Specific Activation Active Focus The Physiological Basis of a Drive

We described earlier the essence of both the innate and acquired drives as a state of specific activation (active focus) in a special population of subcortical and cortical neurons, respectively (see Fig. 11 in Knoll 1969). In the light of the enhancer regulation concept, we may characterize the active focus as an endogenous enhancer substance-induced enhanced excitability in a circumscribed population of mesencephalic and telencephalic neurons that persists until the goal has been reached.

In the case of innate drives enhancer regulation in the mesencephalon is responsible for both the formation of the subcortical active focus that maintains the enhanced orienting-searching reflex activity until the goal is reached and cortical active focus ("the cortical representation of the drive"). As natural conditions are always changing, even the goals determined by innate drives can be reached only with the participation of cortical neurons. The successful operation of an innate drive requires, namely, the continuous acquisition of proper chains of ECRs.

In the case of the acquired drives, however, the essence of the complicated behavioral performance is the activation of enhancer regulation in a special population of cortical neurons, forming a cortical active focus that keeps the organism in action until the goal is reached. Whatever the cortically determined goal is, it cannot be reached without a strong orienting-searching performance resulting from properly enhanced mesencephalic activity. Accordingly, an acquired drive brings the mesencephalic system into the same state of enhanced activity as innate drives do.

In this context the catecholaminergic machinery in the mesencephalic system deserves special consideration. Independent of any goal-directed behavioral performance, with all its cognitive and emotional consequences, the continuous perception of the outer and inner world and the maintenance of homeostasis keep the brain active by themselves. Thus the "engine of the brain" is incessantly in motion. Catecholamines, which influence - activate or inhibit - billions of neurons, are continuously released in the mesencephalon. It was well-documented in the 1970s that an extreme paucity or even lack of synaptic junctions is a common feature of noradrenergic (Ajika and Hok-felt 1973; Calas et al. 1974; Descarries et al. 1977), dopaminergic (Hokfelt 1968; Tennyson et al. 1974), and serotonergic (Richards et al. 1973; Chan-Palay 1975; Calas et al. 1976; Descarries and Leger 1978) nerve terminals. This peculiar situation means that the amount of catecholamines released within a given time interval will determine the extent of the catecholaminergic influence on the whole brain. Enhancer regulation, capable of changing dynamically the amount of free catecholamines in the brain according to need, plays a determinant role in survival.

It is reasonable to assume that whenever a drive is operating the mesen-cephalic enhancer regulation works on a higher activity level. This means that during the operation of a drive a significantly greater amount of cate-cholamines and serotonin can be detected in the mesencephalon. To test the validity of this working hypothesis, we compared the amounts of monoamines released by isolated, discrete brain regions in sated vs food-deprived rats (Miklya et al. 2003b).

We first measured - in a special open field - the orienting-searching reflex activity of rats deprived of food for 48 and 72 h, respectively, and isolated thereafter the discrete brain areas from the mesencephalon and measured the amount of norepinephrine, dopamine, and serotonin released by the tissue samples into an organ bath. The orienting-searching reflex activity of the rats increased proportionally to the time elapsedfrom the lastfeed. Simultaneously the amount of 1. dopamine released from the striatum, substantia nigra, and tuberculum olfactorium, 2. norepinephrine released from the locus coeruleus and 3. serotonin released from the raphe also increased in the hungry rats proportionally to the time of fasting. For example, the amount of dopamine released from the substantia nigra of sated increased after fasting for 48 and 72 h from 4.62 ± 0.20 nM/g wet weight to 5.95 ± 0.37 (P < 0.05) and 10.67 ± 0.44 (P < 0.01), respectively. For details see Miklya et al. (2003b).

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