The 20th Congress of RSCANP,

Băile Felix, 18-21.09.2019

Details on the
20th RSCANP Congress
: news, information, program, registration, fees, abstracts, accommodation, sponsors, contact

The 42st National Conference of Child and Adolescent Neurology and Psychiatry and Allied Professions with international participation


HOW DO WE CREATE NEURAL PATHWAYS BY USING REWARD IN EARLY EDUCATION

Autor: Cristina Petrescu Ghenea Florina Rad Carmen Truţescu Cristina Gianina Anghel Ilinca Mihăilescu Liana Kobylinska Iuliana Dobrescu
Distribuie pe:

In the scientific literature, ever since the beginning of the 20th century, there have been vechiculated a lot of different theories concerning the roles of reward. Understanding and elaborating on this concept may help psychoeducators, mental health practitioners and nevertheless parents develop evidence-based methods to apply in children’s early education. In this article we tried to do a review of the literature about reward using mainly medical search engines. Hyperstimulation with unearned and unnecessary rewards is viewed as the explanation for some of the psychiatric pathology and psychopathy we see rising in adolescents and adults. A future better understanding of areward could be the key in explaining and controlling some challenging behaviors that parents often complain about in their children. Implications of reward process system have also been found in mood disorders or illicit drug use like amphetamines. This review is not intended to adhere to or strictly support one or another theory, but to enumerate and make a brief synopsis of each idea the literature. The years to come, with the new advances in neurosciences and neuroimaging, will lead to more evidence to support the implication of reward in different psychiatric pathologies and to the use of this information in different methods of edication and treatment.

Background

In the educational process, learned from a very early age, without knowing, we educate children using rewards. We all actually run on an already well-known formula:

 

Stimulus – Reaction – Response

 

The novelty and importance of psycho-neuro-biology studies is the discovery that the basis of education, that psycho-educators and therapists talk about that much, giving so many tips and tricks, is building complex mechanisms underlying neuronal circuits. In other words, in the so “simple” education of a child, new parents, doctors or psychologists help build certain neural circuits.

Frequently we hear: “I give you if you do that…” or ” Wait, do not cry, I will make you…”. Basically we “build” the “seven years of home education” through extremely complex forms of subjacent ways that are based on reward.

Through a very carefully developed and only partially known psycho-neuro-biological mechanism, the human brain builds the basis of later observable emotional behaviors. The child is “submissive” or “naughty” is “good and does what you say”, “follows the rules” or “undisciplined and does whatever he wants.”

In this article we present a summary of the data obtained in research laboratories, where scientists have already gone from observing animal behavior to study imaging (PET, SPECT, MRI) of human behavior. We will try to explain as synthetic as possible by reviewing scientific studies in the last decades that a child’s education is not a simple process, but extremely complex, and that actually the implementation of rules and limits must take into account hereditary characteristics – the temperament, but also the environment and the fact that each individual has its own “arousal potential” in the context of which he/she is experiencing maximum pleasure.

It thus remains very current the bio-psycho-social model belonging to the Romanian psychiatrist Petre Branzei  (1970), although in the literature this model is globally attributed to the American psychiatrist Engel (Riga and Riga, 2010).

Each child is “unique” and “unrepeatable” and they even in identical educational conditions they develop their own different mechanisms of reward processing. In psychology this was first treated by the cognitive behavioral theories of Skinner and Albert Elis to Aaron Beck, ending with the most recent and we believe, the most effective application of Paul Stallard with his modern approach to behavioral and cognitive psychological overlapping data and neurobiological theories of “reward processing system” and the brain areas involved.

Tobias Esch and George B. Stefano in 2004 stated that the brain is the most extensively studied neuroscience for finding disease mechanisms, but many more can be studied in relation to brain health. The authors talk about mechanisms implicated in brain health, considering that there are two fundamental forces, namely pleasure and pain. Can the joy or pleasure – they ask – facilitate survival and delay death? The authors begin with the extensive publications on depression and affective disorders but do not describe the possible hidden mechanisms (Esch& Stefano, 2004).

But in neurosciences, there have been identified biological mechanisms mediating behavior and motivated by pleasure, which we will exhibit below.

 

Brief history of the concept of reward

It has been shown that the dopaminergic brain circuitry plays a very important role in organizing both the reward system and motivation. Martin Keitz in 2003 stated that reward or rewarding stimulus, in terms of the evolutionary perspective, can be considered” the driving force of survival for all animal species. “A condition for the survival of vertebrate species is the ability to learn from past experience or, better said, to distinguish between rewarding and non-rewarding stimuli”, “to know which situations should be avoided and which should be addressed” (Martin-Soelch and Leenders , 2001) and JB Pochon et al, 2001. M. Keitz et al, 2003 ( quoted by Blum et al, 2008 ) repeated in recent neuroimaging studies the assumption that underlying the “Reward Processing System in the Brain” are neural changes in the circuits involved in reward.

We review data concerning the history of the concept of reward, the succession describing its various components, as shown in bibliographic information that he had access to. Thorndike in 1913 discussed the combination of pleasure and reward behavior directed toward a goal (“ goal directed “); Skinner in 1938 clarified the concept of “reward” as a positive reward given to a desired behavior; In 1943 C. Hull proposed link between motivation and positive reinforcement and defined the concept of “arousal” as a state of activation that can occur in any body that plays a very important role in the mechanisms of reward (as cited by Keitz et al, 2003); In 1954, Olds and Milner have coined the concept of “reward pathway” and stated that it is a dopaminergic pathway because the laboratory experiments had identified the neural mechanisms responding to positive reinforcement learning and using incentives and intracranial self-stimulation in animals (ICSS); Sem-Jacobsen in 1976 described the existence of “brain stimulation reward in humans”. In 1997 and again in 1999 Rolls Schultz have clarified the concepts of ” pleasurable ” (sense of pleasure, hedonic state of gratification) and some related to “reward” (associating pleasure with purpose) and have resumed talks about “arousal” and “reinforcement”. Pleasure is hard to define, having to deal with a high degree of subjectivity.

Rolls (1999) defined reward as something for which the animal works, and Schultz found that reward has 3 main properties:

 

(1) Reward requires active behavior, prepared or directed toward the goal;

(2) Reward has a high probability of recurrence, that acts as positive reinforcement stimulus initiating the phenomenon of apparent conditioning learning;

(3) Reward causes hedonic subjective feelings in human beings;

  • Also in 1997, Thut et al comunicated the results of psycho-neurobiology studies that identified cerebral pathways and brain areas which become activated to “financial reward” (“monetary reward”) and cortical and cortico-subcortical networks of the dorso-lateral prefrontal cortex and orbitofrontal cortex (DLPFC and OFC); In 2001 Martin-Soelch found differences between types of addiction, namely between smokers and nonsmokers, which activate different areas of the mesolimbic and meso- cortico-limbic brain structures, by this identifying brain reward system (RPS / Brain Reward System) in the limbic system, and in 2002 Martin-Soelch defined reward as the learning and acquisition of adaptive behaviors . (3)

 

Concepts that are part of human behavior as emotions, orientation, arousal, and the reward are again open for exploration in the organization of neuronal circuits due to new methods of investigation used in neuroscience, particularly neuroimaging.

Keitz and Martin-Soelch and Leenders (2001), from the Department of Neurology of the University Hospital Groeningen and the Department of General Cognitive Psychology of the University of Basel, consider that there are four concepts that are related to reward, namely pleasure, orientation, arousal ( high vigilance level ) and reinforcement. (3)

 

Anatomy and physiopathology data involved in reward processing

Dopamine (DA) and noradrenaline (NA) in the process of Reward:

In 1954, Olds and Milner found a direct method to study neural mechanisms using Intracranial Self Stimulation (ICSS). After the electrodes were implanted in different brain regions, the researchers found that animals self stimulate, challenging and pleasure by pressing a tab located in the area of ​​study. In some cases, the animal continues to self stimulate even when they have a state of deprivation showed Aou et al in 1983, continuing Olds and Milner’s study. One of the first observations was that only some regions of the brain respond by creating pleasure after self stimulating pedaling, while in other regions the effect was the opposite and the animal tried to avoid stimulating. The “quiet” ICSS regions were the lateral hypothalamus and the cerebral vicinity in of the medial strip (Olds and Milner, 1954). Subsequent research found other areas involved in ICSS – like frontal cortex (FC), basal ganglia (GB) , septal area, hippocampus and amygdala. Activation of the reward areas was considered “Brain stimulation reward” and regions involved in ICSS were considered sites of reward processing (Rolls et al, 1999). Most sites seem to follow the NA ICSS dorsal strip, from the locus coeruleus to the hippocampus, that then ends the neocortex.

This concept formed the basis of “Noradrenergic hypothesis” which postulated that NA plays an important role in the mediation process in ICSS reward. However, theoretical controversies have emerged. Rolls and his team in 1999 noted that after administration of disulfiram (substance which leads to depletion of NA in the brain) the theoretically expected response does not occur, so in conclusion NA hypothesis is not sufficiently supported.

“Dopaminergic hypothesis” was proposed as an alternative to the noradrenergic one. This hypothesis is supported by at least five research areas: 1. Much of ICSS sites are located in the dopaminergic system; 2. Microdialysis studies show increased release of dopamine (DA) in the region of the projection of the area the ventral tegmental area (VTA), for example in nucleus accumbens; (3). Studies confirm dopaminergic medication because they highlighted the following issues: • DA agonists increase ICSS response rate; • DA antagonists decrease ICSS response rate; • DA receptor blockade with spiroperidol into the nucleus accumbens or the amygdala, hypothalamus decreases self stimulation. Spiroperidol cushions hypothalamic self-stimulation, without lowering arousal; • D-amphetamine injection in the dorsal nucleus accumbens decreases in ICSS threshold VTA (Ranaldi and Beninger, 1994); • Mora et al (1976) have infused apomorphine (agonist) which attenuates self stimulation in the prefrontal cortex (PFC) in rats and in the orbitofrontal cortex (OFC) in monkeys (10). 4. Studies have of brain lesions have shown that: the effective ICSS abolition occurs as a result of increased dopaminergic damage in high-DA density regions (Fibiger et al, 1987); 5. Studies of self-administration of the substances: • Yokel and Wise (1975) have demonstrated that the self-administration of amphetamine is affected by the dopaminergic receptor blockade by pimozide (12); • Pettit and Justice (1989 ) showed that self -administration of cocaine increases DA levels in the nucleus accumbens (13); • DiCyano et al (1995 ) showed that self-administration of D-amphetamine increase DA in the nucleus accumbens • Natural Rewards like sex or food are processed in similar regions involving DA; • Salamone et al (1989, cited by Salamone, 1994) have shown by microdialysis in rats increased DA response to reward – food; •Becker et al (2001) have shown increased dorsal and ventral striatum DA in female rats during sexual activity. Currently are admitted following: • Noradrenergic pathways involved in growth are overall reactive to stimuli of all kinds, – and – • Dopaminergic pathways are involved mainly in increasing responsiveness to specifically rewarding stimuli (Keitz et al, 2003).Studies on primates – come in addition to those stated above. Thus: • Researching the neural organizing of reward processing, Schultz and Romo, 1990 (quoted by Keitz et al 2003) used single cell recordings on Maccachus monkeys linking activation potential amplitude and phases with different stimuli. That showed that DA-ergic neurons are activated by the administration of food and not to visual stimuli. • Apicella et al (1991) investigated the activity of striatal neurons in response to primary reward tasks like “go/no-go tasks” – detecting increased activity in the ventral striatum (17). • Unexpected reward produces “firing” in DA-ergic neurons. The same thing happens when a conditioned stimulus predicts reward. If the reward does not appear, DA-ergic activity falls exactly at the time the stimulus is to appear. Orbitofrontal cortex (OFC) and Medioventral Frontal Cortex (MVFC) is activated only when the reward is given. The conclusion is that the anticipation of reward recruits distinct neuroanatomical mechanisms for consuming and delivering food. The DA is involved in reward, but neural path may differ depending on the purpose of the action (Martin- Soelch, 2001).

 

Human studies

Martin- Soelch and Keitz (3) review reference works published in Brain Research and the Journal of Neuroscience, Clavier ‘s pioneering work, Delgado, Becker, Rolls, Mora, Nakahara from 1970-1980. In 1976, Sem-Jacobsen does the first intracranial stimulation studies in humans. Patients with implanted electrodes in different regions of the brain for therapeutical purposes reported that they felt pleasant or unpleasant odors. PET (Positron Emission Tomography) and fMRI (functional magnetic resonance) led to the possibility of investigating cognitive processes in the brain (Sem – Jacobsen, 1976).

Thut et al, 1997 (quoted Keitz 2003) recorded regional cerebral blood flow (rCBF) related to money reward using PET. Healthy subjects were performing “go/no-go tasks” with 2 different rewards. The authors found activation of cortico- subcortical networks, including the dorsolateral prefrontal cortex regions (DLPFC), orbitofrontal cortex (OFC), thalamus and brainstem (midbrain) in response to material reward. Several things could be concluded using a paradigm similar to that of Thut et al which included 3 different types of rewards: financial/monetary and non-material/non – monetary feedback (Martin-Soelch et al, 2001). Martin-Soelch et al (2001) and Kuenig, 2000 (quoted by Keitz 2003) concludes that different subjects use different circuits. In the addiction to opiates, mesolimbic regions and mesocorticolimbic regions that in healthy subjects respond to material and non-material rewards, responded only to material incentives (monetary feedback).

In those addictive smokers the striatum is activated, but this could not be found in all smokers. Stein et al, 1998 (quoted Keitz et al, 2003) show that iv administration of nicotine increases neuronal activity in the nucleus accumbens, amygdala, cingulate and frontal lobes.

Elliot et al (2000) used a gambling task experiment and found a positive correlation between activation of the brainstem (midbrain) and ventral striatum in the case of winning. Delgado et al, 2000 (quoted Keitz et all, 2003) show that the rewards in money and losing money ( as a form of punishment) is associated with a different neural response. Dorsal and ventral striatum increase or decrease their activity, probably showing differentiation between gain and loss. (Elliot et al, 2000). Esch and Stefano (2010) conclude that the anatomical reward and motivation have  as circuits the ventral tegmental area, at the base of the brain. Neurons send VTA projections to the Frontal lobe and nucleus accumbens. The VTA and the mesolimbic dopamine system are the oldest, but the most effective parts of the motivational system. (Esch and Stefano, 2010).

 

Deficiencies of the reward system

Reward Deficiency Syndrome (RDS) is caused by a dysfunction of “biochemical cascade of reward”. At least one genetic mutation was identified associated with RDS, respectively a variant of the dopamine D2 receptor gene (Blum et al, 2008). If the reward system is deficient it will only respond to material rewards, and not to non-material rewards, as it would happen in healthy subjects. The same occurs in the case of substance abuse. Physiological rationale loses its value because the same effect is obtained by using drugs. It basically creates a short circuit of the reward system. Neurobiologically, there were found physiological and molecular changes that can cause permanent changes in these circuits (Esch and Stefano, 2004). In the case of children we ask ourselves whether by over-stimulating them with so many material stimuli, giving them more than necessary whenever they ask, aren’t we basically short circuiting the reward system? Overstimulation with toys, sweets and with other material stimuli does not lead to “boredom” in children who will not expect eagerly a “Christmas gift”, leading to sad, an hedonic children and a future subsequently unhappy adult population?

 

Conclusions

These research data, from purely scientific literature are very valuable for understanding the importance of neural circuits in the reward system and collating them with the clinical observations raises some pressing questions with practical application:

 

  • Does the training process enable or disable mechanisms of addiction?
  • Can we avoid the force of knowledge some of the educational failures?
  • Will what is “innate” express with certainty?
  • The way of response to material stimulus only in mesolimbic regions is innate or acquired?
  • How can we prevent “short circuiting the reward system”? What should I do to not have children and later an hedonic adults?
  • Can we change the expression of what is innate by positive learning during early education?

 

 

Bibliography

  1. Riga S, Riga D. Restituţie şi patrimoniu în neuroştiinţe şi medicina românească. În: Analele Universităţii din Oradea, fascicula medicală, ed. Universităţii din Oradea, 2010; 17-26.
  2. Esch T, Stefano BG. The neurobiology of pleasure, reward processes, addiction and their health implications, Neuroendocrinology Letters, 2004, 25: 235-251.
  3. Keitz M, Martin-Soelch C,  Leenders KL. Reward processing in the brain: a prerequisite for movement preparation? Neural Plasticity, 2003, 10(1-2): 121-128
  4. Blum K, Chen A, Braverman ER, Comings DE, Chen T, Arcuri V, Blum S, Downs BW, Waite RL, Notaro A, Lubar J, Wiliams L, Prihoda TJ, Palomo T, Oscar-Berman M.Attention deficit hyperactivity disorder and reward deficiency syndrome, Neuropsychiatric Disease and Treatment, 2008, 4(5): 893-917.
  5. Martin-Soelch C, Leenders KL, Chevalley AF, Missimer J, Kunig G, Magyar S, Mino A, Schultz W.Reward mechanism in the brain and their role in dependence: evidence from neurophysiological and neuroimaging studies, Brain Research Reviews, 2001, 36:139-149.
  6. Olds J, Milner P. Positive reinforcement produced by electrical stimulation of septal area and other regions of rat brain, Journal of Comparative and Physiological Psychology, 1954, 47: 419-427.
  7. Rolls ET. The Brain and Emotion. Oxford University Press, New York, USA, 1999, 367.
  8. Nakahara D, Ozaki N, Miura Y, Miura H, Nagatsu T. Increased dopamine and serotonin metabolism in rat nucleus accumbens produced by intracranial self-stimulation of medial forebrain bundle as measured by in vivo microdialysis, Brain Research, 1989,  495 (121):  178–181.
  9. Ranaldi R, Beninger RJ.Rostral-caudal differences in effects of nucleus accumbens amphetamine on VTA ICSS. Brain Res, 1994, 642: 251-258.
  10. Mora F, Rolls ET, Burton MJ, Shaw GS, Shaw GS.Effects of dopamine-receptor blockade on self-stimulation in the monkey. 1976, PharmacolBiochem Behav, 1976, 4: 211-216.
  11. Fibiger HC, LePiane FG, Jakubovic A, Phillips AG.The role of dopamine in intracranial self-stimulation of the ventral tegmental area. J Neurosci, 1987, 7: 3888-3896.
  12. Yokel RA, Wise RA. Increased lever pressing for amphetamine after pimozide in rats: implications for a dopamine theory of reward. Science, 1975, 187: 547-549.
  13. Pettit HO, Justice JB. Dopamine in the nucleus accumbens during cocaine self-admini- stration as studied by in vivo microdialysis. Pharmacol Biochem Behav, 1989, 34: 899-904.
  14. Di Ciano P, Coury A, Depoortere RY, Egilmez Y, Lane JD, Emmett-Oglesby MW. Comparison of changes in extracellular dopamine concentrations in the nucleus accumbens during intravenous self-administration of cocaine or d-amphetamine.Behav Pharmacol, 1995, 6: 311-322.
  15. Salamone JD. The involvement of nucleus accumbens dopamine in appetitive and aversive motivation. Behav Brain Res, 1994, 61: 117-133.
  16. Becker JB, Rudick CN, Jenkins WJ.The role of dopamine in the nucleus accumbens and striatum during sexual behavior in the female rat. J Neurosci, 2001, 21: 3236-3241.
  17. Apicella P, Ljungberg T, Scarnati E, Schultz W.Responses to reward in monkey dorsal and ventral striatum. Exp Brain Res, 1991, 85: 491-500.
  18. Sem-Jacobsen CW. Electrical stimulation and self-stimulation in man with chronic implanted electrodes. Interpretation and pitfalls of results. The Netherlands NHPC, Amsterdam, 1976, 505-520.
  19. Elliot R, Friston KJ, Dolan RJ.Dissociable neural responses in human reward systems, J. Neuroscience, 2000, 20: 6159-6165.
  20. Blum K, Comings D, Cull G., Braverman ER.Reward Deficiency Syndrom, American Scientist, 1996, 84: 132-145.