What motivates a neuron connection looking for behavior
Brain reward system
(brain reward system) consists of branched neuron connections that influence behavior in the sense of a reward and thereby generate states of euphoria, joy, well-being but also motivation. The ventral tegmental area, N. accumbens, frontal cortex, amygdala and the mesolimbic dopaminergic system are involved. Furthermore, systems play a role that use opiates, GABA, and serotonin as transmitters and that interact with the ventral tegmental area and the basal forebrain. The importance of the mesolimbic dopaminergic system for the brain reward system is best studied. The striatum with the Basal ganglia-thalamocortical control circuit receives input from all areas of the cerebral cortex. The striatum in the basal ganglia-thalamocortical loop appears to play the key role in balance as in procedural learning (important role in habit formation and the formation and performance of routine behavior) The projection of the neurons in the striatum is from nigrostriatal dopaminergic input and intrastriatal cholinergic input. dynamically modulated. The brain reward system also plays an essential role in the addiction potential to nicotine, cocaine, heroin and amphetamine, these substances stimulate the brain reward system. The dopamine level rises in the presence of cocaine and amphetamines, but also with other monoamines such as serotonin and noradrenaline; Nicotine works in a similar way. These substances block the reuptake of dopamine. The dopaminergic neurons monitor the general occurrence as well as the timing of a reward. Some researchers assume that changes in the brain reward system also play a role in depression. Depending on the severity of the depression, people seem to respond particularly strongly to the rewarding effect of amphetamines. The dopaminergic reward system is an evolutionarily old system that is addressed by vital stimuli such as food or sexuality. Dopaminergic stimulation of the ventral striatum, the core area of the brain's own reward system, leads to the increased occurrence of all those behaviors that have caused the dopamine release. Drugs with addiction potential stimulate the release of dopamine and thus increase drug consumption. The reason for this reinforcement of behavior is apparently that stimuli that are paired with drugs or alcohol consumption appear to be particularly desirable due to the accompanying dopamine release and motivate the individual to look for these stimulus constellations. The dopaminergic stimulation apparently motivates targeted actions, to obtain a rewarding substance, and is likely to create cravings for that substance. All of this explains why people with Parkinson's disease and possibly also patients with Restless Legs Syndrome rarely develop L-dopa addiction. High doses of the Parkinson's medication can cause euphoria, and the side effects of the high dose are no longer frightening, as with other addictive substances. Hyperkinesia, megalomania, hypersexuality, deviant behavior, anorexia, hallucinations but also suicides have been reported in this context. Most of the time, the doses are well above the therapeutic range. Spigset O, from Scheele C. Nausieda PA.Â AD Lawrence, et al 2003 Â Possibly these findings can be used for dopaminergic drugs in the treatment of depression. On the other hand, this mechanism can also explain why people with depression have an increased risk of developing nicotine or drug addiction. a) â € œNovelty Seekingâ €Â Â h (Behavior activation) (=> Dopamine system) b) â € œHarm Avoidanceâ € œÂ i (Behavioral inhibition) (=> Serotonin system) c) â € œReward Dependenceâ € (Reward dependency) (=> Norepinephrine system) d) â € œPersistenceâ € (Maintaining behavior) (=> General reward system)
Cloninger's behavioral reward system
a) â € œNovelty Seekingâ €Â Â h
(=> Dopamine system)
b) â € œHarm Avoidanceâ € œÂ i
(=> Serotonin system)
c) â € œReward Dependenceâ €
(=> Norepinephrine system)
d) â € œPersistenceâ €
(=> General reward system)
Sources / literature:
L.K. Tremblay et al. Arch. Gen Psychiatry; 59; 2002; 409 ff, Â Prof. Dr. med. Karl MannDt Ã „rztebl 2001; 98: A 2279â € “2283 [Issue 36].Kitabatake, Y., Hikida, T., Watanabe, D., Pastan, I., Nakanishi, S. (2003). Impairment of reward-related learning by cholinergic cell ablation in the striatum. Proc. Natl. Acad. Sci. UNITED STATES. 100: 7965-7970 [Abstract] [Full Text] Kelley, A. E., Berridge, K. C. (2002). The Neuroscience of Natural Rewards: Relevance to Addictive Drugs. J. Neurosci. 22: 3306-3311 [Full Text] McFarland, K., Kalivas, P.W. (2001). The Circuitry Mediating Cocaine-Induced Reinstatement of Drug-Seeking Behavior. J. Neurosci. 21: 8655-8663 [Abstract] [Full Text] Tang, K.-C., Low, M.J., Grandy, D.K., Lovinger, D.M. (2001). Dopamine-dependent synaptic plasticity in striatum during in vivo development. Proc. Natl. Acad. Sci. UNITED STATES. 98: 1255-1260 [Abstract] [Full Text Jog, M.S., Kubota, Y., Connolly, C.I., Hillegaart, V. & Graybiel, A.M. (1999) Science286, 1745-1749 Kaneko, S., Hikida, T., Watanabe, D., Ichinose, H., Nagatsu, T., Kreitman, RJ, Pastan, I. & Nakanishi, S. (2000) Science 289, 633-637Hikida , T., Kitabatake, Y., Pastan, I., Nakanishi, S. (2003). Acetylcholine enhancement in the nucleus accumbens prevents addictive behaviors of cocaine and morphine. Proc. Natl. Acad. Sci. UNITED STATES. 100: 6169-6173 [Abstract] [Full Text] Â Â Zoli, M., Moretti, M., Zanardi, A., McIntosh, J.M., Clementi, F. & Gotti, C. (2002) J. Neurosci. 22, 8785-8789.
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