The Organization of CRF Neuronal Pathways in Toads: Evidence that Retinal Afferents Do Not Contribute Significantly to Tectal CRF Content

2010 ◽  
Vol 76 (1) ◽  
pp. 71-86 ◽  
Author(s):  
James A. Carr ◽  
Jacob Lustgarten ◽  
Nafisa Ahmed ◽  
Nicholas Bergfeld ◽  
Sarah E. Bulin ◽  
...  
Keyword(s):  
Retinal Afferents

scholarly journals Minireview: The Circadian Clockwork of the Suprachiasmatic Nuclei—Analysis of a Cellular Oscillator that Drives Endocrine Rhythms

Endocrinology ◽  
2007 ◽  
Vol 148 (12) ◽  
pp. 5624-5634 ◽  
Author(s):  
Elizabeth S. Maywood ◽  
John S. O’Neill ◽  
Johanna E. Chesham ◽  
Michael H. Hastings
Keyword(s):  
Neural Circuits ◽  
Clock Genes ◽  
Time Base ◽  
Suprachiasmatic Nuclei ◽  
Dark Cycle ◽  
Cellular Mechanisms ◽  
Circadian Control ◽  
Daily Cycles ◽  
Central Clock ◽  
Retinal Afferents

The secretion of hormones is temporally precise and periodic, oscillating over hours, days, and months. The circadian timekeeper within the suprachiasmatic nuclei (SCN) is central to this coordination, modulating the frequency of pulsatile release, maintaining daily cycles of secretion, and defining the time base for longer-term rhythms. This central clock is driven by cell-autonomous, transcriptional/posttranslational feedback loops incorporating Period (Per) and other clock genes. SCN neurons exist, however, within neural circuits, and an unresolved question is how SCN clock cells interact. By monitoring the SCN molecular clockwork using fluorescence and bioluminescence videomicroscopy of organotypic slices from mPer1::GFP and mPer1::luciferase transgenic mice, we show that interneuronal neuropeptidergic signaling via the vasoactive intestinal peptide (VIP)/PACAP2 (VPAC2) receptor for VIP (an abundant SCN neuropeptide) is necessary to maintain both the amplitude and the synchrony of clock cells in the SCN. Acute induction of mPer1 by light is, however, independent of VIP/VPAC2 signaling, demonstrating dissociation between cellular mechanisms mediating circadian control of the clockwork and those mediating its retinally dependent entrainment to the light/dark cycle. The latter likely involves the Ca2+/cAMP response elements of mPer genes, triggered by a MAPK cascade activated by retinal afferents to the SCN. In the absence of VPAC2 signaling, however, this cascade is inappropriately responsive to light during circadian daytime. Hence VPAC2-mediated signaling sustains the SCN cellular clockwork and is necessary both for interneuronal synchronization and appropriate entrainment to the light/dark cycle. In its absence, behavioral and endocrine rhythms are severely compromised.

Demonstration of retinal afferents in the RCS rat, with reference to the retinohypothalamic projection and suprachiasmatic nucleus

1995 ◽  
Vol 282 (3) ◽  
pp. 473-480 ◽  
Author(s):  
Karin Decker ◽  
Ursula Disque-Kaiser ◽  
Mathias Schreckenberger ◽  
Stefan Reuss
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Rcs Rat ◽  
Retinal Afferents

scholarly journals Modeling Development in Retinal Afferents: Retinotopy, Segregation, and EphrinA/EphA Mutants

PLoS ONE ◽  
2014 ◽  
Vol 9 (8) ◽  
pp. e104670 ◽  
Author(s):  
Keith B. Godfrey ◽  
Nicholas V. Swindale
Keyword(s):  
Retinal Afferents

An in vitro study of retinotectal transmission in the chick: Role of glutamate and GABA in evoked field potentials

1996 ◽  
Vol 13 (4) ◽  
pp. 747-758 ◽  
Author(s):  
J. C. Dye ◽  
H. J. Karten
Keyword(s):  
Optic Nerve ◽  
Field Potential ◽  
In Vitro Study ◽  
Bipolar Electrode ◽  
Field Potentials ◽  
Negative Wave ◽  
Evoked Field Potentials ◽  
Thin Slices ◽  
Retinal Afferents

AbstractWe have developed two brain slice preparations for studying tectofugal visual pathways in the chick: conventional, 400-μm slices (“thin slices”), and “thick slices” which encompass the rostral pole of the optic tectum and the contralateral optic nerve. Stimulation was delivered with a bipolar electrode positioned in stratum opticum in thin slices and in the contralateral optic nerve in thick slices. While the latter preparation provided a means of exclusively and unambiguously activating retinal afferents, several lines of evidence also indicated that the evoked field potentials in thin slices were chiefly consequent to retinal afferent excitation: (1) the similarity of evoked field potentials in thin slices to those in thick slice preparations; (2) their precise localization in retinorecipient layers as shown by prelabeling from retina with FITC-coupled cholera toxin; (3) transmission delays appropriate for retinal afferents as established with the thick slice preparation; (4) patterns of labeled afferents resulting from applications of Dil crystals to slices fixed after recording; and (5) the similarity in transmitter pharmacology between thin and thick slice preparations. Pharmacological manipulations carried out with bath-applied antagonists indicated that glutamate is the principal retinotectal transmitter. The broadly active glutamate receptor blocker, kynurenic acid, reversibly eliminated the postsynaptic component of the field potential as confirmed with 0 Ca2+ saline. A complete block was also effected by the non-NMDA antagonists CNQX and DNQX. The specific NMDA antagonist, APS, caused a smaller and variable reduction in response amplitude. The GABA antagonist, bicuculline, caused a prolongation of the monosynaptic field epsp in retinorecipient layers and an enhancement of the long-latency, negative wave in cellular layers below, supporting a late, excitation-limiting role for this inhibitory transmitter.

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