Regulation of c-Fos gene expression in the rat olfactory bulb during olfactory learning.

An immunohistochemical method was used to study the expression of transcription factor c-Fos in the mid part of the main olfactory bulbs in 18-day-old rats after training to seek their mothers using an olfactory orientation cue (propionic acid) in a Y-maze. On the next day, rat pups demonstrated a significant preference for the propionic acid odor in behavioral tests, as compared with control animals trained to the skill without the olfactory orientation cue and pups familiarized with the odor without forming any association between it and any kind of reinforcement. The propionic acid odor evoked an insignificant increase in c-Fos expression, predominantly in the granular layer of the dorsomedial area of the olfactory bulb. Training in a maze lacking the odor signal evoked diffuse activation of c-Fos, in both the mitral and granular layers of all areas of the olfactory bulb. Training with the olfactory orientation cue was also accompanied by an increase in c-Fos expression to a level significantly exceeding that seen after odor-free training, in the granular layer of the dorsomedial area, i.e., the area in which the unreinforced odor acting alone induced insignificant activation of expression. These data provide evidence that, at the level of the regulation of neuronal transcription, associative learning is manifest as summation of the effects of a new neutral stimulus and excitation initiated by the motivational state. In the olfactory bulb, this summation is seen in areas on which non-specific centrifugal excitation and specific afferentation from the signal odor converge.

[Regulation of c-Fos expression in the rat olfactory bulbs during olfactory learning].

The distribution of c-Fos-immunopositive neurons was examined in the mitral/tufted and granular cell layers in the medium part of the main olfactory bulbs of 18-day-old rats after they had been trained for propionic acid vapour-guided search for dam in the Y-maze. On the next day these pups exhibited a strong preference for the propionic acid odor as compared to the control pups trained for this task without the odor cue and odor-familiarized pups exposed to propionic acid as a novel neutral stimulus. Exposure to propionic acid produced a moderate activation of c-Fos expression, mainly in the granular layer of the dorsomedial part of the bulb. Training in the Y-maze devoid of odor cues resulted in diffuse increase in the number of c-Fos-positive neurons both in the mitral and granular cell layers in all parts of the olfactory bulb. Maze training with the odor cue produced activation of c-Fos expression (which significantly exceeded the non-odor Y-maze group) in the dorsomedial olfactory bulb. These data suggest that associative olfactory conditioning results in activation of c-Fos expression that combines the effect of diffuse motivational excitation and specific olfactory input to the neurons which process odor cues.

Comparative analysis of dipsogenic effects of systemic and intracerebral injection of angiotensin II to rats after carotid glomectomy.

Systemic administration of angiotensin II after carotid glomectomy produced a less pronounced dipsogenic effects (consumption of water and NaCl solution) compared to sham-operated control animals. Injection of angiotensin II into the lateral cerebral ventricles of the same glomectomized rats increased water and NaCl consumption to a level surpassing that of sham-operated animals. The number of drinking acts and comfortable grooming acts decreased in glomectomized animals after systemic administration of angiotensin II, but increased after its intracerebral injection compared to the control. The results confirm the hypothesis that carotid chemoreceptors, as the peripheral component of the renin-angiotensin system, participate in the mechanisms of angiotensin-induced thirst, "salt appetite", and associated behavioral forms (comfortable grooming) synergically with the central cerebral receptors.

Formation of taste aversion and preference in protein synthesis inhibition in rats.

The investigation was devoted to the role of the synthesis of protein and peptide factors during the formation of chemosensory memory in rats. Two models of gustatory memorization were used: conditioned taste aversion (CTA), induced by the association of the taste of saccharine with a toxic injection of lithium chloride, and enhanced taste preference (ETP), induced by the influence of preliminary drinking of a saccharine solution on its repeat consumption. It was found that, under conditions of the inhibition of protein synthesis in the brain of 43% by cycloheximide and of 59% by 8-azaguanine, CTA does not form. ETP does not form under the influence of cycloheximide, but not [sic] of 8-azaguanine. A hypothesis was advanced regarding the participation of a varied spectrum of protein and peptide substances in the formation of taste aversion and preference. An influence of protein synthesis blockers on the process of retrieval of gustatory memory was not found.

[The formation of taste aversion and preference under conditions of protein synthesis inhibition in rats]. / Formirovanie vkusovogo otverganiia i predpochteniia v usloviiakh ingibirovaniia sinteza belka u krys.

The study is devoted to the role of protein synthesis in formation of chemosensory memory in rats. Two experimental models of taste memorizing were used, i.e., conditioned taste aversion (CTA) caused by association of succharin intake with being poisoned by lithium chloride, and increased taste preference (ITP) caused by the influence of primary consumption of succharin solution on its repeated intake. It was found out that CTA was not formed under conditions both of 43% inhibition of brain protein synthesis by cycloheximide and of 59% its inhibition by 8-azaguanine. Cycloheximide but not 8-azaguanine prevented formation of ITP. A proposal was made about participation of different spectra of protein and peptide molecules in formation of taste aversion and preference. The effect of protein synthesis inhibitors on the process of taste memory retrieval was not found.