Amygdala complex: physiology of emotions and memory

Abstract

The monograph provides a review of the world’s published scientific literature on the physiology of emotions that are based on the conditioned reflex reaction of fear. A detailed description of electrophysiological, molecular mechanisms of synaptic plasticity of the amygdala complex (amygdala), and their ability for long-term potentiation (LTP), as the basis for emotions and conditioned memory, is presented in this work. There are two categories of fear: innate and learned. Innate fear is realized like an unconditioned reflex by the genetically determined pathways. Learned fear is realized like a conditioned reflex and is formed as a result of learning during the combination of conditioned and unconditioned signals. A convergence of sensory inputs that carry the information on such signals occurs on the neurons of the lateral nuclei of the amygdala. Two types of amygdala cells (glutamatergic projection and GABAergic interneurons) receive inputs from the thalamus and cortex. The synapses of the projection cells are equally effective, while the thalamic synapses of interneurons are more effective. The response of projection neurons to the stimulation of cortical and thalamic afferents includes the monosynaptic excitatory glutamatergic AMPA and NMDA components and disynaptic inhibitory GABAergic components. The most important resources of the regulation of the excitatory efferents of the amygdala are GABAergic interneurons. During the stimulation of the thalamic input, the synapses of the interneurons shunt the membrane of the projection cells more effectively and decrease the level of long-term potentiation in comparison with the stimulation of the cortical input. The stages of the development of long-term potentiation are similar for short-term and long-term memory. The formation of the conditioned reflex is based on a short-term memory on the coincidence of the conditioned signal with an unconditioned traumatizing stimulus, and the consolidation — on the long-term memory. The association of the conditioned reflex reactions and long-term potentiation verify the results of the experiments on the manipulations with genes that encode proteins regulating the synaptic transmission and its plasticity. In animals with a knocked-out gene of gastrin-releasing peptide, easier initiation of long-term potentiation and formation of conditioned reflex reactions of fear are observed. The knock-out of the gene of oncoprotein18/stathmin leads to a deficit of long-term potentiation and complicates the expression of amygdala-dependent conditioned reflexes. The review and analysis of modern publications and the author’s research supplement the Cannon-Bard theory of emotion with evidence that a key role in the regulation of emotions is played by the amygdala complex that is characterized by neuronal mechanisms of stimuli filtration depending on their relevance, education, and formation of stimulus-conditioned memory. The annexes to the article contain the protocols of the electrophysiological experiments and methods of formation of conditioned reflex reaction of fear in animals.