HOW THE BRAIN CONTROLS SEXUAL BEHAVIOUR

HOW THE BRAIN CONTROLS SEXUAL BEHAVIOUR
We can be pretty sure that, in males, the preoptic area is involved in the control of sexual behaviour because:
1. lesions of this region permanently abolish male sexual behaviour;
2. electrical stimulation of this area can elicit copulatory activity;
3. neuronal and metabolic activity is induced in this area during copulation; and
4. small implants of the male hormone testosterone into this area restore sexual behaviour in castrated rats.

[David Buss (1953– ), a professor in the Evolutionary Psychology Research Lab, University of Texas at Austin, has pioneered the use of modern evolutionary thinking in the psychology of human behaviour and emotion. His primary research has focused on human mating strategies and conflict between the sexes. He has championed the idea that men and women have different long-term and short-term mating strategies, and that monogamous and promiscuous mating strategies may coexist. Some interesting extensions to his work include references to sexual jealously and coercion, homicide, battery and stalking. In an effort to find empirical rather than circumstantial evidence to show that human psychological preferences have evolved and are not only learned, Buss has performed many cross-cultural studies containing up to 10,000 participants from many countries around the globe. Overall, his evolutionary psychology has highlighted the dynamic and contextsensitive nature of evolved psychological mechanisms.]

In females, the preoptic area is involved in the control of reproductive cycles, and is probably directly involved in controlling sexual behaviour too. The ventromedial nucleus of the hypothalamus (VMH) is also involved in sexual behaviour. Outputs from the VMH project to the periaqueductal gray of the midbrain, and this region is also necessary for female sexual behaviour, including lordosis (the position adopted by a female to accept a male) in rodents. This behaviour can be reinstated in ovariectomized female rats by injections of the female hormones oestradiol and progesterone into the VMH brain region. Can the brain help us to understand sexual arousal at the sight and smell of someone to whom we are sexually attracted? By receiving inputs from the amygdala and orbitofrontal cortex, the preoptic area receives information from the inferior temporal visual cortex (including information about facial identity and expression), the superior temporal auditory association cortex, the olfactory system and the somatosensory system. It is presumably by these neural circuits that the primary rewards relevant to sexual behaviour (such as touch and perhaps smell) and the learned stimuli that act as rewards in connection with sexual behaviour (such as the sight of a partner) reach the preoptic area. And it is likely that, in the preoptic area, the reward value of these sensory stimuli is modulated by hormonal state, perhaps (in females) related to the stage of the menstrual cycle – women are more receptive to these sensory stimuli when they are at their most fertile. The neural control of sexual behaviour may therefore be organized in a similar way to the neural controls of motivational behaviour for food. In both systems, external sensory stimuli are needed to provide the reward, and the extent to which they do this depends on the organism’s internal state, mediated by plasma glucose concentration for hunger and hormonal status for sexual behaviour. For sexual behaviour, the internal signal that controls the motivational state and the reward value of appropriate sensory stimuli alters relatively slowly. It may change, for example, over four days in the rat oestrus cycle, or over weeks or even months in the case of many animals that only breed during certain seasons of the year.

The outputs of the preoptic area include connections to the tegmental area in the midbrain. This region contains neurons that are responsive during male sexual behaviour (Shimura & Shimokochi, 1990). But it is likely that only some outputs of the orbitofrontal cortex and amygdala that control sexual behaviour act through the preoptic area. The preoptic area route may be necessary for some aspects of sexual behaviour, such as copulation in males, but the attractive effect of sexual stimuli may survive damage to the preoptic . Research findings suggest that, as for feeding, outputs of the amygdala and orbitofrontal cortex can also influence behaviour through the basal ganglia. Much research remains to be carried out into how the amygdala, orbitofrontal cortex, preoptic area and hypothalamus represent the motivational rewards underlying sexual behaviour. For instance, it has recently been found that the pleasantness of touch is represented in the human orbitofrontal cortex (Francis et al. 1999). Findings such as these can enhance our understanding of sexuality in a wider context.

Brain Mechanisms for Eating

BRAIN CONTROLS EATING
Since the early twentieth century, we have known that damage to the base of the brain can influence food intake and body weight. One critical region is the ventromedial hypothalamus. Bilateral lesions of this area (i.e. two-sided, damaging both the left and right) in animals leads to hyperphagia (overeating) and obesity. By contrast, Anand and Brobeck (1951) discovered that bilateral lesions (that is, damage) of the lateral hypothalamus can lead to a reduction in feeding and body weight. Evidence of this type led, in the 1950s and 1960s, to the view that food intake is controlled by two interacting ‘centres’ – a feeding centre in the lateral hypothalamus and a satiety centre in the ventromedial hypothalamus. But problems arose with this dual centre hypothesis. Lesions of the ventromedial hypothalamus were found to act indirectly by increasing the secretion of insulin by the pancreas, which in turn reduces plasma glucose concentration, resulting in feeding. This has been demonstrated by cutti ng the vagus nerve, which disconnects the brain from the pancreas, preventing ventromedial hypothalamic lesions from causing hypoglycaemia, and therefore preventing the consequent overeating. So the ventromedial nucleus of the hypothalamus is now thought of as a region that can influence the secretion of insulin and, indirectly, affect body weight, but not as a satiety centre per se. On the other hand, the hypothesis that damage to the lateral hypothalamus produces a lasting decrease in food intake and body weight has been corroborated by injecting focal neurotoxins (agents that kill brain cells in a very specific manner, such as ibotenic acid), into rats. These damage the local cell bodies of neurons but not the nerve fibres passing nearby. Rats with lateral hypothalamus lesions also fail to respond to experimental interventions that normally cause eating by reducing the availability of glucose (Clark et al., 1991).

A matter of taste
How are taste signals (which provide one of the most significant rewards for eating) processed through different stages in our brains, to produce (among other effects) activation of the lateral hypothalamic neurons.

Some of the brain connections and pathways in the macaque monkey. The monkey is used to illustrate these pathways because neuronal activity in non-human primates is considered to be especially relevant to understanding brain function and its disorders in humans. During the first few stages of taste processing (from the rostral part [rostral towards the head or front end of an animal, as opposed to caudal (towards the tail)] of the nucleus of the solitary tract, through the thalamus, to the primary taste cortex), representations of sweet, salty, sour, bitter and protein tastes are developed (protein represents a fifth taste, also referred to as ‘umami’). The reward value or pleasantness of taste is not involved in the processing of the signal as yet, because the primary responses of these neurons are not influenced by whether the monkey is hungry or satiated. The organization of these first few stages of processing therefore allows the primate to identify tastes independently of whether or not it is hungry. In contrast, in the secondary cortical taste area (the orbitofrontal cortex), [orbitofrontal cortex above the orbits of the eyes, part of the prefrontal cortex, which is the part of the frontal lobes in front of the motor cortex and the premotor cortex] the responses of taste neurons to a food with which the monkey is fed to satiety decrease to zero (Rolls et al., 1989, 1990). In other words, there is modulation or regulation of taste responses in this tasteprocessing region of the brain. This modulation is also sensoryspecific (see, for example, figure 5.6). So if the monkey had recently eaten a large number of bananas, then there would be a decreased response of neurons in this region of the orbitofrontal cortex to the taste of banana, but a lesser decrease in response to the taste of an orange or melon. This decreased responding in the orbitofrontal cortex neurons would be associated with a reduced likelihood for the monkey to eat any more bananas (and, to a lesser degree, any more orange or melon) until the satiety had reduced.
So as satiety develops, neuronal activity in the secondary taste cortex appears to make food less acceptable and less pleasant – the monkey stops wanting to eat bananas. In addition, electrical stimulation in this area produces reward, which also decreases in value as satiety increases (Mora et al., 1979). It is possible that outputs from the orbitofrontal cortex subsequently influence behaviour via the connections of this region to the hypothalamus, where it may activate the feeding-related neurons described earlier.

Brain functions

Brain functions

The surface of the underside of the brain (looking up the string) is much smoother. If we work upwards from where the spinal cord joins the brain, at the brain stem, the first structure is the medulla. This is not just a relay station for incoming and outgoing communications; it also contains nuclei that control basic functions like breathing and heart rate. The brain stem also includes the pons. A variety of motor system connections are routed through the pons, and it includes some of the nuclei that seem to be important in sleep and arousal. Next we reach the midbrain (or mesencephalon). There are important early sensory relays here, particularly for the auditory system. The substantia nigra, which is the critical area lost in Parkinson’s disease patients, is also in this region. The midbrain merges with the thalamus, under which is the hypothalamus (hypo- means ‘under’). The thalamus contains major sensory relays to and from the cortex, but should not be thought of as an exclusively sensory-processing structure; for example, specific nuclei of the thalamus are involved in important functional capacities such as memory. The hypothalamus has major roles in motivation. Hypothalamic damage in one location can lead to gross over-eating (hyperphagia) and obesity,while damage at a different hypothalamic site can result in potentially fatal under-eating. The hypothalamus controls aspects of hormonal function: it can directly control hormone release from the pituitary gland, which lies just beneath the hypothalamus outside the brain itself. Pituitary hormones can themselves control hormone release from other endocrine glands, like the adrenal gland next to the kidneys, whose own hormones can in turn modify both peripheral function and brain function. So the brain and the endocrine system interact.

Further up still, we reach some of the crucial motor system nuclei in the basal ganglia. We also encounter limbic structures, like the hippocampus – crucial for normal memory function – and the amygdala, which appears to play a key role in aspects of emotion, especially fear. Animals with amygdalar damage are less frightened than normal animals by signals of impending shock (LeDoux, 1992). Humans with amygdalar damage cannot recognize facial expressions of emotion, particularly fear and anger (Young et al., 1995), or angry or fearful tones of voice (Scott et al., 1997).


Beyond the hippocampus, which is the simplest example of a cortical layered structure we come to, there are various transitional cortical regions with increasingly complex layered structures, before we reach the neocortex, the most complex of them all. The neocortex has specialized motor areas, sensory processing areas and more general purpose association areas. Within each area there may be further, more specialized, modules. In the visual system, for example, separate modules for colour, form and motion speed up visual processing by handling all these attributes in parallel. This high level of specialization means that damage restricted to particular cortical regions can have very precise effects. For example, people with a condition called prosopagnosia are unable to recognize particular people’s faces, despite other visual abilities remaining quite normal. Sometimes people think of the cortex as the most important part of the brain because it evolved later than other parts, and because of its complexity and its roles in high-level processing and human faculties. But a good deal depends on what you mean by ‘important’. If you ask neuroscientists whether they would prefer to lose a cubic centimetre of cortex or a cubic centimetre of some subcortical region, they would probably choose to give up some cortex. This is because damage to the subcortex tends to be more profoundly disabling. For example, the loss of neurons in the small subcortical region called the substantia nigra results in Parkinson’s disease, which eventually causes almost complete motor disability. The functions of the different areas of the cortex have, until recently, been determined either by experimental studies of monkeys (which have a much more highly developed neocortex than animals like rats) or by neuropsychological studies of the effects of brain damage in clinical patients. The development of functional neuro-imaging methods has given us a new way to study the roles of different brain areas in cognition in healthy humans by allowing us to observe which brain regions are active. Imagine an animal with a simple brain made up of a big blob of neurons. How could such a brain develop, allowing space for extra neurons? It cannot just grow larger. The bigger the blob, the harder it is to sort out all the input and output axons for the cells in the middle. Somehow, all those connections have to find their way through gaps between all the new neurons on the outside of the blob. The alternative solution is to arrange cell bodies in layers. The most complicated structure, the neocortex, is actually made up of six layers of cells (see figure 3.12). This allows all the inputs and outputs to run neatly along in a layer of their own. Fibres divert upwards to contact other cell bodies as needed, facilitated by the cortex being organized into columns. Further development of the brain becomes much easier with this arrangement. You can simply add more columns, or ‘bolt on’ more modules, rather like plugging in a new component on your computer. You would not need to reorganize any pre-existing connections. You can also place cells that need to interact alongside each other, forming cortical modules that minimize inter-cell communication distances. This speeds up communications and saves space. Much the same arrangement is used for laying out printed circuit boards. The wrinkles in the brain, which make it look like an outsized walnut, are all folds in the cortex. A valley, where the cortex is folded inwards, is called a sulcus, while a ridge is called a gyrus. This development enables the maximum cortical area to fit into a volume with minimal outside skull dimensions, just like crumpling up a newspaper to fit it into a small wastepaper basket. The volume and surface area of the newspaper are actually unchanged, but it fits into a neater space.

The neurons that make up the human brain are essentially the same as those making up the brains of other animals. So how do we explain our extraordinary capacity for complex, abstract thought? If you were to flatten out a human cortex, it would cover about four pages of A4 paper, a chimpanzee’s would cover a single sheet, and a rat’s would cover little more than a postage stamp. So we have big brains . . . but size is not everything. In mammals, brain size correlates with body size: bigger animals have bigger brains. But this does not make large animals more intelligent than smaller ones. Adaptable, omnivorous animals like rats are a favourite experimental subject for psychologists partly because they so readily learn new behaviours. Their opportunist lifestyle may well lead to greater behavioural flexibility, compared to larger but more specialized animals like the strictly herbivorous rabbit, whose food keeps still and does not need to be outwitted.

Nonetheless, there is something special about human brain size. Our brains are disproportionately large for our body weight, compared to our primate relatives ( Jerison, 1985). This overdevelopment is especially marked in the most general purpose regions of the cortex, the association areas (though the cerebellum is disproportionately enlarged, too). It is possible that at least some of this enlargement provides extra processing facilities that support the human capacity for abstract thought. The two halves of our brains have different cognitive processing specialities. In most humans, language processing takes place in the left hemisphere. Damage on this side of the brain can leave people unable to speak (aphasic), [aphasia loss of speech ability] though quite capable of understanding spoken language. Paul Broca (1861) was the first to describe a condition known as Broca’s aphasia and to identify the key area of damage responsible for it. Just a few years later, Wernicke (1874) reported that damage at a different point of the language system in the left hemisphere leaves people with a different kind of speech problem, Wernicke’s aphasia. These patients speak perfectly fluently, but what they say makes no sense, and they do not appear to understand what is said to them.

Other neuropsychological conditions are typically associated with right rather than left hemisphere damage. For example, severe hemi-neglect often results from damage to the right parietal lobe. Patients with hemi-neglect may ignore the entire left half of the world, so that they eat only the food from the right side of their plates, shave only the right side of their face, and, when dressing, pull their trousers on to their right leg only. Some patients will even try to throw their left leg out of bed, since they do not consider it as being their own! Neglect of the right-hand side of the world, resulting from left hemisphere damage, is much rarer. The underlying reasons for this are not yet certain, but it suggests that the right hemisphere might be able to support bilateral spatial attentional processes, whereas the left hemisphere (perhaps because of its own specialized allocation to language processing) can only support unilateral spatial attention. This would mean that when the left hemisphere is damaged, the right takes over processes that would normally depend on the left hemisphere. But when the right hemisphere is damaged, the left presumably continues to support its usual processing of events in the right half of the world, but cannot take over processing of events on the left. The two hemispheres are joined together below the surface by the corpus callosum, a massive fibre pathway. Split brain patients have had their corpus callosum cut, for example to stop the spread of epileptic seizures from one side of the brain to the other. This disconnection can have startling consequences. If a split brain patient sees a word briefly flashed up so that it falls on the part of the eye that is connected to the right hemisphere, then the patient cannot read out the word. This is because the visual information has not reached the left hemisphere, and so cannot be processed properly as language. But it is fascinating to see that if the word is the name of an object, the patient can use their left hand (which is connected to the right hemisphere) to select that object from among a variety of others.



[John Hughlings Jackson (1835–1911) was a co-founder of the famous journal Brain. He is sometimes referred to as the father of British neurology. His wife suffered from epilepsy, and perhaps his most important inferences about brain function derived from his observations of the consistency of the patterns of epileptic seizures. Jackson saw that in at least some patients the first signs of an impending seizure were twitchings of particular muscles. In the case of his wife, the seizures would start at one of her hands, then extend to include the arm, then the shoulder and then her face, eventually including her leg (all on the same side) after which the seizure would end. Jackson deduced that this kind of pattern could occur if the epileptic seizure was always initiated at the same point in the brain, from which it spread to related areas, assuming that each motor region of the brain had its own specialized function. He further suggested that the seizures were caused by electrical discharges in the brain, and that the condition might be treated by surgically removing the epileptic focus. In doing this he played an important role in the advance of neurosurgery.]