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At least 199 records · Page 11Linked to original sources
PubMed1989

Neural systems involved in fear-potentiated startle.

The acoustic startle reflex offers a number of advantages for analyzing the neural bases of behavior. Startle apparently is mediated by excitatory amino acids at several of the synapses that comprise the short-latency startle pathway. The reflex is modulated by a variety of neurotransmitters at both the spinal and the supraspinal levels. In addition to showing habituation and sensitization, startle is increased in the presence of a fear stimulus. This may result from activation of the central nucleus of the amygdala which projects directly tot he acoustic startle pathway. A major challenge for future studies will be to determine what neurotransmitters, which are known to modulate startle, are involved in habituation, sensitization, and fear conditioning and to begin to analyze these processes at a cellular level.

Amygdala↗
PubMed1983

Induction of chromosome aberrations by chemical mutagens in neural ganglia of Drosophila melanogaster.

Chromatid aberrations induced by various concentrations of bleomycin, cyclophosphamide and mitomycin C were analyzed in neural ganglia of third-instar larvae of Drosophila melanogaster. A clear dose response was observed with increasing dose after treatment with bleomycin and mitomycin C, whereas no effect was observed after treatment with cyclophosphamide. A comparison with published data for the induction of sex-linked recessive lethals showed that, at least for the 3 drugs tested, the use of both tests eliminates false negatives and might comprise a useful procedure for testing mutagenicity in Drosophila.

Animals↗
PubMed1992

Corticotropin-releasing factor: long-lasting facilitation of the acoustic startle reflex.

Intracerebroventricular infusion of corticotropin-releasing factor (CRF) (0.1-1.0 micrograms) produced a pronounced, dose-dependent enhancement of the acoustic startle reflex in rats. This excitatory effect began about 20-30 min after infusion, grew steadily over the 2 hr test period, and lasted at least 6 hr. Higher doses of CRF (10 micrograms) often produced marked facilitation and then inhibition of startle that oscillated repeatedly with a period of 10-20 min. CRF-enhanced startle did not result from an increase in sensitization produced by repetition of the startle stimulus or from a blockade of habituation. Peripheral injections of the autonomic ganglionic blockers hexamethonium (10 mg/kg) or chlorisondamine (3 mg/kg) slightly attenuated the magnitude of CRF-enhanced startle, suggesting a partial role of peripheral sympathetic activation. Intracerebroventricular infusion of the CRF antagonist alpha-helical CRF9-41 (alpha hCRF; 25 or 50 micrograms) blocked CRF-enhanced startle when infused 5 min prior to CRF, indicating a central site of action. CRF-enhanced startle also was reversed when alpha hCRF was given 90 min after infusion of CRF. This suggests that exogenously applied CRF remains in the brain for a very long time after administration or that CRF given exogenously initiates a process that results in a long-lasting activation of endogenous CRF. Because the startle reflex is elevated by both conditioned and unconditioned fear, these data lend further support to the idea that CRF infusion produces a behavioral state that resembles fear or anxiety. Because startle is mediated by a well-defined neural pathway, CRF-enhanced startle may provide a useful behavioral assay to analyze the neural systems upon which exogenous CRF acts to produce its behavioral effects.

Acoustic Stimulation↗