Motivation and emotion/Book/2017/Hypothalamus and motivation
What is the role of the hypothalamus in motivated behaviour?
- 1 Overview
- 2 Hypothalamus
- 3 Hypothalamus-Pituitary-Adrenal (HPA) axis
- 4 Homeostatic motivation and the hypothalamus
- 5 Reward motivation and hypothalamic functioning
- 6 Social motivation theory and hypothalamic functioning
- 7 Practical implications
- 8 Conclusion
- 9 See also
- 10 References
- 11 External links
Sit there, wait a minute. Can you feel your heartbeat? Can you feel the inhalation and exhalation of your lungs? Most likely yes.
However, can you feel your hypothalamus governing many homeostatic functions? Hmmm, not exactly.
This chapter examines the integral role of the hypothalamus in motivated behaviour, including sleep, hunger, aggression and mating. These behaviours illustrate the principal function of the hypothalamus, which is to maintain homeostasis (Saper & Lowell, 2014).
The motivational properties of the hypothalamus will also be examined through the social motivation theory of autism spectrum disorders, as well as drug-related rewards, which provide a clinical depiction of hypothalamic functioning. Additionally, the case of John is explored to depict a daily real-life example of the hypothalamus in action.
The hypothalamus is a small part of the diencephalon situated anteriorly adjacent to the neural tube, and just under the thalamus. Whilst statistically this structure is only 4 grams of the mean adult brain weight, the hypothalamus plays a principally integrative role relative to incoming stimuli and homeostatic functioning (Saper & Lowell, 2014). Moreover, a dissection of the hypothalamus shows evidence of four anatomical subsections/zones: the periventricular, medial, lateral, and anterior (Saper & Lowell, 2014).
Hypothalamus-Pituitary-Adrenal (HPA) axis
The Hypothalamus-Pituitary-Adrenal (HPA) axis is a peripheral neurological and endocrine pathway consisting of three endocrine glands: the hypothalamus, pituitary and adrenal (Kudielka & Kirschbaum, 2005). The fundamental function of the HPA axis is stress regulation via secretion of glucorticoids (commonly known as cortisol) (Stranahan, Lee, & Matson, 2008). Moreover, a synaptic explanation of stress and the HPA axis suggests a neural plasticity approach. Bains, Wamsteeker Cusulin, and Inoue (2015) ascertain that one stress-induced response stimulates hypothalamic nuclei and causes widespread adaption for future stress responses. Whilst this adaptive modification in itself is not significantly detrimental, prolonged stress activation of the HPA axis and heightened glucorticoid secretion is indicative of maladaptive daily functioning responses (Bains et al., 2015).
Overall, this research proposes an imperative importance of the HPA axis explicitly relative to stress. However, whilst the hypothalamus is an integral part of this axis, this chapter focuses on how the hypothalamus affects motivated behaviours.
Homeostatic motivation and the hypothalamus
The principal function of the hypothalamus is to maintain homeostasis (Saper & Lowell, 2014). Thus, the proceeding motivation processes influenced by the hypothalamus are goal-directed behaviours and maintainance of homeostatic state for daily functioning.
Physiological studies frequently examine the facilitatory and regulatory mechanisms of sleep with the analogy of 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 (see Figure 3) (Montagna, 2006). The ability to maintain wakefulness is a motivated taxing process, and a dysregulation to this pathway results in chronic sleepiness, subsequently hindering motivation and alertness (Montagna, 2006).
Moreover, the preoptic hypothalamus and the medial preoptic nucleus are attributable to sleep regulation, promoted[say what?] to have implications in sleep deprivation (Alam, Kumar, McGinty, Alam, & Szymusiak, 2013). These areas are saturated with neurons such as adenosine which have regulatory functions in the initial onset of sleep and maintenance of sleep, with heightened adenosine production denoted as an antecedent to sleep deprivation (Alam et al., 2013). Damage to these areas results in widespread homeostatic dysfunctions, such as chronic sleepiness, a core deficit of sleep deprivation(Alam et al., 2013). Sleep deprivation also has motivational implications, such as impaired job performance due to decreased intrinsic motivation (Dinges & Kribbs, 1991). However, extrinsic motivators such as incentives may increase work performance and subsequent motivation in individuals with sleep deprivation (Hull, Wright, & Czeisler, 2003)
|John's Case Study:
John has remained awake all day to finish an assignment. He then puts down his laptop climbs into bed and starts to sleep
Hunger motivation and satiety
Empirical research has extensively examined the hypothalamus relative to the pathophysiology of eating behaviours, specifically related to excessive energy intake.[factual?] This exponential growth and widespread interest has prompted the term; Hypothalamic Obesity (HyOb) (Bereket et al., 2012). Subsequently, overwhelming literature has denoted the ventromedial hypothalamus (VH) as the control centre of satiety, providing the cornerstone of numerous HyOb illnesses, specifically that of hyperphagia. Hyperphagia is a highly motivated eating behaviour denoted as an abnormal excessive energy intake (Wren et al., 2001).
Ogawa, Niizuma, and Tominaga (2017) implemented a structural examination of the hypothalamus specifically investigating hyperphagia. From preoperative scanning of patients, it was postulated that VH anatomical abnormalities (i.e., tumours) were associated with hyperphagia. Thus, implying a dysregulation of the VH increases the abnormal motivated desire of excessive food intake (Ogawa et al., 2017). However, this research was largely explorative, and subsequent studies should implement distinct control groups and further use experimental apparatus such as functional magnetic resonance imaging (fMRI) scans.
An explicit link between hypothalamic hyperphagia and motivation is ascertained by rat hyperphagia studies (see Figure 4). A seminal review by Singh (1973) suggested that VH lesions in rats results in hyperphagia and consequently has a direct effect on increased hunger motivation. However, subsequent studies[factual?] contradict these findings, proposing that the motivation to attain food is hindered in hyperphagic rats.
Teitelbaum (1950) proposed an experimental design in which rats were to undertake a series of tasks to obtain food. The subjects employed were both hyperphagic rats and matched controls. Results were as follows:
- On low fixed-ratio reinforcement (pressing a bar to obtain food) both rat groups were almost similar in results
- On high fixed-ratio reinforcement (moving weighted hinged lids to obtain food) hyperphagic rats performed significantly worse, indicative of a lower motivation to obtain food (Teitelbaum, 1950).
These results indicate that whilst excessive food intake is the cornerstone to hyperphagia, this is not indicative of higher motivation. However, this research is largely seminal and the implementation of secondary studies with better methodological controls and assessment of confounds should be administered. Moreover, hypothalamic functioning is also examined at the molecular metabolic level, as the peptide of ghrelin commonly found in the gastrointestinal tract, is attributable to signalling the hypothalamus to maintain energy and conduct metabolic homeostasis (Kageyama, Takenoya, Shiba, & Shioda, 2009).
The widely cited drive-reduction theory has been examined relative to an expansive array of biological mechanisms, specifically in the physiological need of hunger (Berridge, 2004). Clark Hull, the pioneering founder of drive-reduction theory suggested that humans are motivated to conduct goal-directed behaviour to satisfy a drive and retain an equilibrium (Berridge, 2004). This theoretical application is attributable to the hypothalamus as the VH and Lateral Hypothalamus (LH) conduct motivated behaviours to fulfil the hunger drive.
Through an extensive review of hunger literature, Stellar (1954) postulated the dual-control theory to examine the two independent hypothalamic regions working in cyclical fashion to regulate eating and satiety. This theory suggests that:
- The VH works as the integration centre for satiety
- Whilst the LH is suggested to be the predominant brain region relative to hunger (Broberger, 2005).
If one region in this pathway is dysregulated, this has severe implications evident in the example of hyperphagia (King, 2006). Moreover, both hunger and satiety mechanisms are postulated as appetitive motivators. 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 due to obtainment of food (Marchant, Millan, & McNally, 2012).
|John's Case Study:
"Oh my goodness am I hungry" John grabs a bowl of chips and starts munching on them "well that hit the spot I'm not hungry anymore"
The anatomical breakdown of the hypothalamus suggests that there is widespread underlying physiological mechanisms of attack behaviours in numerous zones (Hrabovsky et al., 2005). Moreover, the mediobasal hypothalamus (coined the Hypothalamic Aggression Area) is also postulated to be an integrative structure relative to aggressive cognitions and motivated aggressive behaviours in humans and mammalians (Toth, Fuzesi, Halasz, Tulogdi, & Haller, 2010). Additionally, the anterior hypothalamus (AH) is one hypothalamic zone imperative for the modulation of aggressive responses (Hrabovsky et al., 2005). The synthesis of hormones and the stimulation of nuclei within the AH coincides with conspecific[explain?] aggression and attack behaviours between primal species, a somewhat maladaptive motivated response (Hrabovsky et al., 2005).
Moreover, Schwartzer and Melloni (2010) support this proposition through the anatomical examination of hamsters. Postulating that the AH acts as an integration centre for neurochemicals responsible for aggression, especially dopamine[grammar?]. 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).
|John's Case Study:
John has noticed his girlfriend Bec loves his friend Paul and starts to anticipate a fight
Neural imaging techniques have been implemented to discern a neurological root of motivated sexual behaviours, emphasising the role of gender differences (Yang et al., 2013). Explicitly, the medial preoptic nucleus is predominantly involved in the selectivity and manifestation of masculine sexual behaviour, whilst the VH is associated with female sexual behaviour (Swanson, 2000). However, contradictory evidence postulates that the VH 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 in VH nuclei has expansive reproductive implications in mammals. Specifically, relative to females, a dysfunction [where?] restricts the ability to exhibit the motivated sexual receptivity posture of lordosis, hindering intraspecific copulation (see Figure 6) (Kim et al., 2013). Moreover, this research is reinforced by seminal brain stimulation studies, suggesting direct stimulation of the VH facilitates lordosis in mammalian species (Pfaff & Sakuma, 1979).
Whilst a 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). 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). Specifically, the hypothalamus is partially responsible for initiating sexual behaviours such as penile erection as well as sexual arousal to erotic stimuli (Walter et al., 2008). However, this hypothalamic activation is specifically related to male sexual behaviour, with inconsistent results obtained in females, thus future studies should implement gender controls to further infer generalisability of results (Poeppl et al., 2016; Walter et al., 2008).
|John's Case Study:
John is anticipating a night alone, ten minutes passes and he receives a sexually arousing image from his girlfriend Bec
Reward motivation and hypothalamic functioning
Preponderance of literature thus far has explained the influence of hypothalamic functioning through the lens of appetitive motivators such as hunger[grammar?]. However, an important implication of hypothalamic functioning is discernible in the field of reward and extrinsic motivation. A neurological examination proposed by Marchant et al. (2012) postulates that the hypothalamus is an integral brain structure for both appetitive and reward motivational states.
A pioneering study by Olds and Milner (1954) examined the extrinsic motivation of rats to obtain reinforcement by the employment of self-induced brain stimulation. Prior to the commencement of the reinforcement paradigm, electrodes were placed in the rat's brain. This experiment employed the comprehensively implemented skinner box, where a rat would press a lever to receive short electrical stimulation of brain regions. Results determined that 71 percent of the time that the rats would continue pressing the lever was due to stimulation of the hypothalamic region (Olds & Milner, 1954). You may be thinking what does this have to do with reward? Olds and Milner (1954) suggest that this type of stimulation is attributable to a conventional primary reward, suggesting the rats would press the lever to obtain rewards.
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 hypothalamic functioning and reward is discernible in drug-seeking behaviours. Marchant et al. (2012) suggest that the LH 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 LH (Marchant et al., 2012).
Orexin in the LH becomes stimulated by cues relative to extrinsic consummatory reward behaviours such as drugs, a hallmark in addictive behaviour (Harris, Aston-Jones, & Wimmer 2005). Marchant et al. (2012) further proposed that the influence of drug-related stimuli (e.g., a beer) is mediated in the LH encoding its motivational significance (e.g., trying to attain this beer). Moreover, if the motivational significance of drug-related stimuli is constantly strong, orexin is secreted continuously, and hypothalamic neurons potentiate in strength (Marchant et al., 2012). These heightened physiological responses are subsequently denoted as a hallmark of addiction, and consequently maladaptive to daily functioning (Marchant et al., 2012).
|John's Case Study:
John is at a party, his friend passes him a beer "Come on mate you can have another one" his friend says
Social motivation theory and hypothalamic functioning
Hypothalamic functioning is also attributable to the epidemiological field of autism spectrum disorders (ASD), explicitly in the symptoms of impaired social motivation. Social motivation theory postulates that social interaction motivation 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 this core social motivational deficit of ASD into behavioural, biological and evolutionary perspectives (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).
MRI techniques have reinforced these findings, suggesting that vasopressin and oxytocin are attributable to deficits in social interaction (Heinrichs, von Dawans, & Domes, 2009). Primarily, the synthesis of oxytocin within the supraoptic and paraventricular hypothalamic nuclei is attributable to inducing empathy, facial expression, and the motivation to seek trusting/loving relationships (Heinrichs et al., 2009). Thus, literature ascertains that marked deficits in these social variables observed in ASD are partially attributable to a structural deficit of the hypothalamus.
Kurth and colleagues (2011) implemented an image acquisition design with ASD subjects and matched IQ, age and gender controls to propose a neurological explanation of social motivation. 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. Thus suggesting that a dysfunction and/or deterioration in hypothalamic nuclei can propose a neurological explanation for social motivational deficits in ASD[grammar?].
A subsequent study administered by Chamidale and colleagues (2015) corroborates the influence of hypothalamic functioning on 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 heightened 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.
|John's Case Study:
John is not on the spectrum for ASD but some of these findings may be generalised for severe maladaptive social interactions
How can the hypothalamus be utilised for self-improvement? Dysregulation in hypothalamic regions causes negative implications for daily functioning (e.g., drug addiction). Whilst numerous pharmacological interventions assess these implications, underlying knowledge of the hypothalamus is important to examine the efficacy of these interventions. For example, Yeoh et al. (2012) suggest that knowing the underlying hypothalamic regions associated with drug-seeking behaviours can provide insight into the development of interventions. These interventions may, in turn, prevent relapse, increase positive cognitions, and enhance the patient's quality of life.
Moreover, this insight is also beneficial for ASD, as knowing the underlying biological mechanisms may provide biological "markers" which can improve self-insight and understanding of treatment throughout critical periods of development (de la Torre-Ubieta, Won, Stein, & Geschwind, 2016).
The role of the hypothalamus is to regulate hunger, sleep, aggression, and sex. Moreover, whilst a highly functioning hypothalamus turns physiological mechanisms into goal-directed behaviour, such as the dual-control theory of hunger and the drive-reduction theory. A dysfunction in hypothalamic zones results in an expansive array of maladaptive behaviours such as hyperphagia, sleep deprivation, and inhibited copulation. Furthermore, the reward properties of the hypothalamus help to explain our responses to drug-related stimuli and the aetiology of addiction. Moreover, social motivation theory is consistent with decreased grey matter in hypothalamic nuclei being connected to social motivational deficits in children with ASD.
Whilst physiological mechanisms are not directly observable, gaining insight into the underlying hypothalamic mechanisms can promote pharmacological and behavioural interventions, which in turn, increase individual self-development (de la Torre-Ubieta et al., 2016). This insight fosters a sense of acknowledgement of not only your own, but other people's motivated behaviours.
Bains, J. S., Wamsteeker Cusulin, J. I., & Inoue, W. (2015). Stress-related synaptic plasticity in the hypothalamus. Nature Reviews. Neuroscience, 16, 377-388. http://dx.doi.org/10.1038/nrn3881
Bereket, A., Kiess, W., Lustig, R. H., Muller, H. L., Goldstone, A. P., Weiss, R., . . . Hochberg, Z. (2012). Hypothalamic obesity in children. Obesity Reviews, 13, 780-798. http://dx.doi.org/10.1111/j.1467-789X.2012.01004.x
Berridge, K. C. (2004). Motivation concepts in behavioral neuroscience. Physiology & Behavior, 81, 179-209. http://dx.doi.org/10.1016/j.physbeh.2004.02.004
Broberger, C. (2005). Brain regulation of food intake and appetite: Molecules and networks. Journal of Internal Medicine, 258, 301-327. http://dx.doi.org/10.1111/j.1365-2796.2005.01553.x
Chaminade, T., Da Fonseca, D., Rosset, D., Cheng, G., & Deruelle, C. (2015). Atypical modulation of hypothalamic activity by social context in ASD. Research in Autism Spectrum Disorders, 10, 41-50. http://dx.doi.org/10.1016/j.rasd.2014.10.015
Chevallier, C., Kohls, G., Troiani, V., Brodkin, E. S., & Schultz, R. T. (2012). The social motivation theory of autism. Trends in Cognitive Sciences, 16, 231. http://dx.doi.org/10.1016/j.tics.2012.02.007
de la Torre-Ubieta, L., Won, H., Stein, J. L., & Geschwind, D. H. (2016). Advancing the understanding of autism disease mechanisms through genetics. Nature Medicine, 22, 345. http://dx.doi.org/10.1038/nm.4071
Harris, G. C., Aston-Jones, G., & Wimmer, M. (2005). A role for lateral hypothalamic orexin neurons in reward seeking. Nature, 437, 556-559. http://dx.doi.org/10.1038/nature04071
Heinrichs, M., von Dawans, B., & Domes, G. (2009). Oxytocin, vasopressin, and human social behavior. Frontiers in Neuroendocrinology 30, 548-557. http://dx.doi.org/10.1016/j.yfrne.2009.05.005
Hrabovszky, E., Halász, J., Meelis, W., Kruk, M. R., Liposits, Z., & Haller, J. (2005). Neurochemical characterization of hypothalamic neurons involved in attack behavior: Glutamatergic dominance and co-expression of thyrotropin-releasing hormone in a subset of glutamatergic neurons. Neuroscience, 133, 657-666. http://dx.doi.org/10.1016/j.neuroscience.2005.03.042
Kageyama, H., Takenoya, F., Shiba, K., & Shioda, S. (2010). Neuronal circuits involving ghrelin in the hypothalamus-mediated regulation of feeding. Neuropeptides, 44, 133-138. http://dx.doi.org/10.1016/j.npep.2009.11.010
King, B. M. (2006). The rise, fall, and resurrection of the ventromedial hypothalamus in the regulation of feeding behavior and body weight. Physiology & Behavior, 87, 221-244. http://dx.doi.org/10.1016/j.physbeh.2005.10.007
Kudielka, B. M., & Kirschbaum, C. (2005). Sex differences in HPA axis responses to stress: A review. Biological Psychology, 69, 113-132. http://dx.doi.org/10.1016/j.biopsycho.2004.11.009
Kurth, F., Narr, K. L., Woods, R. P., O'Neill, J., Alger, J. R., Caplan, R., . . . Levitt, J. G. (2011). Diminished gray matter within the hypothalamus in autism disorder: A potential link to hormonal effects? Biological Psychiatry, 70, 278-282. http://dx.doi.org/10.1016/j.biopsych.2011.03.026
Marchant, N. J., Hamlin, A. S., & McNally, G. P. (2009). Lateral hypothalamus is required for context-induced reinstatement of extinguished reward seeking. Journal of Neuroscience, 29, 1331. http://dx.doi.org/10.1523/JNEUROSCI.5194-08.2009
Marchant, N. J., Millan, E. Z., & McNally, G. P. (2012). The hypothalamus and the neurobiology of drug seeking. Cellular and Molecular Life Sciences, 69, 581-597. http://dx.doi.org/10.1007/s00018-011-0817-0
Montagna, P. (2006). Hypothalamus, sleep and headaches. Neurological Sciences, 27, 138-143. http://dx.doi.org/10.1007/s10072-006-0589-8
Ogawa, Y., Niizuma, K., & Tominaga, T. (2017). Fine morphological evaluation of hypothalamus in patients with hyperphagia. Acta Neurochirurgica, 159, 865-871. http://dx.doi.org/10.1007/s00701-017-3112-5
Olds, J., & Milner, P. (1954). positive reinforcement produced by electrical stimulation of septal area and other regions of rat brain. Journal of Comparative and Physiological Psychology, 47, 419-427. http://dx.doi.org/10.1037/h0058775
Pfaff, D. W., & Sakuma, Y. (1979). Facilitation of the lordosis reflex of female rats from the ventromedial nucleus of the hypothalamus. The Journal of Physiology, 288, 189-202. http://dx.doi.org/10.1113/jphysiol.1979.sp012690
Poeppl, T. B., Langguth, B., Rupprecht, R., Safron, A., Bzdok, D., Laird, A. R., & Eickhoff, S. B. (2016). The neural basis of sex differences in sexual behavior: A quantitative meta-analysis. Frontiers in Neuroendocrinology, 43, 28-43. http://dx.doi.org/10.1016/j.yfrne.2016.10.001
Ricci, L. A., Schwartzer, J. J., & Melloni, R. H. (2009). Alterations in the anterior hypothalamic dopamine system in aggressive adolescent AAS-treated hamsters. Hormones and Behavior, 55, 348-355. http://dx.doi.org/10.1016/j.yhbeh.2008.10.011
Saper, C. B., & Lowell, B. B. (2014). The hypothalamus. Current Biology : CB, 24, 1111-1116. http://dx.doi.org/10.1016/j.cub.2014.10.023
Schwartzer, J. J., & Melloni, R. H. (2010). Dopamine activity in the lateral anterior hypothalamus modulates AAS-induced aggression through D2 but not D5 receptors. Behavioral Neuroscience, 124, 645-655. http://dx.doi.org/10.1037/a0020899
Singh, D. (1973). Effects of preoperative training on food-motivated behavior of hypothalamic hyperphagic rats. Journal of Comparative and Physiological Psychology, 84, 47-52. http://dx.doi.org/10.1037/h0035022
Stranahan, A. M., Lee, K., & Mattson, M. P. (2008). Central mechanisms of HPA axis regulation by voluntary exercise. NeuroMolecular Medicine, 10, 118-127. http://dx.doi.org/10.1007/s12017-008-8027-0
Toth, M., Fuzesi, T., Halasz, J., Tulogdi, A., & Haller, J. (2010). Neural inputs of the hypothalamic "aggression area" in the rat. Behavioural Brain Research, 215, 7. http://dx.doi.org/10.1016/j.bbr.2010.05.050
Walter, M., Bermpohl, F., Mouras, H., Schiltz, K., Tempelmann, C., Rotte, M., . . . Northoff, G. (2008). Distinguishing specific sexual and general emotional effects in fMRI—Subcortical and cortical arousal during erotic picture viewing. Neuroimage, 40, 1482-1494. http://dx.doi.org/10.1016/j.neuroimage.2008.01.040
Wren, A. M., Small, C. J., Abbott, C. R., Dhillo, W. S., Seal, L. J., Cohen, M. A., . . . Bloom, S. R. (2001). Ghrelin causes hyperphagia and obesity in rats. Diabetes, 50, 2540-2547. http://dx.doi.org/10.2337/diabetes.50.11.2540
Yang, C. F., Chiang, M. C., Gray, D. C., Prabhakaran, M., Alvarado, M., Juntti, S. A., . . . Shah, N. M. (2013). Sexually dimorphic neurons in the ventromedial hypothalamus govern mating in both sexes and aggression in males. Cell, 153, 896-909. http://dx.doi.org/10.1016/j.cell.2013.04.017
Yeoh, J. W., James, M. H., Jobling, P., Bains, J. S., Graham, B. A., & Dayas, C. V. (2012). Cocaine potentiates excitatory drive in the perifornical/lateral hypothalamus. The Journal of Physiology, 590, 3677-3689. http://dx.doi.org/10.1113/jphysiol.2012.230268