Brain research
-
When two brief flashes presented in rapid succession (<100 ms apart) are paired with a single auditory stimulus, subjects often report perceiving only a single flash [Andersen, T. S., Tiippana, K., Sams, M., 2004. Factors influencing audiovisual fission and fusion illusions. ⋯ PD180 was found to covary in amplitude across subjects with the visual evoked N1 component (148-184 ms), suggesting that inter-individual differences in perceiving the illusion are based at least in part on differences in visual processing. A trial-by-trial analysis found that the PD180 as well as a subsequent modulation in visual cortex at 228-248 ms was diminished on trials when the two flashes were perceived as one relative to trials when two flashes were correctly reported. These results suggest that the sound induced flash fusion is based on an interaction between polysensory and visual cortical areas.
-
The sphenopalatine ganglia (SPG) receive their preganglionic innervation from the ventro-lateral reticular formation and nuclei of the caudal pons, and are involved in parasympathetic control of cranial glandular and vascular components including the blood supply to specific brain areas. In 53% of all SPG neurons, a particular member (MOL2.3) of the odorant receptor superfamily is co-expressed with green fluorescent protein (GFP) in MOL2.3 transgenic mouse pups. Choline acetyltransferase and vesicular acetylcholine transporter (VAChT) could be demonstrated in 90% of the GFP-positive, and 60% of the GFP-negative cells, these cells thus representing cholinergic neurons. ⋯ Inhibition of cholinergically induced intracellular calcium signalling by various omega-conotoxins indicated functional expression of alpha 3 beta 4 and alpha 7 nAChR subtypes in murine SPG cells, which could be supported by RT-PCR analysis of the neonatal mouse SPG. With regard to secondary cholinergic activation, L- but not N-subtype voltage-gated calcium channels might represent a prime target. Nicotinic signal transduction did not prove to be different in GFP-positive as compared to-negative murine SPG neurons.
-
The central nucleus of the amygdala (CeA), the nociceptive amygdala, serves as the major output nucleus of the amygdala and participates in receiving and processing pain information. Considering the abundance of GABA(A) receptors in the CeA and also the attributed bidirectional roles for GABA in controlling nociception, we examined the effects of bilateral intra-CeA microinjection of a different dose of the GABA(A) receptor agonist, muscimol, and the GABA(A) receptor antagonist, bicuculline, on pain modulation using a tail-flick test. Adult rats were exposed to intra-CeA microinjection of a selective GABA(A) receptor antagonist, bicuculline, (50,100,200,400 ng/side) or a selective GABA(A) receptor agonist, muscimol, (62.5, 125,250,500 ng/side) and subjected to the tail-flick test. ⋯ Microinjection of bicuculline and muscimol into the CeA increased and decreased tail-flick latency, respectively in a dose-dependent fashion. The hyperalgesic effect of muscimol (500 ng) microinjected into the CeA was attenuated (P<0.001) by a prior microinjection of bicuculline (50 ng) at the same site. The results of the present study showed that locally released GABA in the CeA is involved in pain modulation and suggests the existence of a GABA(A) mediated inhibitory system in the CeA on pain control.
-
We investigated the profile of CART immunoreactivity in some discrete hypothalamic nuclei following chronic ethanol treatment and withdrawal conditions. Adult, male, Sprague-Dawley rats were fed with liquid diet (pair-fed) or liquid diet containing ethanol (ethanol-fed) for 15 days. Thereafter, all the animals were given access to ethanol free nutritionally balanced liquid diet and killed at 0, 24, 48 and 72 h post-withdrawal, and their brains processed for immunocytochemistry using monoclonal antibodies against CART. ⋯ The immunoreactive profile in the LH, TC and DMH resembled that of the pair-fed groups at 48 and 72 h post-withdrawal intervals. However, CART-immunoreactive profile in the supraoptic nucleus did not respond to the chronic ethanol treatment and/or withdrawal. We suggest that transient up-regulation of CART in some discrete hypothalamic nuclei following ethanol withdrawal, at least in part, may contribute to the pathogenesis of ethanol withdrawal-induced symptoms like anxiety and anorexia.