Brain has architecture that is specific to a given species and gradually develops during evolution and during individual existence, though correspondence within the species is not ideal. Subtle structural peculiarities of the brain can depend on heredity, but they are not decisive for brain function. On the contrary, brain functions tend to remain steady after a light or even an intermediate crash in morphological structure. Brain morphology of an adult human has the most complex organization. Therefore, the brain cannot be considered as the gland that produces behavior. Rather, neurobiologists and theorists are inclined to accept another extreme and consider the brain as a super perfect construction with an ideal structural design. Given appropriate neural centers, it would be naturally at the beginning of a topic on brain to describe the functions of all brain sections. Although such a description is out of the scope of our topic, we will be compelled sometimes to appeal to localization of some brain functions. Unfortunately, at the present time, we know the roles of various brain centers only approximately. Some functions of brain seem to be distributed within neural tissue and some brain centers seem to have reference to a great number of functions. For example, brain imaging studies in humans indicate that learning and memory involve many of the same regions of the cortex that process sensory information and control motor output [1287].
There are obstacles preventing comprehension of function localizations in the brain. In order to determine functions of a neural center we may observe activity in this center (electrical or chemical processes, temperature, blood flow, etc.) during functioning or evaluate the peculiarity of functioning after influence to this center (electrostimulation, pharmacological blockage, cooling, extirpation, etc.). Both methods are beneficial for simple systems but inappropriate for complex ones with relation to complex functions. We know what makes heart, kidney, chewing muscle, tear glands and so on. We can explain what functions brain performs although somewhat more vaguely and verbosely than, say, kidney. Yet, we do not know what functions are performed by the neocortex, hippocampus, nucleus caudatus or amygdala if we are not satisfied by simplistic responses like, "Neocortex is the center of high nervous functions". Which of brain’s supposed functions ought we to choose: excitation or inhibition, synthesis of amino acids or endorphins, elaboration of temporary rhythms or carrying out the relay functions, unit of errors or unit of forecasts, a memory store or only the memory about something special? Artificial hindrance of performance of a function by a given neural center may not illuminate the problem, since brain possesses strong compensatory capabilities and function must be preserved at the expense of another brain area. Many functions are not, really, scattered in the brain, but they are capable of being compensated. This would not mean, however, that removed of a brain center was not essential in the normal conditions. Much more important would be those discoveries that demonstrate irreversible damage of a function after brain damage. However, a powerful mechanism of compensation prevents irreparable damage or makes it infrequent.
Recently, methods have been developed for visualization of living brain activity during normal behavior: positron emission tomography and functional magnetic resonance. These methods give admirable portraits of the working brain and bring to light sequences of activations in many brain areas during normal behavior. It is also possible now to do non-invasive irritation of deep brain areas. Although these methods are based on recording of nonspecific processes such as oxygen consumption, glucose turnover and blood flow, they have disclosed some important details of neural function.
There are many examples that point to a given brain area as being related to a given brain function, but this pertains to input and output that is sensory and motor functions. Injury of afferent or efferent pathways damages image recognition or motor control and leads to the most prominent impairment of behavior. This is a trivial result, since interruption of direct connection must result in the failure of corresponding function. For example, olfactory nerve damage inevitably leads to anosmia. In the same way, it was established that rostral regions within the neocortex control motor and executive functions, whereas caudal regions process sensory signals [1196]. In vertebrates (except fish), each motor neuron is always part of a pool of tens, hundreds, or thousands of similar neurons that serve a common purpose. This repetitive arrangement contrasts with the pattern of connections in invertebrate muscle, where one, or at most a few, identifiable motor neurons innervate each identifiable muscle fiber, forming a stereotyped circuit exclusively dedicated to a particular function [738]. Relatively strict localization of some particular brain functions does exist [58]. Certain neural functions specifically depend on physiological processes that happen in restricted areas of brain. Even individual neurons may play a role in performing cognitive functions of the brain. Many specific cognitive functions such as language disorders, face detection and mathematical disability, are carried out by groups of highly specialized neurons whose roles are genetically predetermined. A famous example is the speech center (Broca’s area) in the opercular and triangular sections of the inferior frontal gyrus of the frontal lobe of the human cortex, which is involved in language processing, speech production and comprehension. A linguistic processing system located in a specific domain in the left hemisphere is specialized for language independently of the particular modalities through which language is perceived and expressed (deficit of reading, writing or spoken language). In this area, damage leads to a specific language disorder. The circadian rhythm is also a function of individual neurons and is determined by intracellular molecular processes. Their dysfunctions cannot be compensated by other elements of the nervous system or by a reconstruction of interneuron connections within networks [58].
There are specific brain areas for emotions and cognitive signals1 and separate brain regions are involved in different aspects of emotion2 (positive negative, fear sadness, emotion with cognitive demands and instrumental behavior).
A local brain area may be responsible for face recognition in primates. Recently it has been described that cells in the medial temporal lobe and the hippocampus of humans were responding to individual objects (famous persons such as actresses Jennifer Aniston and Julia Roberts, ex-president Bill Clinton, the basketball player Michael Jordan, the Beatles and landmark buildings or objects) [1005]. The prominent feature of these results was the consistency of responses across different images of the same object. Sometimes neurons generated specific reaction not only to the given pictures, but also even by letter strings with their names. The number of images in the given screening session was around 100. 14% of units were selective to only a small amount of images, as 3% of the projected pictures. The cells had a very low baseline activity and responded in a selective manner. Clearly, this was a kind of invariance based on learned associations, not geometric transformation of visual structure, and these cells encode memory-based concepts rather than visual appearance. Nevertheless, detection of 3 out of 100 pictures is far from ideal as face recognition. It would be impossible to find a specific neuron for a specific face, if ideal specificity exists. It is necessary to make a reservation that this criticism is not proof that "grandmother cells" (cells corresponding grandmother, my or yours) are absent in the brain, but only that a search for them is labor and time consuming [500]. However, less selective neurons that differentiated face from non-face were found and there is a direct causal link between the activity of face-selective neurons and face perception. Microstimulation of face selective sites in the inferior temporal cortex of primates, but not other sites, strongly prejudiced the monkeys’ decisions towards the face category [8] and damage of this or related systems can lead to an impairment in recognizing individuals by the sight of their faces [1037]. It was also revealed that there exists discrimination between faces according to an emotional relationship to a given face. So, when participants alternately viewed a photograph of their beloved and a photograph of a familiar individual (the head only), activation specific to the beloved occurred in dopamine-rich areas associated with mammalian reward and motivation, namely the right ventral tegmental area and the right postero-dorsal body and medial caudate nucleus. Activation in the left ventral tegmental area was correlated with facial attractiveness scores [57]. Interestingly, local damage to a specific area in the visual association cortex in both hemispheres or in the right hemisphere can cause face agnosia, that is, face-selective neurons in the temporal cortex are located differently on areas responsible for face agnosia [58]. Nevertheless, some face-selective neurons in the inferior temporal cortex altered the relative degree to which they responded to different members of a set of novel faces over the first few presentation of the set [1037] and, hence, response to a given face is not predetermined. Activation of some parietal neurons is necessary for visual contents but is not in itself sufficient [72].
Another example of sensory specificity is "neurons of place". In the hippocampus was found the cells that are activated only when animals were settled down in the determined place [908]. Neurons of place were found also in the neocortex. Neurons of place are not something that never changes. Ensembles of place cells in the hippocampus undergo extensive "remapping" in response to changes in the sensory or motivational inputs to the hippocampus. The nature of hippocampal remapping can be predicted by ensemble dynamics in place-selective grid cells in the medial entorhinal cortex, one synapse upstream of the hippocampus [439]. Sensory maps of the neocortex are adaptively altered to reflect recent experience, pharmacological influences and learning. Plasticity occurs at multiple sites. This view contrasts with the classical model in which map plasticity reflects a small set of cortical synapses [377].
Nevertheless, participation of a given area in a given function does not exhaust all aspects of given function maintenance, especially in connection with mechanisms of memory. For instance, the basolateral complex of the amygdala is involved in modulation of memory for aversively motivated behavior. Even so, memory for this kind of training is modulated by post-training drug infusions administered to many other brain regions. Modulation within the amygdala is not sufficient to effect memory. So, inactivation of the amygdala with lidocaine prior to retention testing did not block memory of any kind of training [821]. Paradoxically, lesion of the basolateral complex of the amygdala sometimes improves learning. Insufficiency of reversal learning after orbitofrontal damage is eliminated by additional lesions of the basolateral amygdala [1167].
Beside, damage to a specific function concerning a specific area, damage to a specific area of the brain leads to partial impairment of irrelevant functions of areas distantly located from the injured place. For instance, extirpation of the visual cortex prevents elaboration of a conditioned reflex to light, but also slows down elaboration of a conditioned reflex to sound [767]. Similarly, people with comparatively restricted lesions of the ventral right hemisphere show longer reaction times in response to targets on the left side when they pertained to the right side. The dorsal parietal area was the only brain region that increased activity on the lesioned side during the acute to the chronic stages. This was accompanied by reduced activity in the non-lesioned hemisphere [263]. Moreover, even impairment of sensory systems and efferent control may be compensated after injury. For instance, damage to cortical representation of the leg leads to lack of motor control, and then gradual recovery the function. Surprisingly, after recovery, it is impossible to find new cortical representation of the same leg [1255]. Likewise, the post-lesion lack of vestibular input of central vestibular neurons may be compensated for by changes in the efficacy of the remaining sensory inputs. However, the compensational process can also rapidly become independent of these external cues. Vestibular compensation first relies on external cues and finally on changes in the intrinsic properties of the vestibular neurons themselves [1304]. Nevertheless, the damaged function is not recovered completely. So, even if damage to vision after a stroke is ameliorated, in the chronic stage patients improved in their ability to detect stimuli, while even after many years they had a large deficit in reaction time [263]. The most remarkable example of recovery pertains to sexual function. Sexual behavior is severely compromised in rats after removal of the medial preoptic area, the main sexual center. However, sexual behavior does not disappear completely: fewer than 30% of rats with medial preoptic area lesions mounted, fewer than 15% intromissed, and fewer than 3% ejaculated [758]. In humans, sexual arousal without erection includes cortical, limbic, and paral-imbic areas, but only a subpart of these areas participate in the development of an articulated sexual response including full penile erection [383].
We may conclude that some general functions have specific localization in normal brain. These are particular and ancient functions, such as circa-dian rhythm, breathing, self-reception in determined places, simple emotions, image receptions and efferent control having inherent or even an automatic nature. In some cases, but not as a rule, damage to these areas leads to irreversible failure of the corresponding functions. Unexpectedly, contemporary functions having a voluntary nature such as control of language and face recognition also have precise localization. This is, evidently, determined by an increase in the degree both of brain differentiation and of function localization in higher animals and especially in humans. To a lesser degree, localization of functions concerns those functions acquired during learning and connected with memory. These neural functions after brain damage are in most cases only partially deteriorated and later they are recovered, although this improvement is, nevertheless, incomplete.
