The Conception that Whatever Humans Achieved Derives from the Unrestricted Capacity of Their Brain to Acquire Drives

It was already discovered in ancient times that the behavior of some mammalian species can be manipulated by proper training. The animals acquire a drive for an unnatural goal and humans make use of it. The horse and the dog are probably the best examples of domesticated species that for thousands of years played an important role in the everyday life of humans. Their faithfulness and devotion to their master, their cleverness and special skill to be helpful in complicated situations is legendary. The essence of domestication is clear by now. The manipulation of the brain of domesticated animals, which enables their exploitation after proper training, is based on the ability of their cortex to acquire drives. Yet the overwhelming majority of vertebrates is devoid of this ability.

In the light of our present knowledge I conjecture that living organisms on earth arrived at the attainable peak of sophistication with the evolution of a cortex capable of acquiring drives. This concept already took shape in the early 1950s when we successfully built into the brain of rats the glass-cylinder-seeking drive, while we were unable to force mice to acquire a similar drive. This was a clear hint that the potentiality to acquire drives represents a higher level of cortical organization. A lifelong, thorough examination of rats that had acquired the glass-cylinder-seeking drive played a decisive role in the experimental foundation of this idea. It catalyzed new lines of research, ultimately leading to the realization that enhancer regulation is the neurochemical basis of the drives (Knoll 2003).

Observationofany actinthe endlessfightforexistencedramain nature illustrates the crucial importance of enhancer regulation. When the eagle pounces upon a rabbit with lightning speed, life or death is in the balance. Both the attacker and the potential victim have only a split second to become properly activated. The chance for the eagle to obtain its food and for the rabbit to save its life lies in the efficiency of a specific mechanism that activates the brain and through it the whole organism. The participant with the more efficiently activated brain will reach its goal (see Knoll 1969, 1994, 2001, 2003, for review). The rabbit's only chance of survival depends upon its split-second transformation from a relaxed state to a state of excitation that enables it to mobilize all resources and run for its life. Enhancer regulation is the brain mechanism responsible for this change. The term "drive", used to cherish illusions that we know what is happening, is just a resounding phrase to describe the phenomenon.

We can easily understand the essential, drive-induced, behavioral consequences by observing the movement of rats in an open field with numbered squares in which activity is measured by the number of squares crossed in a 30-min period and by the total area covered during this period. Due to the innate orienting-searching reflex activity, a naive rat put in this open field looks searchingly around for a short while and then stops moving.

A rat urged on by an innate or an acquired drive behaves qualitatively differently. The orienting-searching reflex activity seems to be inextinguishable. The reason for the difference, in my interpretation, is as follows: In the mesencephalon of the naive rat put in the open field only the best performing catecholaminergic neurons react to the new surrounding. In the "drive" situation endogenous enhancer substances raise the excitability of the cate-cholaminergic neurons and a significantly higher number of neurons respond to the same stimulation. This is the essence of the change.

The characteristic behavioral consequences of the operation of an innate or acquired drive is shown in rats in an open field in Table 1. The data were taken from a recently published series of experiments (Miklya et al. 2003b) that corroborated our earlier findings published between 1955 and 1957 (see Knoll 1969, for review).

Table 2.1 demonstrates that rats supplied ad libitum with food and water crossed on average 11 squares within 30 min and covered 9.2% of the total area (Series no. 1). Rats driven by the deprivation of food for 72 h, however, crossed 73 squares and covered 54.6% of the total area (Series no. 3), and rats that acquired the "glass-cylinder-seeking drive" and were activated through the specific CS, crossed 265 squares and covered 88.4% of the total area (Series no. 8). It is obvious that the drive-induced enhanced orienting-searching-reflex activity is essential for ultimately reaching, by trial and error, a goal that is not perceivable by the senses at the start of the experiment.

This is further clearly shown by comparing the drive-induced purposeful increase in activity with the purposeless hypermotility caused by amphetamine treatment. Amphetamine induces a continuous, irresistible release of cate-cholamines from their intraneuronal stores in the mesencephalon and this leads to aimless hyperactivity. Groups of rats treated with 1, 2 or 5 mg/kg amphetamine crossed in average 98, 216, and 369 squares, respectively, but the total area covered by the animals was on average 8.0,9.8, and 7.1% (Series no. 4,5, 6), the same as covered by rats devoid of a drive (Series no. 1). Moreover, amphetamine completely inhibited the goal-directed activity enhancement, induced by an innate (Series no. 7), or an acquired drive (Series no. 9).

Table 2.1. Demonstration of the drive-induced, essential behavioral consequences in an open field in rats: The qualitative difference between an innate-, or acquired-drive-induced purposeful hypermotility, due to enhanced orienting-searching reflex activity,3 on the one hand, and amphetamine-induced purposeless hypermotility, due to continuous release of catecholamines from their intraneuronal stores, on the other

Table 2.1. Demonstration of the drive-induced, essential behavioral consequences in an open field in rats: The qualitative difference between an innate-, or acquired-drive-induced purposeful hypermotility, due to enhanced orienting-searching reflex activity,3 on the one hand, and amphetamine-induced purposeless hypermotility, due to continuous release of catecholamines from their intraneuronal stores, on the other

No.

Type of experiment

Average number of squares crossed in the open field within 30 min

Average percentage of the total area of the open field covered within 30 min

1

Control

11

9.2

2

Food-deprivation for 48 hb

57

36.8

3

Food-deprivation for 72 hb

73

54.6

4

Amphetamine (1 mg/kg)d

98

8.0

5

Amphetamine (2 mg/kg)d

216

9.8

6

Amphetamine (5 mg/kg)d

369

7.1

7

Amphetamine (5 mg/kg) treatment of rats deprived of food for 72 hd

311

8.2

8

Glass-cylinder-seeking ratsc

265

88.4

9

Amphetamine (5 mg/kg) treatment of glass-cylinder-seeking ratsc,d

377

14.4

a The orienting-searching reflex activity was measured in an open field in rats according to Knoll (1957). b Food-deprivation experiments were performed on three-month-old male Wistar rats (n = 20).

c Glass-cylinder-seeking rats (n = 5) were trained according to the method of Knoll (1969).

d Amphetamine was injected subcutaneously 30 min prior to the trial period.

At the end of the 3rd week after birth enhancer regulation in the rat's mesencephalon starts working on a significantly higher activity level. This is the discontinuation of breast feeding, the crucially important first step to living separately from the mother (Knoll and Miklya 1995). Weaning is obviously the onset of the developmental (uphill) phase of the individual life of the mammalian organism (Knoll 1994, 2001). The period, characterized by a higher basic activity, lasts until the rat develops full-scale sexual maturity (Knoll et al. 2000).

One of the telltale signs which makes the operation of the mesencephalic enhancer mechanism evident is the enhanced basic activity of the catecholamin-

ergic and serotonergic systems, as measured by the significantly enhanced release of catecholamines and serotonin from discrete brain regions isolated from the brain of rats after weaning. Reaching sexual maturity this change disappears and the basic activity of the catecholaminergic and serotoninergic systems returns to the preweaning level (Knoll and Miklya 1995).

Sexual hormones seem to be responsible for the transition from the developmental, uphill phase of life into the postdevelopmental, downhill period, characterized by the slow age-related decay of brain performance terminated by natural death (Fig. 6 in Knoll 2001). Weighty arguments speak in favor of the assumption that the slow, continuous age-related decline of enhancer regulation in the mesencephalic neurons plays a key role in the progressive decay of behavioral performances with the passing of time (see Sect. 3.5.1.1 for details).

According to our present knowledge the nigrostriatal dopaminergic neurons that maintain the enhanced orienting-searching reflex activity indispensable for successful goal-seeking behavior are the most rapidly aging units in the human brain. Over age 45 the dopamine content of the human caudate nucleus decreases steeply, at a rate of 13% per decade. If dopamine sinks below 30% of the normal level, symptoms of Parkinson's disease appear. About 0.1% of the population over 40 years of age develops Parkinson's disease and prevalence increases sharply with age. Parkinson's disease is an especially convincing example of an age-related neurodegenerative disease due to the unusually fast deterioration of an enhancer-sensitive group of midbrain neurons (see Sect. 3.5.1.2.1 for details).

Although the decay of enhancer regulation starts with the full scale development of sexual hormonal regulation (Knoll et al. 2000), this does not mean that the sexually mature individual is immediately converted to a significantly lower performer in his or her fight for existence. Learning, the modification of behavior through experience, training, or practice ensures a rapid and successful goal-directed performance without the need for the high-level specific activation of enhancer-sensitive midbrain neurons. This is nature's most ingenious method to enhance the chances for survival even in the downhill period of living. The experienced organism works in an economic manner and is always reaching its goal with much lower energy investment than the inexperienced one. Nevertheless, the progressive age-related decay of enhancer regulation is irresistibly weakening the ability to acquire new information. As a consequence, vitally important adaptability to a new situation is necessarily on a progressive decline. Thus, even the most experienced, aged organism becomes more and more vulnerable in its struggle for life with the passing of time.

The progressive deterioration of the brain engine's performance with the passing of time is paralleled by the proportional decay in the ability of naive cortical neurons to change by training their functional state. This is manifested by the progressive age-related decline of the capacity to build ECRs, fix ICRs and acquire drives. Thus, the stability of already fixed information is in inverse relationship to the time of its acquisition. This helps explain why aged people vividly relive their youth but forget their most recent experiences.

To ecphorize already fixed chains of ICRs and activate acquired drives does not require significant effort. In contrast, the acquisition of new information, the transformation of a naive cortical neuron into an experienced one, is the most complicated operation. It requires the highest energy investment and is therefore the most vulnerable function of the cortical neurons. Clinical experiences, based on thousands of reliable case histories, support this conclusion.

The famous pathography that describes the illness of the great musician, Maurice Ravel, published by his physician Alajouanine (1948), is a convincing example. This case clearly demonstrates the high vulnerability of the mechanism in the cortical neurons responsible for the fixation of chains of ICRs and for the acquisition of drives. Ravel, who died in 1937, wrote his two last compositions (two brilliant piano concertos) in 1929-1930 because, suffering a severe cerebral lesion on both sides of his brain, he later completely lost his ability to compose or even learn a piece of music unknown to him. This in no way hindered him, however, from playing his own compositions, and he easily ecphorized other music known to him before his illness. This case demonstrates that it is easy to revive an engram that was already irreversibly fixed in the past and bring it into consciousness even from a seriously lesioned brain, but to transform naive neurons into trained ones is the most complicated, most vulnerable process in the brain.

The leading idea of this monograph is the view that in a species capable of acquiring drives the function of the cortical neurons changes in response to training in three consecutive phases. Each of these represents a characteristic form of behavior, as follows:

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