The Dissertation is devoted to study basic electrical, morphological, synaptic and pharmacological properties of second-order sensory pain-related neurons in Substantia Gelatinosa (SG) of the rat spinal cord. The variety in observed morphological types of nerve cells includes central, islet, vertical, medio-lateral and radial neurons. The morphological features however do not correlate significantly with cells' functional characteristics and appear to reflect mainly 3-dimensional organization of the spinal cord. Based on the type of characteristic electrical activity (pattern) in response to sustained depolarization, SG neurons can be subdivided on three types: with tonic, adapting and delayed firing of action potentials (APs). Using such principle in nerve cells' analysis seems to be justified because it correlates well with physiological functions of a given neuron in pain signaling. For example, cells with tonic firing are likely excitatory glutamatergic interneurons in SG networks. An applicability of such approach is additionally strengthened by observation of similar electrical patterns in those types of neurons in high brain regions (hipothalamus, thalamus, cortex), which possess well-known physiological functions. Thus, elucidation of mechanisms of electrical patterns formation is of fundamental neurobiological significance. A specific electrical behavior of SG nerve cells is formed due to expression in their membranes of specific sets of voltage-gated ionic channels. Tonic firing activity is produced via interplay of only two conductances, fast Na+ (GNa) and delayed rectification K+ (KDR). The adapting firing in neurons results from reduced density of, primarily, Na+ channels. The pattern of delayed firing is explained by an expression in respective neurons of additional conductance (to GNa and KDR) in high density - potassium of A-type. Calcium and Ca2+-dependent ionic currents were not necessary to form basic electrical patterns, however they participate in modulation of firing activity by changing level of membrane potential and frequency of APs. The mechanisms of electrical activity regulation in SG neurons by central analgesics (opioids, neuropeptide Y) has been studied as well. The latter acts on their respective somato-dendritic receptors (of mu- and Y1-type) and promptly, within minutes, inhibits electrical activity and reduces excitability of neurons acting on voltage-independent (but not voltage-gated) ionic conductances. The likely molecular effectors of their action are G-protein dependent K+ channels of inward rectification (GIRK). The characteristic feature of both analgesics is their cell' type specificity - they acts almost exclusively on tonic firing neurons. As far as the latter are likely excitatory interneurons in SG networks, such selective suppression of their activity by opioids and neuropeptide Y represent one of the mechanisms underlying the behavioral anesthesia of those substances. In addition, neuropeptide Y acts also presynaptically and modulates the processes of mediator release. Similar to opioids, the neuropeptide reduces non-selectively the activity in excitatory (via Y2-receptors) and inhibitory (via Y1-receptors) synapses. These presynaptic effects do not depend on the type of firing activity in postsynaptic neuron. Overall, the obtained data show a significant diversity of second-order sensory neurons in SG and highlights on a principal role of electrical parameters in physiological analysis of these cells in pain signaling. Key words: spinal cord, Substantia Gelatinosa, pain, neurons, electrical properties, firing pattern, action potentials, excitability, ionic channels, analgesics, opioids, neuropeptide Y, receptors, synapses, glutamate, glycine, GABA.
