A neural theory of punishment and avoidance, II: quantitative theory

Abstract

Quantitative neural networks are derived from psychological postulates about punishment and avoidance. The classical notion that derive reduction is reinforcing is replaced by a precise physiological alternative akin to Miller's “Go” mechanism and Estes's “amplifier” elements. Cell clusters A + f and A - f are introduced which supply negative and positive incentive motivation, respectively, for classical conditioning sc sensory-motor acts. The A + f cells are persistently turned on by shock (on-cells). The A - f cells are transiently turned on by shock termination (scf-cells). The rebound from A + f cell activation to A - f cell activation replaces drive reduction in the case sc shock. Classical conditioning from sensory cells L to the pattern sc activity playing on arousal cells A f = ( A + f , A - f ) can occur. Sufficiently positive net feedback from A f to L can release sampling, and subsequent learning, by prescribed cells in L sc motor output controls. Once sampled, these controls can be reactivated by L on recall trials. This concept avoids some difficulties sc two-factor theories sc punishment and avoidance. Recent psychophysiological data and concepts are analyzed in terms sc network analogs, and some predictions are made. The rebound from A + f cell activation to A - f cell activation at shock termination is interpreted to be a consequence sc different rates sc transmitter accumulation — depletion in the parallel neural channels associated with A + f and A - f . This interpretation culminates in an analogy with adrenergic and cholinergic interactions at lateral and ventromedial hypothalamic sites, dependent on phasic sensory input and tonic reticular formation input. Mechanisms are suggested for such phenomena as: the greater rewarding effect sc reducing J units sc shock to J/2 units than sc reducing J/2 units to 0 units; a relationship between the rewarding effect sc reducing J units sc shock to J/2 units and the possibility sc releasing a conditioned avoidance response in the presence sc fearful cues; two kinds sc depressed emotional affect, one due to overarousal, that can also be associated with massive associational confusions and poor paying attention, and one due to underarousal, that can also be associated with overreactive fear and relief responses; persistent nonspecific fear that biases interpretation sc specific cues, and can “resist” new learning or “repress” old learning; different effects sc gradual and abrupt shock on response suppression; response generalization from one shock level to another; reduction sc pain in the presence sc loud noise (analgesia); influences sc drugs, such as carbachol, atropine, and scopolamine on conditioned emotional and avoidance responses, and on self-stimulation via implanted hypothalamic electrodes; sensory-drive heterarchy that allows changes in situational cues to release responses compatible with any sc several nonprepotent drives; feedback inhibition sc adrenergic transmitter production; potentiation sc adrenergic production by presynaptic spiking, and by postsynaptic spiking via a feedback loop that controls higher-order instrumental conditioning; learning at cholinergic synapses.