Roles of periventricular neurons in retinotectal transmission in the optic tectum

2006 ◽  
Vol 79 (2) ◽  
pp. 112-121 ◽  
Author(s):  
Masae Kinoshita ◽  
Etsuro Ito

2005 ◽  
Vol 484 (2) ◽  
pp. 249-259 ◽  
Author(s):  
Masae Kinoshita ◽  
Masahiro Fukaya ◽  
Takuro Tojima ◽  
Satoshi Kojima ◽  
Hironori Ando ◽  
...  




Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 637
Author(s):  
Nicholas S. Moore ◽  
Robert A. Mans ◽  
Mackenzee K. McCauley ◽  
Colton S. Allgood ◽  
Keri A. Barksdale

Evidence from human and animal studies indicate that disrupted light cycles leads to alterations of the sleep state, poor cognition, and the risk of developing neuroinflammatory and generalized health disorders. Zebrafish exhibit a diurnal circadian rhythm and are an increasingly popular model in studies of neurophysiology and neuropathophysiology. Here, we investigate the effect of alterations in light cycle on the adult zebrafish brain: we measured the effect of altered, unpredictable light exposure in adult zebrafish telencephalon, homologous to mammalian hippocampus, and the optic tectum, a significant visual processing center with extensive telencephalon connections. The expression of heat shock protein-70 (HSP70), an important cell stress mediator, was significantly decreased in optic tectum of adult zebrafish brain following four days of altered light exposure. Further, pSer473-Akt (protein kinase B) was significantly reduced in telencephalon following light cycle alteration, and pSer9-GSK3β (glycogen synthase kinase-3β) was significantly reduced in both the telencephalon and optic tectum of light-altered fish. Animals exposed to five minutes of environmental enrichment showed significant increase in pSer473Akt, which was significantly attenuated by four days of altered light exposure. These data show for the first time that unpredictable light exposure alters HSP70 expression and dysregulates Akt-GSK3β signaling in the adult zebrafish brain.



1991 ◽  
Vol 146 (2) ◽  
pp. 278-291 ◽  
Author(s):  
Deni S. Galileo ◽  
Adrian P. Gee ◽  
Paul J. Linser
Keyword(s):  


2001 ◽  
Vol 18 (4) ◽  
pp. 549-558 ◽  
Author(s):  
A. KURAS ◽  
N. GUTMANIENĖ

Nicotinic acetylcholine receptors are localized on retinotectal axons' terminals in lower vertebrates. The effects of activation of these receptors by endogenous acetylcholine were observed under stimulation of mass optic fibers. This study was designed to determine whether endogenous acetylcholine facilitates frog retinotectal transmission, provided only the synapses of an individual optic axon are activated, and to evaluate the feasible extent of nicotinic facilitation in these synapses by applied agonist. To this end, the effects of cholinergic drugs on the extracellular action and synaptic potentials recorded from the terminal arborization of a separate retinotectal fiber (in layer F of the tectum) were investigated in vivo. Glutamatergic nature of retinotectal synapses was reexamined by treatment with kynurenic acid. Both kynurenic acid (0.25–1 mM) and d-tubocurarine chloride (10–15 μM) significantly depressed the synaptic potentials. Carbamylcholine chloride (50–150 μM) evoked a large augmentation of the synaptic potentials and a slight but statistically significant decrease of the action potentials. D-tubocurarine reduced the effect of carbamylcholine. Pilocarpine hydrochloride (50 μM) had only a weak effect. The paired-pulse facilitation of the synaptic potentials changed significantly under the action of carbamylcholine and d-tubocurarine. The obtained results suggest that the glutamate release from activated synapses of individual retinotectal axons is facilitated by endogenous acetylcholine via presynaptic nicotinic receptors. Under used stimulation conditions, this modulation mechanism was employed only partially since its activation by applied carbamylcholine could enhance synaptic transmission up to 2.8 times.





1986 ◽  
Vol 370 (2) ◽  
pp. 365-369 ◽  
Author(s):  
N. Tumosa ◽  
W.K. Stell ◽  
C.D. Johnson ◽  
M.L. Epstein


1991 ◽  
Vol 307 (2) ◽  
pp. 335-349 ◽  
Author(s):  
M. Jes�s Manso ◽  
Ram�n Anadon
Keyword(s):  


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