- Joined
- Mar 18, 2012
- Messages
- 2,759
Something I happened upon this morning of interest:
Effects of AAS on reward pathways:
Dopamine is the main transmitter in the mesolimbic pathway, also known as the reward pathway, and numerous animal studies have shown that AAS affect the dopamine system in the brain. Long-term administration of nandrolone increased dopamine transporter density in the rat caudate putamen.. (Kindlundh et al., 2002; Kindlundh et al., 2004).
In addition, the density of dopamine receptors was affected by AAS administration; D1 receptors were down-regulated in the striatum and nucleus accumbens, and D2 receptors were down-regulated in the nucleus accumbens, but up regulated in the caudate putamen (Kindlundh et al., 2001).
In a recent study, nandrolone administration decreased the expression of the D1 dopamine receptor in the nucleus accumbens of adult mice (Martinez-Rivera et al., 2015). Furthermore, studies have reported decreased activity of the dopamine-metabolizing enzymes monoamine oxidase A and B and a decrease in the levels of the dopamine metabolites 3,4-dihydroxyphenylacetic acid and homovanillic acid after repeated nandrolone administration (Birgner et al., 2007; Birgner et al., 2008).
Another signalling system highly associated with reward and dopamine signalling is the endogenous Opioid system (Herz, 1997; Spanagel et al., 1992).
Several studies have reported AAS-induced changes in the levels of opioid peptides and their receptors in the CNS (for review (Nyberg and Hallberg, 2012)). For example, administration of nandrolone for two weeks in male rats has been shown to affect endogenous opioid peptides in the caudate putamen, nucleus accumbens, and periaqueductal grey (Johansson et al., 2000).
Increased gene expression of PDYN, encoding the opioid peptide precursor prodynorphin, was found in the hippocampus of male rats after two weeks of nandrolone administration (Magnusson et al., 2009a).
In addition to dopamine and opioids, the neurotransmitter Serotonin plays an important role in the context of reward (Kranz et al., 2010), and AAS administration induces alterations in the
serotonergic system (Ambar and Chiavegatto, 2009; de Souza Silva et al., 2009; Rainer et al.,
2014). For example, long-term and irreversible effects on the serotonergic system following AAS administration in hamsters have been reported (Grimes and Melloni, 2006).
A recent study demonstrated that chronic administration (4 weeks, 5 mg/kg) of nandrolone caused a decrease in dopamine, serotonin, and noradrenaline concentrations in the nucleus accumbens (Zotti et al., 2014). From the studies described in this section, it is clear that AAS has significant effects on monoaminergic activity in brain regions associated with reward.
Effects of AAS on other signaling systems in the brain, for example the Glutamatergic, and various neuropeptidergic systems, have also been demonstrated (Hallberg, 2011; Le Greves et al., 1997; Rossbach et al., 2007).
Glutamate is known to bind with high affinity to N-methyl-D aspartate (NMDA) receptors, which are important for neuronal plasticity, including learning and memory. A study examining the effects of two week administration of nandrolone on the NMDA receptor subunits found a decrease in the mRNA expression of GluN2A and GluN2B in certain brain regions. The expression of GluN2B subunits was attenuated by steroid treatment in the hypothalamus, whereas GluN1 subunit expression was decreased in the nucleus accumbens (Le Greves et al., 1997). In addition, even a single injection of nandrolone was shown to affect NMDA receptor subunit expression in the rat hippocampus (Rossbach et al., 2010; Rossbach et al., 2007).
To summarize, although AAS do not induce acute rewarding affects at the same magnitude as
other drugs of abuse, animal studies provide evidence that AAS have rewarding properties and affect the reward pathways in the brain. Several studies also suggest that non-genomic actions of AAS could play an important role in mediating these effects?
Effects of AAS on reward pathways:
Dopamine is the main transmitter in the mesolimbic pathway, also known as the reward pathway, and numerous animal studies have shown that AAS affect the dopamine system in the brain. Long-term administration of nandrolone increased dopamine transporter density in the rat caudate putamen.. (Kindlundh et al., 2002; Kindlundh et al., 2004).
In addition, the density of dopamine receptors was affected by AAS administration; D1 receptors were down-regulated in the striatum and nucleus accumbens, and D2 receptors were down-regulated in the nucleus accumbens, but up regulated in the caudate putamen (Kindlundh et al., 2001).
In a recent study, nandrolone administration decreased the expression of the D1 dopamine receptor in the nucleus accumbens of adult mice (Martinez-Rivera et al., 2015). Furthermore, studies have reported decreased activity of the dopamine-metabolizing enzymes monoamine oxidase A and B and a decrease in the levels of the dopamine metabolites 3,4-dihydroxyphenylacetic acid and homovanillic acid after repeated nandrolone administration (Birgner et al., 2007; Birgner et al., 2008).
Another signalling system highly associated with reward and dopamine signalling is the endogenous Opioid system (Herz, 1997; Spanagel et al., 1992).
Several studies have reported AAS-induced changes in the levels of opioid peptides and their receptors in the CNS (for review (Nyberg and Hallberg, 2012)). For example, administration of nandrolone for two weeks in male rats has been shown to affect endogenous opioid peptides in the caudate putamen, nucleus accumbens, and periaqueductal grey (Johansson et al., 2000).
Increased gene expression of PDYN, encoding the opioid peptide precursor prodynorphin, was found in the hippocampus of male rats after two weeks of nandrolone administration (Magnusson et al., 2009a).
In addition to dopamine and opioids, the neurotransmitter Serotonin plays an important role in the context of reward (Kranz et al., 2010), and AAS administration induces alterations in the
serotonergic system (Ambar and Chiavegatto, 2009; de Souza Silva et al., 2009; Rainer et al.,
2014). For example, long-term and irreversible effects on the serotonergic system following AAS administration in hamsters have been reported (Grimes and Melloni, 2006).
A recent study demonstrated that chronic administration (4 weeks, 5 mg/kg) of nandrolone caused a decrease in dopamine, serotonin, and noradrenaline concentrations in the nucleus accumbens (Zotti et al., 2014). From the studies described in this section, it is clear that AAS has significant effects on monoaminergic activity in brain regions associated with reward.
Effects of AAS on other signaling systems in the brain, for example the Glutamatergic, and various neuropeptidergic systems, have also been demonstrated (Hallberg, 2011; Le Greves et al., 1997; Rossbach et al., 2007).
Glutamate is known to bind with high affinity to N-methyl-D aspartate (NMDA) receptors, which are important for neuronal plasticity, including learning and memory. A study examining the effects of two week administration of nandrolone on the NMDA receptor subunits found a decrease in the mRNA expression of GluN2A and GluN2B in certain brain regions. The expression of GluN2B subunits was attenuated by steroid treatment in the hypothalamus, whereas GluN1 subunit expression was decreased in the nucleus accumbens (Le Greves et al., 1997). In addition, even a single injection of nandrolone was shown to affect NMDA receptor subunit expression in the rat hippocampus (Rossbach et al., 2010; Rossbach et al., 2007).
To summarize, although AAS do not induce acute rewarding affects at the same magnitude as
other drugs of abuse, animal studies provide evidence that AAS have rewarding properties and affect the reward pathways in the brain. Several studies also suggest that non-genomic actions of AAS could play an important role in mediating these effects?
