[Administration of aggregated beta-amyloid peptide (25-35) causes change in long-term potentiation in the hippocampus]. / Vvedenie agregirovannogo beta-amiloidnogo peptida (25-35) vyzyvaet izmenenie dlitel'noi potentsiatsii v gippokampe in vivo.

A month after intracerebroventricular injection of aggregated beta-amyloid fragment 25-35 (7.5 nmol/ventricle), a significant change in in vivo long-term potentiation in hippocampus was demonstrated. The time course of the long-term potentiation was compared with that in sham-operated animals, a powerful and stable increase in the evoked potential amplitude was observed. This phenomenon can be related with the oxidative stress that was revealed in this model in our previous studies, and, as a consequence, with deterioration of ion homeostasis.

[Effects of C-terminal fragment of substance P-CP 5-11 on the activity of neurons of the dorsal raphe nucleus]. / Vliianie C-kontsevogo fragmenta substantsii P-CP 5-11 na aktivnost' neironov dorsal'nogo iadra shva.

The experiments on Wistar rats showed that microinjection of C-terminal fragment of substance P-CP5-11 (1 microgram) into one of the antinociceptive system structure--dorsal raphe nucleus, caused a prolonged (24 hours of observation) analgetic effect by the hot plate test. Neuronal activity of dorsal raphe nucleus simultaneously enhanced. The CP5-11 antinociceptive activity was higher than the CP1-11 one. The conclusion is that CP1-11 and in particular its C-terminal fragment CP5-11 play a role in activation of antinociceptive system.

[Changes in electric activity of neurons of dorsal raphe nuclei in the development of generator of pathologically enhanced excitation in the nociceptive system]. / Izmeneniia élektricheskoi aktivnosti neironov dorsal'nogo iadra shva pri razvitii generatora patologicheski usilennogo vozbuzhdeniia v notsitseptivnoi sisteme.

In the experiments on rats it was proved by the method of extracellular registration of impulse neuron activity of dorsal raphe nucleus, that the formation of generator of pathologically enhanced excitation (GPEE) in nociceptive structures of spinal brain underlying the pain syndrome of spinal origin, results in a change of electric neuron activity of dorsal raphe nucleus. These changes are manifested by growing number of background nucleus neurons, the increase of middle frequency of discharges, and assuming pack character of impulse activity. These changes are greater marked in a ventral nucleus part, than in a dorsal one, which is evident of the activation of this antinociceptive system structure. The changes of electric activity of dorsal raphe neurons are stable for a long time after GPEE is formed in nociceptive system, and participate in suppression of GPEE and corresponding pain syndrome.

[The effect of substance P on the neuronal activity of the antinociceptive system]. / Vliianie substantsii P na aktivnost' neironov antinotsitseptivnoi sistemy.

The experiments on rats showed that the 1 micrograms substance P injection to dorsal raphe nucleus caused prolonged (24 hours of study) analgetic effect--it enhances the reaction latent period to thermal nociceptive stimulation, intensifies the background impulse activity, rises the middle frequency of neuron discharges and creates high-frequency neurons as well as the neurons with burst impulse activity. The supposition is being confirmed that the mechanism of antinociceptive structures activation leads to analgesia caused by substance P.

[Effects of substance P and its fragments in physiological and pathological pain]. / Vliianie substantsii P i ee fragmentov na fiziologicheskuiu i patologicheskuiu bol'.

It has been shown that substance P and its fragments can produce under certain conditions an analgetic effect on both physiological and pathological pain (i.e. on pain syndrome of spinal origin). The data obtained give evidence that prolonged hypoalgesia is caused by the injection of substance P and its fragments to nucleus raphe dorsal--a structure of the antinociceptive system. This analgetic effect can be initiated by the activation of the antinociceptive system influenced by substance P and or its fragments.

[Effect of the spinal pain syndrome on pain reactions caused by nociceptive thermal stimuli]. / Vliianie bolevogo sindroma spinal'nogo proiskhozhdeniia na bolevye reaktsii, vyzvannye notsitseptivnym termicheskim vozdeistviem.

It has been shown that the reaction of both limbs to thermal pain stimulation was suppressed during spinal pain syndrome development caused by generators of pathologically enhanced excitation (GPEE) formed in the dorsal horns of the spinal cord lumbosacral segments on one side. The analgetic effect on physiological pain was retained long after pain syndrome disappearance (48 hours), the effect was bilateral and was independent of the type of agent producing GPEE. It was shown that neuronal activity in the antinociceptive system key structure (nucleus raphe dorsal) increases. It is assumed that physiological pain relief is caused by enhanced activity in antinociceptive system structures in pain syndrome.

[Analysis of the associative properties of visual cortex neurons in the local joint action of mediators]. / Analiz assotsiativnykh svoistv neironov zritel'noi kory pri lokal'nom sochetannom deistvii mediatorov.

The neuronal spike activity in the visual cortex of awake nonanesthetized rats during paired local action of glutamate and acetylcholine has been investigated. In some neurons the specific associative activity modifications were recorded in form of chemosensitivity changes to the analog of conditioned stimulus (1-glutamate) mainly. The initial reactivity of neurons to the paired stimuli is not enough to form the associative effects.