In contrast, when FL was given to the hippocampus in a previous investigation, enhanced anxiety-like behavior was seen, probably as a consequence of interaction between the medication and targets other than ARs. Interaction of ND and FL with ARs in brain areas such as the hypothalamus, basal ganglia, amygdala, septum, hippocampus, motor nuclei in the brain stem, cerebellum, spinal cord, and cerebral cortex is known to contribute to anxiety-related behavior by interfering with serotonergic, glutamatergic, and dopaminergic pathways, which may lead to anxiety reduction and memory impairment.
Minkin et al., on the other hand, discovered that after ND administration (10 or 50 mg/week for 8 weeks), Long-Evans rats (gonadally intact or gonadectomized) spent more time in the open-field edges (i.e. thigmotaxis), indicating an elevated degree of anxiety. Minkin and Meyer observed similar findings because anxiogenic responses were elicited in rats treated with ND during the open field test.
Nandrolone increases synaptic currents mediated by the GABAA receptor in the hypothalamic ventromedial nucleus but decreases them in the preoptic region. These effects are determined by the GABAA receptor's subunit makeup. Blockade and augmentation of GABAA-mediated currents in the dorsomedial hypothalamus are linked with anxiogenic and anxiolytic responses, respectively [48, 49].
