Behavioral effects of para-chlorophenylalanine in gonadectomized male rats.

Para-chlorophenylalanine restores impaired conditioning and retention of active avoidance reaction in castrated animals and improved their behavior in the open field test.

The effects of peripheral endocrine hormone deficiencies on the processes of behavior, learning, and memory.

The effects of thyroid and adrenal cortex hormone and sex hormone deficiencies on the ability to learn, store memory traces, and behave were compared in male rats. These studies showed that removal of peripheral endocrine glands led to disruption of the learning process and the ability to reproduce learned information and also produced alterations in behavior. Analysis of the results showed that corticosteroid hormones are directly involved in the processes of learning and behavior. Sex and thyroid hormones appear to have modulatory effects on higher nervous activity.

The effects of the hormones of peripheral endocrine glands on the processes of behavior, learning, and memory.

The effects of systemic administration of thyroid, adrenal cortex, and sex hormones on learning ability, memory trace retention, and behavior were compared in male rats. These studies showed that thyroid, corticosteroid, and sex hormones had no effect on passive learning. Excess quantities of sex hormones disrupted active learning and subsequent reproduction of received information; an excess of thyroid hormone improved the acquisition and retention of the active avoidance habit. Increases in the levels of adrenal cortex hormones worsened active learning and the retention of memory traces, and also increased the level of behavioral activity.

Effect of L-tryptophan on active avoidance response in male rats with increased testosterone level.

The effects of L-tryptophan on acquisition and extinction of active avoidance response and open field behavior were studied in male rates with elevated testosterone content. L-tryptophan improved learning in rats with elevated androgen content without affecting their behavior.

The effect of taurine derivative on lipid peroxidation and interhemispheric asymmetry of phospholipids from the brain synaptosomes in rats after immobilization stress.

Malondialdehyde (MDA) as an indicator of lipid peroxidation (LPO), content and composition of phospholipids (PL) were analyzed in synaptosomes of the rat brain hemispheres using immobilization stress without and with pretreatment with a new synthetic taurine derivative (STD). The stress was accompanied by a decrease MDA content, inversion of the initial asymmetry of total phospholipids (TPL) and modification PL composition in the brain hemispheres of rats. STD administration to the rats after stress antagonized the decrease of the MDA level, attenuates stress induced inversion TPL asymmetry and normalized PL composition in the brain hemispheres. Prevention or diminution of synaptosomal PL changes in the rat brain hemispheres are interpreted as one of the possible mechanisms of the neuroprotective effect of STD.

Comparative characteristics of learning and behavior processes in conditions of elevated sex hormone levels.

The effects of elevated levels of sex hormones resulting from systemic administration of hormone preparations on the abilities to learn and retain memory traces and on behavior were studied in rats of both sexes. Experiments were performed using models of conditioned active and passive avoidance reflexes and in the "open" field test. Increases in testosterone and estradiol levels had no effect on passive learning. Increases in testosterone levels in male rats led to derangement of active learning but had no effect on animal behavior. Elevated estradiol levels in female rats accelerated active learning and increased the animals' behavioral activity.

Meiotic mutants of rye Secale cereale L. II. The nonhomologous synapsis in desynaptic mutants sy7 and sy10.

We studied the expression and inheritance of two spontaneous mutations found in different populations of rye Secale cereale L. that cause high univalent frequency in meiosis and low fertility. Both mutations were inherited as monogenic recessives. For each of the mutations the corresponding gene symbols (sy7 and sy10) were suggested although their allelism has not been studied. These mutants differ in chiasma frequency and in the number of univalents per meiocyte. Electron microscopy of the wholemount surface-spread synaptonemal complexes (SCs) from microsporocytes of both mutants revealed that during meiotic prophase I random synapsis began and progressed that involved not only homologous but also nonhomologous chromosomes. SCs were formed with frequent changes of pairing partners (switches) and intrachromosomal foldbacks of unpaired axial elements. As a result, incompletely synapsed, non-homologous and multivalent SCs were formed in mutants by the stage analogous to pachytene in normal plants. In sy7 a maximum in the number of switches and foldbacks were observed at zygotene, whereas in sy10 this occurred at pachytene. We suggest that it is the process of recognition of homology that is impaired in both mutants. This leads to indiscriminate synapsis and prevents chiasma formation. Both mutants may be classified as desynaptic.

Meiotic mutants of rye Secale cereale L. : I. Synaptic mutant sy-1.

A mutant form of weedy rye characterized by male and female sterility and having a hereditary block in the chromosome synapsis has been found and described. Genetic analysis has shown the synapsis block to be determined by the recessive allele of a gene designated as sy-1. Electron microscopy of surface-spread microsporocyte nuclei revealed the complete absence of the synaptonemal complex over the whole meiotic prophase I, although the axial cores were perfectly formed by each chromosome. Only univalents were observed at metaphase I, their average number ranging from 13.1 to 14.0 per cell. A precocious distribution of univalents at the poles is observed at metaphase I. All of the later stages of meiosis were irregular and resulted in the formation of abnormal microspores. Thus, the mutant proves to be asynaptic because of the blocked initiation of synapses at prophase I.