1993
DOI: 10.1016/0006-8993(93)91665-f
|View full text |Cite
|
Sign up to set email alerts
|

Glutamate immunoreactivity in terminals of the retinohypothalamic tract of the brown Norwegian rat

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1

Citation Types

2
46
0
1

Year Published

1995
1995
2005
2005

Publication Types

Select...
10

Relationship

0
10

Authors

Journals

citations
Cited by 116 publications
(51 citation statements)
references
References 28 publications
2
46
0
1
Order By: Relevance
“…The putative photopigment, melanopsin, and the neurotransmitters, glutamate and pituitary adenylate cyclase-activating polypeptide (PACAP), are thought to mediate the communication of light information to the SCN because (1) melanopsin is distinctly localized in retinal ganglion cells that are endogenously responsive to light (Hattar et al, 2002); (2) glutamate and PACAP have been identified as the principal neurotransmitters of the RHT (De Vries et al, 1993;Hannibal et al, 2000;van den Pol, 1993); (3) transgenic deletion of genes encoding melanopsin, PACAP, and PACAP receptors influences the phase-shifting responses of the murine circadian clock to light (Colwell et al, 2004;Hannibal et al, 2001;Harmar et al, 2002;Ruby et al, 2002); and (4) infusion of glutamate or PACAP into the SCN phase shifts circadian rhythms in a manner comparable to light (Harrington et al, 1999;Meijer et al, 1988). Thus, neonatal EtOH exposure may chronically increase both the entraining and phaseshifting effects of light on the SCN clock by enhancing melanopsin-mediated phototransduction or by potentiating glutamate and/or PACAP function in the communication of photic signals to the SCN.…”
Section: Discussionmentioning
confidence: 99%
“…The putative photopigment, melanopsin, and the neurotransmitters, glutamate and pituitary adenylate cyclase-activating polypeptide (PACAP), are thought to mediate the communication of light information to the SCN because (1) melanopsin is distinctly localized in retinal ganglion cells that are endogenously responsive to light (Hattar et al, 2002); (2) glutamate and PACAP have been identified as the principal neurotransmitters of the RHT (De Vries et al, 1993;Hannibal et al, 2000;van den Pol, 1993); (3) transgenic deletion of genes encoding melanopsin, PACAP, and PACAP receptors influences the phase-shifting responses of the murine circadian clock to light (Colwell et al, 2004;Hannibal et al, 2001;Harmar et al, 2002;Ruby et al, 2002); and (4) infusion of glutamate or PACAP into the SCN phase shifts circadian rhythms in a manner comparable to light (Harrington et al, 1999;Meijer et al, 1988). Thus, neonatal EtOH exposure may chronically increase both the entraining and phaseshifting effects of light on the SCN clock by enhancing melanopsin-mediated phototransduction or by potentiating glutamate and/or PACAP function in the communication of photic signals to the SCN.…”
Section: Discussionmentioning
confidence: 99%
“…Previous studies have indicated that excitatory amino acids may be involved in photic entrainment of circadian rhythms and melatonin production (Cowell et al 1991;Ohi et al 1993;Poeggeler et al 1995). Further studies have shown that glutamate, the dominant excitatory neurotransmitter in the central nervous system, mediates photic entrainment (DeVries et al 1993). Pharmacological studies have revealed that antagonists of postsynaptic receptors that mediate the actions of this neurotransmitter block the light induced suppression of melatonin (Cowell et al 1991;Ohi et al 1993).…”
Section: Discussionmentioning
confidence: 99%
“…GLU was targeted as a potential RHT neurotransmitter following a series of studies that (1) found GLU receptors in the SCN (Nishino & Koizumi, 1977;; (2) located GLU in the RHT (Castel eta/., 1993;de Vries et a/., 1993;van den Pol, 1991); (3) determined that GLU was released following optic nerve stimulation ; (4) showed GLU release in the SCN via optic nerve stimulation resulted in phase dependent resetting, mimicking the effects of light (de Vries et a/., 19194); and (5) established that prior bath application of Kynurenate, an excitatory amino acid (EAA) antagonist, blocked phase shifts to optic nerve stimulation (Cahill & Menaker, 1987). GLU's role in photic :signalling was clouded, however, by results from an in vivo study showing that GLU injedions directly into the SCN resulted in phase shifts that differed from those to light (Meijer et a/., 1988).…”
Section: Glutamate and The Rhtmentioning
confidence: 99%