Motivation and emotion/Book/2017/Hypothalamus and motivation
What is the role of the hypothalamus in motivated behaviour?
- 1 Overview
- 2 Case study
- 3 Hypothalamus
- 4 Hypothalamus-Pituitary-Adrenal (HPA) Axis
- 5 Homeostatic motivation and the hypothalamus
- 6 Reward motivation and hypothalamic functioning
- 7 Social motivation theory and hypothalamic functioning
- 8 Conclusion
- 9 See also
- 10 References
- 11 External links
Sit there, wait a minute. Can you hear your heartbeat? Even feel your heartbeat? Can you feel the inhalation and exhalation of your lungs? These physiological responses are crucial for everyday life. However, can you feel the small almond sized hypothalamus governing many homeostatic functions? Hmmm not exactly.
Physiological responses of motivational behaviour, whilst not explicitly observable, constitute an imperative role in life. Specifically, that of the hypothalamus, which is the focus of this book chapter. Throughout exploration of hypothalamic function relative to motivation, the themes of sleep, hunger, thirst, aggression and mating will emerge in great detail. These terms are not mutually exclusive and are derived from the umbrella term of homeostasis: the principal regulatory function of the hypothalamus. Homeostasis and motivation (drive theory explain)
The hypothalamus is a small part of the Diencephalon situated anteriorally adjacent to the neural tube, and just under the thalamus. Whilst statistically this structure contributes 0.29 percent to the mean developed adult brain weight, the hypothalamus plays a principally integrative role relative to incoming stimuli and is imperative to homeostatic functioning (Saper & Lowell, 2014). Moreover, a dissection of this integrative brain structure provides evidence of the proceeding anatomical subsections:
|Periventricular||Preoptic||Medial Preoptic Nucleus|
|Medial||Supraoptic / Anterior||Anterior Hypothalamic Nucleus|
|Dorsal Premammillary Nuclei|
|Ventral Premammillary Nuclei|
Hypothalamus-Pituitary-Adrenal (HPA) Axis
The Hypothalamus-Pituitary-Adrenal (HPA) axis is a peripheral neurological and endocrine pathway consisting of the three endocrine glands of the hypothalamus, pituitary and adrenal (reference). The fundamental function of the HPA axis is the regulation and synthesis of stress-related threats and responses (reference). Preponderance of literature of this Axis has concurrently examined secretion of Glucocorticoids and the role of stress-induced physiological responses (Stranahan, Lee, & Matson, 2008). (What are glucocorticoids)
Moreover, a synaptic explanation of stress and hypothalamic functioning denotes a neural plasticity approach. Bains, Wamsteeker Cusulin, and Inoue (2015) ascertain that one stress-induced response stimulates paraventricular hypothalamic nuclei and causes widespread adaptive modification of future stress responses. Explicitly stating that stressful experiences and subsequent physiological responses, alter neural plasticity throughout development (Bains, Wamsteeker Cusulin, & Inoue, 2015). Whilst this adaptive modification in itself is not significantly detrimental, prolonged activation of the HPA axis and subsequent dysfunction in glucocorticoid production is indicative of maladaptive daily functioning responses.
One psychobiology model assessing prolonged stress responses is the General Adaption Syndrome model (See Figure 3.) (explain)
Homeostatic motivation and the hypothalamus
Neurological and physiological studies frequently examine the hypothalamus with the analogy of a switch. Proposing the facilitatory and regulatory mechanisms within the human body relative to sleep are governed by a hypothalamic switch (Montagna, 2006). This proposed switch is turned 'off' within the Anterior Hypothalamus to facilitate sleep and 'on' in the Posterior Hypothalamus to govern and maintain wakefulness, as shown in the below table (Montagna, 2006). The ability to maintain wakefulness is a highly motivated taxing job, and is also moderately correlated with alertness and motivational factors, such as motivation to stay awake (reference). A dysregulation and/or damage to this pathway may subsequently result in sleepiness and coma, a paradoxical effect which may hinder motivation and alertness
Table 1. An exemplification of hypothalamic zones and subsequent functions relative to sleep (Montagna, 2006)
|Anterior Hypothalamus||Sleep Facilitation|
|Posterior Hypothalamus||Maintain Wakefulness|
|Preoptic Hypothalamus and Medial Preoptic Nucleus||Sleep Regulation|
Moreover, the Preoptic Hypothalamus and the Medial Preoptic Nucleus are attributable to sleep regulation, promoted to have implications in sleep deprivation (in the analogy of the switch, these areas provide the ability to switch between on and off) (Alam, Kumar, McGinty, Alam, & Szymusiak, 2013). These areas are saturated with neurons such as adenosine (explain) which have regulatory functions in the initial onset of sleep and maintenance of sleep, with heightened adenoise production specifically denoted to maintain prolonged slow-wave activity indicative of sleep deprivation (Alam et al., 2013). Damage to the these areas is also attributable to homeostatic dysfunctions, and chronic sleepiness, a hallmark of sleep deprivation (Alam et al., 2013). This sleep deprivation also has motivational implications, shown in impaired motivation and subsequent impairment in job performance (re-write this) (Dinges and Kribbs, 1991). However, whilst intrinsic motivation may be hindered in those with sleep deprivation, extrinsic motivators such as; incentives, rewards, or competitions may increase performance levels and subsequent motivation in individuals with sleep deprivation (Hull, Wright, & Czeisler, 2003) (See Figure 4).
Hunger Motivation and Satiety
Empirical research has extensively examined the hypothalamus relative to the pathophysiology of feeding and eating behaviours, specifically those related to excessive energy intake. This exponential growth and widespread interest relative to hypothalamic functioning has prompted the term; Hypothalamic Obesity (HyOb) (Bereket et al., 2012). Subsequently, overwhelming literature has denoted the ventromedial hypothalamus as the control centre of satiety, providing the cornerstone of numerous HyOb illnesses, specifically that of Hyperphagia.
Hyperphagia is a highly motivated eating behavior sometimes coined as an excessive food intake. However, whilst these terms are not mutually exclusive, Yanovski as cited in (insert reference) suggests that on the continuum of excessive food intake, hyperphagia is the most extreme. See External Links for an in-depth analysis of hyperphagia
Ogawa, Niizuma, and Tominaga (2017) implemented a structural examination of the hypothalamus relative to severe eating behaviors, specifically investigating hyperphagia. From preoperative scanning of patients, it was evident that medial hypothalamic anatomical abnormalities such as tumours, were associated with severe hyperphagia. Thus, implying a dyregulation of the medial zone of the hypothalamus increases the abnormal motivated desire to consume large quantities of food (Ogawa, Niizuma, & Tomonaga, 2017). However, this research was largely explorative, and subsequent studies should further implement distinct control groups and use experimental apparatus such as functional MRI scans.
A discernible link between hypothalamic hyperphagia and motivation is also ascertained by rat hyperphagia studies (see Figure 4). A seminal review postulated by Singh (1973) suggests that ventromedial hypothalamic lesions in rats results in hyperphagia and subsequently has a direct effect on increased hunger motivation. However, subsequent studies contradict these findings, proposing that the motivation to attain food is hindered in animals with ventromedial hypothalamic lesions. Teitelbaum (1950) proposed an experimental design of which rats were to undertake a series of tasks to obtain food. The subjects employed were both hyperphagia rats and matched controls. On low fixed-ratio reinforcement, (pressing a bar to obtain food) both rat groups were almost similar in results, however, on high fixed-ratio reinforcement (moving weighted hinged lids and running down an alley to obtain food) hyperphagia rats performed significantly worse, indicative of a lower motivation to obtain food (Teitelbaum, 1950). This cumulative evidence suggests that whilst an excessive intake of food is the cornerstone to hyperphagia, this is not indicative of higher motivation as ascertained by the aforementioned study. Moreover, this research is largely seminal and the implementation of secondary studies with larger methodological controls and assessment of confounds should be administered.
Moreover, it is imperative to note that hypothalamic functioning is also examined at the molecular metabolic level. This is specifically related to the peptide of ghrelin commonly found in the gastrointestinal tract, and is attributable to signalling the hypothalamus to conduct and maintain energy and metabolism homeostasis (Kageyama, Takenoya, Shiba, & Shioda, 2009).
This empirical evidence further postulates that the medial hypothalamus plays a role in satiety alongside that of the ventromedial nucleus.
As aforementioned, there are widespread applications of the hypothalamus relative to hunger and satiety. As this may be overwhelming there are a few key points to be aware of:
The anatomical breakdown of the hypothalamus suggests that there is widespread underlying physiological mechanisms of attack behaviours in numerous zones, including the ventromedial and anterior hypothalamus (AH) regions (Hrabovsky et al., 2005).The synthesis of hormones and the stimulation of nuclei within the AH coincides with conspecific aggression and attack behaviours between primal species, a somewhat maladaptive motivated survival response (Hrabovsky et al., 2005). Moreover, Schwartzer and Melloni (2010) supported this proposition through the anatomical examination of hamsters. Postulating that during the developmental period of adolescence the AH acts as an integration center for neurochemicals responsible for aggression, especially dopamine. Heightened levels of dopamine in the AH, modulates and alters the aggressive response, especially in the onset of an aggressive encounter (Schwartzer & Melloni, 2010; Ricci, Schwartzer, & Melloni, 2009). The mediobasal hypothalamus (coined the Hypothalamus Aggression Area) is also postulated to be an integrative structure relative to aggressive cognitions and motivated aggressive behaviours in humans as well as mammalians (reference).
Neural imaging techniques have been implemented to discern a neurological root of motivated sexual behaviours, emphasising the role of hypothalamic nuclei concurrently with gender differences (Yang et al., 2013). Explicitly, the medial preoptic nucleus is predominantly involved in the selectivity and manifestation of masculine sexual behavior and preference, whilst the ventrolateral ventromedial nucleus is associated with female sexual behaviour (Swanson, 2000). However, contradictory evidence postulates that the ventromedial hypothalamus governs mating preferences in both sexes (Yang et al., 2013). These inconsistencies, in part, have been mediated by the production of hormone-responsive neurons, explicitly progesterone in female sexual receptivity (Yang et al., 2013)
A dysfunction or damage in the ventromedial hypothalamic nuclei has expansive adaptive and motivationally driven reproductive implications in mammalians. Specifically, relative to females, a dysfunction restricts the ability to exhibit the sexual receptivity posture of lordosis, (see Figure 7) hindering intraspecific copulation (Kim et al., 2013; Pfaff & Sakuma, 1979). Moreover, this research is reinforced by seminal brain stimulation studies, suggesting direct stimulation of the ventromedial nucleus facilitates lordosis in mammalian species (Pfaff & Sakuma, 1979). Lordosis is frequently denoted as a motivated state (Explain).
Whilst preponderance of literature has examined mammalian sexual motivation explicitly in the context of lordosis, limited studies have examined human sexual motivation and hypothalamic functioning. However, a neurological brain imaging meta-analysis discerned three perspectives of human sexual behaviour; cognitive, emotional and motivational (Redouté et al., 2012). Relative to this model, activity in the posterior hypothalamus is attributable to the motivational aspect of sexual behaviour, explicitly in overt sexual behaviour and goal-directed motivation to obtain sex (Redouté et al., 2012 as cited in Poeppl et al., 2016). Specifically, the hypothalamus is in part, responsible for initiating sexual behaviours such as penile erection as well as sexual arousal to stimuli such as erotic images (Walter et al., 2008). However, this hypothalamic activation is specifically related to male sexual behaviour, with inconsistent results obtained in females (Poeppl et al., 2016; Walter et al., 2008).
Reward motivation and hypothalamic functioning
Preponderance of literature examined thus far has explained the influence of hypothalamic functioning on physiological needs and appetitive motivators such as; hunger and thirst. Appetitive motivation is a term utilised to define the subset of behaviours which refer to obtaining a reward, for example hunger is an appetitive motivator as you are trying to obtain food (Marchant, Millan & McNally, 2012). Moreover, an important implication of hypothalamic functioning is discernible in the field of reward and extrinsic motivation. A neurological examination proposed by Marchant, Millan and McNally (2012) postulates that the hypothalamus is an integral brain structure for both appetitive motivational states and reward motivation.
The pioneering study by Olds and Milner (1954) primarily examined the extrinsic motivation for rats to obtain reinforcement by the employment of self-induced stimulation of the hypothalamic region. Prior the commencement of the reinforcement paradigm, electrodes were placed in the rats brain. This experiment employed the comprehensively implemented Skinner box, where a rat would press the lever to receive short electrical stimulation of multiple brain regions. Results determined that 71 percent of the time pressing the lever was indicative of the stimulation of the hypothalamus ( Olds & Milner, 1954). You may be thinking what does this stimulation have to do with reward? Olds and Milner (1954) suggest that this type of mammalian stimulation is attributable to conventional primary reward, suggesting that the rat would press the lever to obtain this reward.
This somewhat arbitrary example of reward with the employment of rats, is not as applicable to understand human behaviour and implications of motivation. Perhaps the most direct relationship between human hypothalamic functioning and reward is discernible in drug-seeking and additive behaviours. Marchant, Millan and McNally (2012) suggest that the Lateral Hypothalamus is the integral hypothalamic region associated with drug seeking and drug related rewards. At the neurological level, the neuropeptide of orexin is heightened in reward-related behaviours with the most density of orexin observed in the lateral hypothalamus (Marchant, Millan and McNally, 2012). Orexin in the lateral hypothalamus becomes stimulated by cues relative to extrinsic consummatory reward behaviours such as food and drugs, a hallmark in addictive behaviour (Harris, Wimmer, & Aston-Jones, 2005). Moreover, Marchant, Millan and McNally (2012) further propose that the influence of drug related stimuli (e.g. a beer) for example, is mediated in the lateral hypothalamus encoding its motivational significance (e.g. trying to attain this beer). However, this effect is bi-directional, as after extinguishment of a drug addiction, the lateral hypothalamus has strong implications of the renewal of drug-related behaviours. (Reference).
Social motivation theory and hypothalamic functioning
Hypothalamic functioning has also been attributable to the clinical epidemiological field of Autism spectrum disorders (ASD). Maladaptive social and motivational impairment has been frequently denoted as the hallmark of ASD (Reference). Social Motivation theory postulates that the motivation for social interaction is imperative for guiding human behaviour, with a deficit attributable to the onset of ASD (Chevallier, Kohls, Troiani, Brodkin & Schultz, 2012). Moreover this theory divides the core social motivational deficit of ASD into three streams: behavioural, biological and evolutionary (Chevallier et al., 2012). Relative to the biological stream, it is postulated that the hypothalamus underlies this social deficit through the synthesis of oxytocin (Chamidale et al., 2015).
Stuctural Magnetic Resonance Imaging (MRI) techniques have reinforced this findings, suggesting the two neuropeptides and hormones of vasopression and oxytocin are attributable to deficits in social interaction. Primarily, the synthesis of these hormones, especially oxytocin within the supraoptic and paraventricular hypothalamic nuclei are attributable to inducing empathy, facial expression, eye-contact encoding, and the motivation to seek trusting/loving relationships (Heinrichs, von Dawans, & Domes, 2009, as cited in Kurth et al., 2011). Thus, literature has ascertained that a marked deficit in these social variables are shown? in individuals with ASD, and are in part, attributable to a structural deficit in the aforementioned hypothalamic nuclei.
Kurth and colleagues (2011) implemented an image acquisition design with ASD subjects and matched IQ, age and gender controls to ascertain a neurological root of socially motivated behaviours. Through the employment of structural MRIs, a diminished volume of grey matter was observed in the supraoptic and paraventricular nuclei in the hypothalamus within ASD subjects. This study reinforces the aforementioned results, suggesting that a dysfunction or in this case, deterioration in this hypothalamic nuclei can in part, provide a neurological explanation for social motivational deficits in ASD.
A subsequent study administered by Chamidale and colleagues (2015) cooberates this aforementioned effect of hypothalamic functioning and the social aspects in ASD. ASD individuals and matched controls were invited to undertake a competitive game, postulated to induce a social evaluative situation. Through medical imaging, an observed hieghtened secretion of oxytocin in hypothalamic regions was discernable in matched controls, comparative to ASD subjects. Chamidale and colleagues (2015) attribute that the synthesis and secretion of oxytocin in hypothalamic regions is attributable to the intrinsic motivating significance of positive social interactions. Due to a significantly higher secretion of oxytocin in matched controls comparative to ASD subjects, this suggests a deficit in oxytocin within the hypothalamus is a neurological pointer for ASD. Stavropoulos and Carver (2013) also reinforce these findings, suggesting that hypothalamic nuclei deficits significantly decrease intrinsic motivation to seek socially rewarding interactions, shown in ASD.
Explain Intrinsic motivation
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