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5.2: Motivation

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    About Drives and Motives

    Motivation is an extended notion, which refers to the starting, controlling and upholding of corporal and mental activities. It is declared by inner processes and variables which are used to explain behavioral changes. Motivations are commonly separated into two types:

    1.Drives: describe acts of motivation like thirst or hunger that have primarily biological purposes.

    2.Motives: are driven by primarily social and psychological mechanisms.

    Motivation is an interceding variable, which means that it is a variable that is not directly observable. Therefore, in order to study motivation, one must approach it through variables which are measurable and observable:

    • Observable terms of variation (independent variables [1])
    • Indicators of behavior (dependent variables[2]) e.g.: rate of learning, level of activity, ...

    There are two major methodologies used to manipulate drives and motives in experiments:

    Stimulation: Initiating motives by aversive attractions like shocks, loud noise, heat or coldness. On the other side attractions can activate drives which lead to positive affective states, e.g. sexual drives.

    Deprivation: means that you prohibit the access to elementary aspects of biological or psychological health, like nutrition or social contacts. As a result it leads it to motives or drives which are not common for this species under normal conditions.

    A theory of motivations was conceived by Abraham Maslow in 1970 (Maslow's hierarchy of needs). He considered two kinds of motivation:

    1. Defected motivation: brings humans to reconsider their psychical and physical balance.

    2. Adolescence motivation: gets people to pass old events and states of their personal development.

    Maslow argues that everyone has a hierarchy of needs(see picture).

    Regarding to this, our innate needs could be ordered in a hierarchy, starting at the “basic” ones and heading towards higher developed aspects of humanity. The hypothesis is that the human is ruled by lower needs as long as they are not satisfied. If they are satisfied in an adequate manner, the human then deals with higher needs. (compare to chapter attention)


    Hierarchy of needs, Maslow (1970)

    Nevertheless, all throughout history you can find examples of people who willingly practiced deprivation through isolation, celibacy, or by hunger strike. These people may be the exceptions to this hypothesis, but they may also have some other, more pressing motives or drives which induce them to behave in this way.

    It seems that individuals are able to resist certain motives via personal cognitive states. The ability of cognitive reasoning and willing is a typical feature of being human and can be the reason for many psychological diseases which indicates that humans are not always capable to handle all rising mental states. Humans are able to manipulate their motives without knowing the real emotional and psychological causes. This introduces the problem that the entity of consciousness, unconsciousness and what ever else could be taken into account is essentially unknown. Neuroscience cannot yet provide a concrete explanation for the neurological substructures of motives, but there has been considerable progress in understanding the neurological procedures of drives.

    The Neurological Regulation of Drives

    The Role of the Hypothalamus

    The purpose of drives is to correct disturbances of homeostasis which is controlled by the hypothalamus. Deviations from the optimal range of a regulated parameter like temperature are detected by neurons concentrated in the periventricular zone of the hypothalamus. These neurons then produce an integrated response to bring the parameter back to its optimal value. This response generally consists of

    1. Humoral response

    2. Visceromotor response

    3. Somatic motor response

    When you are dehydrated, freezing, or exhausted, the appropriate humoral and visceromotor responses are activated automatically,[3] e.g.: body fat reserves are mobilized, urine production is inhibited, you shiver, blood is shunted away from the body surface, … But it is much faster and more effective to correct these disturbances by eating, drinking water or actively seeking or generating warmth by moving. These are examples of drives generated by the somatic motor system, and they are incited to emerge by the activity of the lateral hypothalamus.

    For illustration we will make a brief overview on the neural basis of the regulation of feeding behavior, which is divided into the long-term and the short-term regulation of feeding behavior.

    The long-term regulation of feeding behavior prevents energy shortfalls and concerns the regulation of body fat and feeding. In the 1940s the “dual center” model was popular, which divided the hypothalamus in a “hunger center” (lateral hypothalamus) and a “satiety center” (ventromedial hypothalamus). This theory developed from the facts that bilateral lesions of the lateral hypothalamus causes anorexia, a severely diminished appetite for food (lateral hypothalamic syndrome) and on the other side bilateral lesions of the ventromedial hypothalamus causes overeating and obesity (ventromedial hypothalamic syndrome). Anyway, it has been proved that this “dual model” is overly simplistic. The reason why hypothalamic lesions affect body fat and feeding behavior has in fact much to do with leptin signaling. Adipocytes (fat cells) release the hormone leptin, which regulates body mass by acting directly on neurons of the arcuate nucleus[4] of the hypothalamus that decreases appetite and increase energy expenditure. A fall in leptin levels stimulates another type of arcuate nuleus neurons[5] and neurons in the lateral hypothalamus,[6] which activate the parasympathetic division of the ANS, and stimulate feeding behavior. The short-term regulation of feeding behavior deals with appetite and satiety. Until 1999 scientists believed that hunger was merely the absence of satiety. This changed with the discovery of a peptide called ghrelin, which is highly concentrated in the stomach and is released into the bloodstream when the stomach is empty. In the arcuate nucleus it activates neurons,[7] that strongly stimulate appetite and food consumption. The meal finally ends by the concerted actions of several satiety signals, like gastric distension and the release of insulin.[8] But it seems that animals not only eat because they want food to satisfy their hunger. They also eat because they like food in a merely hedonistic sense. Research on humans and animals suggests that “liking” and “wanting” are mediated by separate circuits in the brain.

    The Role of Dopamine in Motivation

    In the early 1950s, Peter Milner and James Olds conducted an experiment in which a rat had an electrode implanted in its brain, so the brain could be locally stimulated at any time. The rat was seated in a box, which contained a lever for food and water and a lever that would deliver a brief stimulus to the brain when stepped on. At the beginning the rat wandered about the box and stepped on the levers by accident, but before long it was pressing the lever for the brief stimulus repeatedly. This behavior is called electrical self-stimulation. Sometimes the rats would become so involved in pressing the lever that they would forget about food and water, stopping only after collapsing from exhaustion. Electrical self-stimulation apparently provided a reward that reinforced the habit to press the lever. Researches were able to identify the most effective sites for self-stimulation in the different regions of the brain: the mesocorticolimbic dopamine system. Drugs that block dopamine receptors reduced the self-stimulation behavior of the rat. In the same way this drugs greatly reduced the pressing of a lever for receiving of food even if the rat was hungry. These experiments suggested a mechanism by which natural rewards (food, water, sex) reinforce particular behavior. Dopamine plays an important role in addiction of drugs like heroin, nicotine and cocaine. Thus these drugs either stimulate dopamine release (heroin, nicotine) or enhance dopamine actions (cocaine) in the nucleus accumbens. Chronic stimulation of this pathway causes a down-regulated of the dopamine “reward” system. This adaption leads to the phenomenon of drug tolerance. Indeed, drug discontinuation in addicted animals is accompanied by a marked decrease in dopamine release and function in the nucleus accumbens, leading to the symptom of craving for the discontinued drug. The exact role of dopamine in motivating behavior continues to be debated. However, much evidence suggests that animals are motivated to perform behaviors that stimulate dopamine release in the nucleus accumbens and related structures.

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