Have you had your DHT checked, or are you going by how you feel. It's no mystery that DHT and dopamine are the driving force in libido for males. But as with all things, it's a lot more complicated than any one variable.
When you start on exogenous testosterone, a whole lot of changes are happening in your body and your brain. Changes to the CNS, neurotransmitter balance, HPTA axis and hormonal balance. All of these have an effect, good or bad, on libido.
Dopamine and testosterone are interrelated and have a very strong effect on each other:
While testosterone is often thought of for male libido, the nervous system has a crucial role as well. In fact, three major nervous system messengers (neurotransmitters)—dopamine, glutamate and serotonin—impact male sexual health.
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Nerves and Male Libido
The male libido is complex. It results from a combination of the physical and emotional aspects of the body. To integrate these areas, the body uses hormones and neurotransmitters. Steroid hormones, such as testosterone, prime the body to respond to sexual cues. They do so, in part, by affecting neurotransmitter function.2 However, the nervous system signals are the fast-acting, “in the moment” actors.2
Dopamine and Testosterone: A Two-Way Path
The relationship between dopamine and testosterone are interrelated. Dopamine can influence testosterone and the converse is true as well. In males, a key area of the brain for sexual function is the medial preoptic area (MPOA).
One study found that microinjecting dopamine agonists (which mimic dopamine function) in the MPOA of rats led to an increase in sexual activity.3 Another study found castrated male rats showed no interest in sex. And, dopamine was not released in the MPOA. After testosterone injections, the castrated rats engaged in sexual intercourse. There was also an increase in dopamine release in the MPOA.4
These studies reveal how critical dopamine is for libido. They also highlight testosterone’s role in dopamine release. While the MPOA is important for performance, there are two other brain regions critical for the sexual drive that involves dopamine.
One part of the brain is known for its role in pleasure and reward (VTA). Dopamine is the primary neurotransmitter in this system. Here, the actions of dopamine elicit the desire to engage in sexual activity.2 What dopamine’s activity does for sexual desire, it does in another region of the rat brain to motivate physical activity.2,5
But as stated above, the dopamine-testosterone relationship is not one-sided.
You can hypothesize that by adding exogenous testosterone you are affecting neurotransmitter balance. This can happen from a variety of mechanisms.
Also, once exogenous testosterone is introduced to the body, you cease to produce LH. Luteinizing Hormone receptors have been identified in the CNS and the brain. They are there for a reason.
This article is part of a Special Issue “SBN 2014”.Hormonal dysfunction due to aging, especially during menopause, plays a substantial role in cogniti…
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Luteinizing hormone: Evidence for direct action in the CNS
Abstract
This article is part of a Special Issue “SBN 2014”.
Hormonal dysfunction due to aging, especially during menopause, plays a substantial role in cognitive decline as well as the progression and development of
neurodegenerative diseases. The hypothalamic–pituitary–gonadal (HPG) axis has long been implicated in changes in
behavior and neuronal morphology. Most notably, estrogens have proven beneficial in the healthy brain through a host of different mechanisms. Recently,
luteinizing hormone (LH) has emerged as a candidate for further investigation for its role in the CNS. The basis of this is that both LH and the LH receptor are expressed in the brain, and serum levels of LH correlate with
cognitive deficits and
Alzheimer's disease (AD) incidence. The study of LH in cognition and AD primarily focuses on evaluating the effects of downregulation of this peptide. This literature has shown that decreasing peripheral LH, through a variety of pharmacological interventions, reduces cognitive deficits in
ovariectomy and AD models. However, few studies have researched the direct actions of LH on neurons and
glial cells. Here we summarize the role of luteinizing hormone in modulating cognition, and we propose a mechanism that underlies a role for brain LH in this process.
Graphical abstract
In the aged female brain estrogen replacement after ovariectomy does not improve cognitive function or associated underlying mechanisms such as dendritic spine density changes. Drugs that reduce peripheral levels of LH, which surge after ovariectomy or during menopause, rescue ovariectomy-dependent cognitive dysfunction, increases signaling events associated with synaptic plasticity. The LH receptor is localized to cognition-associated areas and its functionality is described both at a level of function and plasticity. Brain-derived LH protein levels are present in cognition associated areas and reduced by ovariectomy. These levels are normalized by drugs that reduce peripheral LH levels and this normalization of brain-LH positively correlates with markers of neuroplasticity and cognitive improvement.
