Talk:Cognitive euphoria: Difference between revisions

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==Neurological Analysis==

===Electrodes can reliably induce euphoria when stimulating the nucleus accumbens===

"Recent studies on deep brain stimulation (DBS) of the nucleus accumbens (NA)—a center of the brain well known to mediate reward, pleasure, and addiction—have provided proof of principle evidence that DBS might be able to induce euphoria in a rapid, well-modulated manner, with potentially much higher efficacy than previous neuropsychiatric interventions"

"These examples of euphoria—inducible in a rapid and very titratable fashion by a simple linear increase of DBS voltage—certainly provide an only preliminary empirical basis for further ethical discussion. More studies in larger patient groups are required to confirm these effects and study their nature in more detail. Nevertheless, at least in principle, an effect of euphoria induced by NA DBS seems highly plausible based on the fact that the NA is a critical center for the experience of reward and pleasure: Increases in NA neuron activity and dopamine release are observed during expectations and experience of rewards (Adinoff, 2004; de la Fuente-Fernandez et al. 2002; Doyon et al. 2005; Schultz, 2004), and neuroimaging studies have shown increases in ventral striatal activity associated with euphoric responses to dextroamphetamine (Drevets et al. 2001), cocaine-induced euphoria (Breiter et al. 1997), monetary reward (Cohen et al. 2005; Knutson et al. 2001), pleasurable responses to music (Blood and Zatorre 2001), and viewing attractive faces (Aharon et al. 2001)."<ref>Synofzik, M., Schlaepfer, T. E., & Fins, J. J. (2012). How happy is too happy? Euphoria, neuroethics, and deep brain stimulation of the nucleus accumbens. AJOB Neuroscience, 3(1), 30-36. https://doi.org/10.1080/21507740.2011.635633</ref>

===Enkephalin, Noradrenaline, and Dopamine systems work in tandem to mediate euphoria===

"These results suggest that central grey self-stimulation may depend on the activation of both noradrenaline-containing and enkephalin-containing neurones (sic); indeed, since all of the enkephalin-rich self-stimulation sites referred to above are also rich in catecholamines(17), it is possible that the reward process may generally be regulated by the interaction of noradrenaline, dopamine, and enkephalin systems. Studies on intravenous self-administration of opiate drugs similarly suggest that catecholamine mechanisms are involved in opiate reinforcement(19,20)."<ref>Belluzzi, J. D., & Stein, L. (1977). Enkephalin may mediate euphoria and drive-reduction reward. Nature, 266(5602), 556. https://doi.org/10.1038/266556a0</ref>

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"Amphetamine and ketamine produced euphoria and emotional distress, predominantly tension or anxiety. However, the amphetamine euphoria was associated with psychomotor activation and hostility, whereas that of ketamine was associated with sedation. This distinction may be relevant to the behavioral effects of alcohol, where dopamine may contribute to the stimulant-related “high” associated with the ascending blood alcohol levels, and blockade of NMDA receptors may contribute to the sedative effects associated with high levels of alcohol consumption and descending blood alcohol levels.46,47 In summary, the present data suggest that despite some overlap, ketamine and amphetamine produce distinct profiles of cognitive and behavioral effects."<ref>Krystal, J. H., Perry, E. B., Gueorguieva, R., Belger, A., Madonick, S. H., Abi-Dargham, A., ... & D’Souza, D. C. (2005). Comparative and interactive human psychopharmacologic effects of ketamine and amphetamine: implications for glutamatergic and dopaminergic model psychoses and cognitive function. Archives of general psychiatry, 62(9), 985-995. https://doi.org/10.1001/archpsyc.62.9.985</ref>

===Acute ethanol administration correlates euphoria with alpha band brainwaves===

"Alpha power was significantly increased by high dose ethanol at 15, 30 and 45 min after drinking while the low dose ethanol did not alter alpha power. Alpha power declined to control levels by 45 min after subjects had finished consuming high-dose ethanol. The incidence of euphoria episodes paralleled this bimodal change in alpha power (y=0.49x+5.61; r~=0.89) and was highly correlated

(r=0.95). Only a single short episode of euphoria was reported by one subject who had received low dose ethanol. While the absolute plasma ethanol levels after both doses were not significantly different up to 45 min after drinking began, the slopes were significantly different during the 25-50 min period when the greatest incidence of reported euphoria occurred. The slopes and 95% confidence intervals for high dose- and low dose-induced plasma ethanol curves were 0.599 (0.432-0.767) and 0.153 (0.091-0.214) mg/dl/min"

"Previous studies have demonstrated that ethanol produces increased alpha activity and a slowing of the alpha frequency [9, 10, 13]."<ref>Lukas, S. E., Mendelson, J. H., Benedikt, R. A., & Jones, B. (1986). EEG alpha activity increases during transient episodes of ethanol-induced euphoria. Pharmacology Biochemistry and Behavior, 25(4), 889-895. https://doi.org/10.1016/0091-3057(86)90403-X</ref>

===Neuropathological implications of depression in reward-based behaviors===

@@ Line 1: / Line 1: @@
 ==Neurological Analysis==
+===Electrodes can reliably induce euphoria when stimulating the nucleus accumbens===
+"Recent studies on deep brain stimulation (DBS) of the nucleus accumbens (NA)—a center of the brain well known to mediate reward, pleasure, and addiction—have provided proof of principle evidence that DBS might be able to induce euphoria in a rapid, well-modulated manner, with potentially much higher efficacy than previous neuropsychiatric interventions"
+"These examples of euphoria—inducible in a rapid and very titratable fashion by a simple linear increase of DBS voltage—certainly provide an only preliminary empirical basis for further ethical discussion. More studies in larger patient groups are required to confirm these effects and study their nature in more detail. Nevertheless, at least in principle, an effect of euphoria induced by NA DBS seems highly plausible based on the fact that the NA is a critical center for the experience of reward and pleasure: Increases in NA neuron activity and dopamine release are observed during expectations and experience of rewards (Adinoff, 2004; de la Fuente-Fernandez et al. 2002; Doyon et al. 2005; Schultz, 2004), and neuroimaging studies have shown increases in ventral striatal activity associated with euphoric responses to dextroamphetamine (Drevets et al. 2001), cocaine-induced euphoria (Breiter et al. 1997), monetary reward (Cohen et al. 2005; Knutson et al. 2001), pleasurable responses to music (Blood and Zatorre 2001), and viewing attractive faces (Aharon et al. 2001)."<ref>Synofzik, M., Schlaepfer, T. E., & Fins, J. J. (2012). How happy is too happy? Euphoria, neuroethics, and deep brain stimulation of the nucleus accumbens. AJOB Neuroscience, 3(1), 30-36. https://doi.org/10.1080/21507740.2011.635633</ref>
 ===Enkephalin, Noradrenaline, and Dopamine systems work in tandem to mediate euphoria===
 "These results suggest that central grey self-stimulation may depend on the activation of both noradrenaline-containing and enkephalin-containing neurones (sic); indeed, since all of the enkephalin-rich self-stimulation sites referred to above are also rich in catecholamines(17), it is possible that the reward process may generally be regulated by the interaction of noradrenaline, dopamine, and enkephalin systems. Studies on intravenous self-administration of opiate drugs similarly suggest that catecholamine mechanisms are involved in opiate reinforcement(19,20)."<ref>Belluzzi, J. D., & Stein, L. (1977). Enkephalin may mediate euphoria and drive-reduction reward. Nature, 266(5602), 556. https://doi.org/10.1038/266556a0</ref>
@@ Line 11: / Line 16: @@
 "Amphetamine and ketamine produced euphoria and emotional distress, predominantly tension or anxiety. However, the amphetamine euphoria was associated with psychomotor activation and hostility, whereas that of ketamine was associated with sedation. This distinction may be relevant to the behavioral effects of alcohol, where dopamine may contribute to the stimulant-related “high” associated with the ascending blood alcohol levels, and blockade of NMDA receptors may contribute to the sedative effects associated with high levels of alcohol consumption and descending blood alcohol levels.46,47 In summary, the present data suggest that despite some overlap, ketamine and amphetamine produce distinct profiles of cognitive and behavioral effects."<ref>Krystal, J. H., Perry, E. B., Gueorguieva, R., Belger, A., Madonick, S. H., Abi-Dargham, A., ... & D’Souza, D. C. (2005). Comparative and interactive human psychopharmacologic effects of ketamine and amphetamine: implications for glutamatergic and dopaminergic model psychoses and cognitive function. Archives of general psychiatry, 62(9), 985-995. https://doi.org/10.1001/archpsyc.62.9.985</ref>
+===Acute ethanol administration correlates euphoria with alpha band brainwaves===
+"Alpha power was significantly increased by high dose ethanol at 15, 30 and 45 min after drinking while the low dose ethanol did not alter alpha power. Alpha power declined to control levels by 45 min after subjects had finished consuming high-dose ethanol. The incidence of euphoria episodes paralleled this bimodal change in alpha power (y=0.49x+5.61; r~=0.89) and was highly correlated
+(r=0.95). Only a single short episode of euphoria was reported by one subject who had received low dose ethanol. While the absolute plasma ethanol levels after both doses were not significantly different up to 45 min after drinking began, the slopes were significantly different during the 25-50 min period when the greatest incidence of reported euphoria occurred. The slopes and 95% confidence intervals for high dose- and low dose-induced plasma ethanol curves were 0.599 (0.432-0.767) and 0.153 (0.091-0.214) mg/dl/min"
+"Previous studies have demonstrated that ethanol produces increased alpha activity and a slowing of the alpha frequency [9, 10, 13]."<ref>Lukas, S. E., Mendelson, J. H., Benedikt, R. A., & Jones, B. (1986). EEG alpha activity increases during transient episodes of ethanol-induced euphoria. Pharmacology Biochemistry and Behavior, 25(4), 889-895. https://doi.org/10.1016/0091-3057(86)90403-X</ref>
 ===Neuropathological implications of depression in reward-based behaviors===