Molecular mechanisms of neuronal plasticity during learning: The role of secondary messengers

Abstract

We present published data along with our own results concerning the role of second messengers and their intracellular receptors in molecular mechanisms associated with the plasticity of neurons during learning. The participation of cyclic 3',5'-adenosine monophosphate, cyclic 3',5'-guanosine monophosphate, calcium, calmodulin, and also the metabolic products of inositol phospholipids, inositol-1,4,5-triphosphate, diacylglycerol and the protein kinase C activated by it, arachidonic acid, and the products of its lipoxygenase oxidation during the regulation of neuronal plasticity over the course of prolonged potentiation, sensitization, habituation, and classical associative training are discussed.

Correlations between the psychological peculiarities of an individual and the efficacy of a single neurofeedback session (by the EEG characteristics)

“…It can be supposed that such correlations are to a significant extent based on structural and neurochemical changes in the monoaminergic brainstem neuronal systems, which are formed under the influence of the life experience [34,35].…”

Cholinoreceptor neurons of the snail: Identification, plasticity, and its regulation by opioids and second messengers

“…The intracellular Ca 2+ receptor calmodulin is also associated with the regulation of the plasticity of CR, since a number of its blockers, R 24571 (20-50 ~zM), chlorpromazine (20-60 ~M), trifluoperazine (50-200 ~M), and prenylamine lactate (30-400 ~M), reversibly attenuate the rate and depth of extinction [1,8,11].…”

“…Activators of guanylate cyclase, the nitrogen-containing compounds Na nitroprusside (0.5-1 mM) and Na azide (0.5-1 mM) that increases [sic] the content of cGMP in the cell, intensify the extinction of the ACh-reactions [1,8,10,33]. In the RPa4 neuron the nitrogen-containing compounds increase the rate and depth of extinction, while not altering the duration of the spontaneous recovery of the extinguished response.…”

“…The pharmacological effects on the adenylate cyclase system of the cell have no influence on the extinction of the ACh-reaction [1,7,8]. Neither forskolin (20-60 ~M), an activator of adenylate cyclase, which increases the content of cAMP, nor imidazole (5 mM), a phosphodiesterase activator that decreases the basal level of cAMP, alter extinction.…”

Adenosine A3 Receptor and Brain

“…In view of the presence of A 3 receptors in the gerbil brain, 59 and of the potent effect of their preischemic stimulation in the latter species (see below), it is highly unlikely that the treatment with chronic IB‐MECA is completely indifferent. The absence of any cognitive response in gerbils is even more surprising considering both the rapid desensitization of A 3 receptor‐associated G proteins following prolonged stimulation, 11 and the fact that activation of the A 3 receptor triggers several neuronal systems 5 known to be involved in learning and memory 43,44 …”