Traditionally, the hypothalamus was seen as comprising two main regions, the lateral hypothalamus (LH), and the ventromedial hypothalamus (VMH), which were hypothesized to control feeding and satiety respectively. The VMH was implicated as a ‘satiety center’ when a series of studies (e.g. Hetherington & Ranson; 1940) showed that lesions to the VMH resulted in hyperphagia and obesity in rats. Similarly, lesions to the LH resulted in aphagia, thus suggesting the LH to be the ‘feeding centre’ of the brain. (Anand & Brobeck, 1951). Such theories have been largely displaced of late, owing to two main experimental findings. Firstly, the hypothalamus has been found to regulate energy metabolisation rather than eating per se; and secondly, effects previously attributed to LH & VMH lesions, have been shown to actually result from damage to surrounding brain structures such as the dopaminergic axons of the nigrostriatal (Stricker & Zigmond; 1976), the noradrenergic bundle (Gold et al.; 1977) or the para-ventricular nuclei (Leibowitz, et al 1981). Present research in this area has focused upon the role of two neurotransmitters secreted by neurons, within the lateral hypothalamus and their activation (i.e. hunger signals) via neuropeptide Y (NPY) which also has at least two sites within the thalamus (Carlson; 2001).
The hypothalamus has also been implicated in sexual behaviour. For example, it has been noted that males have larger preoptic (Swaab & Fliers; 1985), anterior (Allen et al., 1989) and suprachiasmatic (Swaab et al.; 1994) hypothalamic regions than females. Furthermore, male sexual behaviour is regulated by a tract connecting the medial preoptic are and the lateral tagmental field, whilst in females the corresponding tract runs from the ventromedial nucleus to the periaqueductal gray (Pinel; 2000; p307).
Another highly important structure of the limbic system is the amygdala, “…an almond shaped nucleus that is located in the medial temporal lobe, just anterior to the hippocampus [and which]…links feelings of fear and anxiety to appropriate stimuli and defensive responses.” (Pinel & Edwards 1998; p190). Kluver-Bucy’s-syndrome (e.g. Kluver & Bucy;1937) was the first indication that this structure was implicated in emotional perception and expression. Subsequent research has demonstrated the amygdala’s importance in the acquisition of conditioned emotional responses (e.g. LeDoux; 1995; Bechara et al.; 1995 ), and modified startle responses (Davis el al.; 1994); and in the recognition of emotional facial expressions (Adolphs et al.; 1994) . Such functions are further supported by functional imaging studies involving both PET scans (Isenberg et al.; 1999) and MRI (Benkelfat et al. 1995). Of course the importance of such functions would be diminished greatly if one were unable to retain such information. Thankfully, however, another limbic system structure, namely the hippocampus, facilitates in this acquisition (Maren & Baudry; 1995).
The hippocampus, located at the medial-temporal lobes, extends from the anterior amygdala to the posterior of the fornix. The most significant suggested function of the hippocampus arose from O’Keefe & Dostrovsky’s (1971) discovery of hippocampal pyramidal cells. These so-called ‘place cells’ have been found to fire in relation to where the animal ‘thinks’ it is (Wilson & McNaughton; 1993) and thus are important spatial locators. There are three main contemporary explanations of such functions. O’Keefe & Nadel (1978) proposed ‘cognitive map theory’ stating that the hippocampus constructs and stores allocentric maps of the external environment, based upon sensory input. Whilst Rudy & Sutherland (1992) suggest that the hippocampus facilitates long-term retention of the behavioural significance of stimuli as opposed to the stimuli per se. Thirdly, Whishaw et al. (1997) propose ‘path-integration-theory,’ which suggests that the hippocampus plays a ‘mediating’ role, integrating past, present, and future location vis-à-vis ones movement. Whatever its exact function, the hippocampus can nonetheless be noted as being pertinent to both spatial location and the process of memory.
A further structure of the limbic system, namely, the cingulate cortex, has been implicated in the perception of pain. More specifically, recent research suggests that it is important in the detection of aversiveness of stimulus. For example, Rainville et al. (1997) found that hypnotized subjects (who had reported less aversion to a painful stimulus than experimental controls) correspondingly, showed less activation of the cingulate cortex as measured via PET scans.
An important point of note, is that whilst all of the above structures and functions were presented individually for ease of conceptualization, the greatest understanding of their significance is to be grained when they are considered collectively. To borrow the old Gestalt idiom – ‘the whole is greater that the sum of its parts.’ But how then, might all of the above information, be integrated into a tenable set of principles capable of explaining the collective functions of the limbic system?
Firstly, as has been noted previously, the limbic system is thought to equip us with survival value, and indeed from the evidence outlined above this appears to be true. For example in the case of the, the cingulate cortex, it helps us to interpret the severity, or aversiveness of any threatening stimuli and thus can prepare us for the flight or flight response. This is of particular importance to the hypothalamus, which can exert control on the ANS (fundamental to the fight or flight response) and is involved in the regulation of sexual behaviour (and thus continuation of ones gene-pool) as well as eating and drinking behaviour (necessary to remain healthy). Similarly, the amygdala facilitates the recognition of emotional facial expression in others, affects our ability to perceive threatening situations, and is fundamental to the acquisition of conditioned emotional responses. Whilst the hippocampus helps us to form memories of that information (all of which are behaviours which are of obvious value to the survival of the individual, and thus the species as a whole).
Secondly, it is important to remember also, that those structures outlined above, are but only some of the components of which the limbic system comprises. Indeed, when we consider their function vis-à-vis other main structures (e.g. the olfactory cortex, or the fornix ) we begin to gain an appreciation of just how complex the limbic system actual is. That is, it constitutes a circuit which is flexible enough to receive information from several different sources at once, relay this information to all other relevant structures, (re)interpret the feedback received from those structures and still, somehow integrate all this information into a coherent course of action for use by one or more of its structures.
REFERENCE
Adolphs, R. Tranel, D. Damasio, H. Damasio, A. (1994). ‘Impaired Recognition of
Emotion in Facial Expressions Following Bilateral Damage to the Human Amygdala’. Nature 372: 669-672.
Allen, L.S., Hines, M., Shryne, J.S. & Gorski, R.A. (1989). ‘Two sexually dimorphic cell
groups in the human brain.’ The Journal of Neuroscience 9: 497-506.
Anand BK, Brobeck JR. (1951) ‘Hypothalamic control of food intake in rats and cats.’
Yale J Biol Med 24:123-140, 1951.
Bechara A, Tranel D, Damasio H, Adolphs R, Rockland C, Damasio AR, (1995) ‘Double
Dissociation of Conditioning and Declarative Knowledge Relative to the Amygdala and Hippocampus in Humans." Science 269:1115-1118
Benkelfat C, Bradwejn J, Meyer E, Ellenbogen M, Milot S, Gjedde A, Evans AC (1995)
‘Functional neuroanatomy of CCK4-induced anxiety in normal healthy volunteers’ Am J Psych 152: 1180--1184
Carlson, N.R 2001, ‘Physiology of Behaviour.’ (7th Ed.) Boston : Allyn & Bacon,
Davis, J.D. & Campbell, C. S. (1973) ‘Peripheral control of meal size in the rat:effect of
sham feeding on meal size and drinking rate’. Journal of comparative and
Physiological psychology, 83, 379-387.
Gold, R. M.; Jones, A. P. Kapatos, G. (1977) ‘Paraventricular area: Critical focus of a
longitudinal neurocircuitry mediating food intake.’ Physiology & Behaviour, 18, 1111-1119.
Hetherington, A. W. & Ranson, S. W. (1940) ‘Hypothalamic lesions and adiposity in the
rat.’ Anatomical Record, 78: 149.
Kandel, E. R., Schwartz, J. H., and Jessel, T. M. (2000). ‘Principles of Neural Science.’
Elsevier.
Kluver, H. & Bucy, P.C. (1939) ‘Preliminary analysis of functions of the temporal lobes
in monkeys.’ Archives of Neurological Psychiatry, 42, 979-1000.
Leibowitz, S.F. & Hammer, N.J. & Chang, A.K. (1981). ‘Hypothalamic paraventricular
nucleus lesions produce overeating and obesity in the rat.’ Physiology & Behavior, 27, 1031-1040.
LeDoux J.E. (1994). ‘Emotion, memory and the brain.’ [Review]. Scientific American,
270(6): 50-57
MacLean PD (1949). ‘Psychosomatic disease and the "visceral brain": Recent
developments bearing on the Papez theory of Emotion.’ Psychosom. Med. 11:338-353.
MacLean PD (1985). Evolutionary psychiatry and the triurne brain. Psychological
medicine, 15:219-221.
Maren, S. & Baudry, M. (1995). ‘Properties and mechanisms of long-term synaptic
plasticity in the mammalian brain: Relationships to learning and memory.’ Neurobiology of Learning and Memory, 63:1- 18.
O'Keefe, J. and J. Dostrovsky (1971). ‘The hippocampus as a spatial map: preliminary
evidence from unit activity in the freely moving rat.’ Brain Research 34: 171-175.
O'Keefe J, Nadel L. The hippocampus as a cognitive map’. Oxford: Clarendon Press,
1978.
Papez, J. (1937) ‘A proposed mechanism of emotion.’ Arch. Neurol. Psychiat. 38:725-
743.
Pinel, J.P.J. and Edwards, M. (1998). ‘A Colourful Introduction to the Anatomy of the
Human Brain. Allyn and Bacon.’
Pinel, J.P. (2000). ‘Biopsychology’ (4th ed.). Toronto: Allyn & Bacon.
Rainville, P., Duncan, GH, Price, DD, and BUSHNELL, MC. ‘Pain affect coded in
human anterior cingulate but not somatosensory cortex.’ Science 227: 968-971
Reber, A.S. & Reber, E.S. (2001). ‘Dictionary of Psychology’, (3rd Ed) London: Penguin
Books, Ltd
Rudy, J. W. & Sutherland, R. J. (1992). ‘Configural and elemental associations and the
memory coherence problem.’ Journal of Cognitive Neuroscience, 4, 208-216.
Stricker ED, Zigmond MJ (1976) ‘Recovery of function following damage to central
catecholamine containing neurons; a neuro-chemical model of the lateral hypothalamic syndrome.’ In:Sprague JM, Epstein AN (eds) Progress in psychobiology and physiological psychology. New York: Academic Press,
Swaab, D. F. and Hofman, M. A. (1990), "An Enlarged Suprachiasmatic Nucleus in
Homosexual Men" Brain Research, vol. 537, pages 141-148.
Swaab, D.F., Zhou, J.N., Ehlhart, T. and Hofman, M.A.(1994) ‘Development of
vasoactive intestinal polypeptide neurons in the human suprachiasmatic
nucleus in relation to birth and sex.’ Brain Res., 79 (1994) 249- 259.
Wilson, M.A. and McNaughton, B.L. (1993). ‘Dynamics of the hippocampal ensemble
code for space.’ Science, 261, 1055-1058.
Whishaw IQ. McKenna JE. Maaswinkel H. (1997). ‘Hippocampal lesions and path
integration. Current Opinion in Neurobiology.’ 7(2), 228-34.