Protection from neuronal damage evoked by a motivational excitation is a driving force of intentional actions.
Motivation may be understood as an organism's subjective attitude to its current physiological state, which somehow modulates generation of actions until the organism attains an optimal state. How does this subjective attitude arise and how does it modulate generation of actions? Diverse lines of evidence suggest that elemental motivational states (hunger, thirst, fear, drug-dependence, etc.) arise as the result of metabolic disturbances and are related to transient injury, while rewards (food, water, avoidance, drugs, etc.) are associated with the recovery of specific neurons. Just as motivation and the very life of an organism depend on homeostasis, i.e., maintenance of optimum performance, so a neuron's behavior depends on neuronal (i.e., ion) homeostasis. During motivational excitation, the conventional properties of a neuron, such as maintenance of membrane potential and spike generation, are disturbed. Instrumental actions may originate as a consequence of the compensational recovery of neuronal excitability after the excitotoxic damage induced by a motivation. When the extent of neuronal actions is proportional to a metabolic disturbance, the neuron theoretically may choose a beneficial behavior even, if at each instant, it acts by chance. Homeostasis supposedly may be directed to anticipating compensation of the factors that lead to a disturbance of the homeostasis and, as a result, participates in the plasticity of motivational behavior. Following this line of thought, I suggest that voluntary actions arise from the interaction between endogenous compensational mechanisms and excitotoxic damage of specific neurons, and thus anticipate the exogenous compensation evoked by a reward.
Tsitolovsky
Lev E
LE
Department of Life Science, Bar-Ilan University, Ramat-Gan 52900, Israel. tsitol@mail.biu.ac.il
D000818:Animals; D001519:Behavior / Q000502:physiology; D006801:Humans; D033182:Intention; D009042:Motivation; D009420:Nervous System / Q000503:physiopathology; D009474:Neurons / Q000502:physiology*