DØpÁmıne Autoreceptors are well known to control (reduce) the amount of dopamine being SYNTHESIZED (Produced) AND the amount being released (active) as well as the firing rate (spontaneity and frequency of activity). The general consensus is that sufficient Dopamine is necessary for sexual desire as well as arousal/erection. Dopamine has some anti-sympathetic effects meaning when activating the D2 autoreceptors in particular it also may reduce the amount of active adrenaline in the blood - leading to easier sexual response.
Although in theory, because blocking dopamine autoreceptors causes more dopamine to be released ; this should increase libido and sexual function. Unfortunately, things that look good 'on paper' do not always turn out to be so linear in the real scientific equation...and activating AUTORECEPTORS that REDUCE dopamine actually is what is necessary for erection/arousal and desire.
That does not mean we don't need the dopamine D2L (long allele) receptors or the D1/D5 complex for sexual functioning - we need these as well; but these seem to be involved more in the attentive process and with the vascular system. So therefore the D2's are more to do with libido and fantasies whereas the D1's increase energy metabolism and keep blood pressure under control...
REMEMBER, you WANT to seek the endorphin rush and pleasure associated with sex so therefore if you are already adrenaline fueled or just have a ridiculous flood of dopamine CONSTANTLY then you already fueled with sufficiency...additionally, dopamine D2 receptors decrease beta-endorphin and too much beta-endorphin blocks sexual desire and arousal to an extent. So it all adds up, doesn't it?
THE HARD SCIENCE
**REFERENCES**
The Yawning-penile erection syndrome as a putative model for dopamine autoreceptor activity
Differential behavioral response to dopamine D₂ agonists by sexually naive, sexually active, and sexually inactive male rats.
Dopamine D1 receptor agonists induce penile erections in rats.
Although in theory, because blocking dopamine autoreceptors causes more dopamine to be released ; this should increase libido and sexual function. Unfortunately, things that look good 'on paper' do not always turn out to be so linear in the real scientific equation...and activating AUTORECEPTORS that REDUCE dopamine actually is what is necessary for erection/arousal and desire.
That does not mean we don't need the dopamine D2L (long allele) receptors or the D1/D5 complex for sexual functioning - we need these as well; but these seem to be involved more in the attentive process and with the vascular system. So therefore the D2's are more to do with libido and fantasies whereas the D1's increase energy metabolism and keep blood pressure under control...
REMEMBER, you WANT to seek the endorphin rush and pleasure associated with sex so therefore if you are already adrenaline fueled or just have a ridiculous flood of dopamine CONSTANTLY then you already fueled with sufficiency...additionally, dopamine D2 receptors decrease beta-endorphin and too much beta-endorphin blocks sexual desire and arousal to an extent. So it all adds up, doesn't it?
THE HARD SCIENCE
- Dopamine D2-autoreceptors decrease cyclic AMP (cAMP) which leads to reduction in net sympathetic nervous system activity and alters the rate of calcium ion flow.
- Dopamine synthesis decreases because cAMP is a messenger recruited to form the dopamine production enzyme; tyrosine hydroxylase.
- However, dopamine enhances or provides sexual desire by a pathway involving oxytocin and neuronal nitric oxide synthase...which also both interact with N-type calcium channels (but not L-TYPE)
**REFERENCES**
The Yawning-penile erection syndrome as a putative model for dopamine autoreceptor activity
Differential behavioral response to dopamine D₂ agonists by sexually naive, sexually active, and sexually inactive male rats.
Dopamine D1 receptor agonists induce penile erections in rats.
No comments:
Post a Comment