Research reportEffects of excitatory amino acid transmitters on hypothalamic corticotropin-releasing hormone (CRH) and arginine-vasopressin (AVP) release in vitro: implications in pituitary-adrenal regulation
References (27)
- et al.
Effects of serotonergic agonists and antagonists on corticotropin-releasing hormone secretion by explanted rat hypothalami
Peptides
(1989) - et al.
Anatomical organization of excitatory amino acid receptors and their pathways
Trends Neurosci.
(1987) Modulation of oxytocin and vasopressin release from rat neurosecretosomes: the roles of VIP, oxytocin and GABA
Neuropeptides
(1991)- et al.
Region-selective stress-induced increase of glutamate uptake and release in rat forebrain
Brain Res.
(1990) - et al.
Quantitative mapping of glutamate presynaptic terminals in the supraoptic nucleus and surrounding hypothalamus
Brain Res.
(1993) - et al.
Hypothalamic site of action for N-methyl-d-aspartate (NMDA) on LH secretion
Life Sci.
(1988) - et al.
Application of glutamic acid and substance P to the substantia nigra modulates in vivo [3H]serotonin release in the basal ganglia of the cat
Brain Res.
(1982) - et al.
Neuroactive amino acids influence gonadotropin output by a suprapituitary mechanism in either rodents or primates
Brain Res.
(1983) - et al.
Agonists and antagonists for excitatory amino acid receptors
Trends Neurosci.
(1987) - et al.
Acute effects of N-methyl-DL-aspartate on the release of pituitary gonadotropins and prolactin in the adult female monkey
Brain Res.
(1982)
Contrasting actions of amino acids, acetylcholine, noradrenaline and leucin enkephalin on the excitability of supraoptic vasopressin-secreting neurons
Neuroendocrinology
In vivo evidence for an inhibitory glutamatergic control of serotonin release in the cat caudate nucleus: involvement of GABA neurons
Brain Res.
Direct activation of gonadotropin-releasing hormone secretion through different receptors to neuroexcitatory amino acids
Neuroendocrinology
Cited by (31)
Riluzole and d-amphetamine interactions in humans
2008, Progress in Neuro-Psychopharmacology and Biological PsychiatryGlutamate agonists activate the hypothalamic-pituitary-adrenal axis through hypothalamic paraventricular nucleus but not through vasopressinerg neurons
2005, Brain ResearchCitation Excerpt :The primary site of action of glutamate has been suggested to be at the level of the hypothalamus via the control of hypothalamic releasing factors. According to this suggestion in in vitro studies, EAA could influence CRH and AVP secretion from hypothalamic slides [13,24,41]. However, ACTH release could be evoked with EAA injection into other brain regions as well (dorsomedial hypothalamus in rat [5], locus coeruleus and dorsal rostral pons of cat [10,11], nucleus trigeminus caudalis in cat [6]).
Chapter 4.7 Modulation of glutamatergic and GABAergic neurotransmission by corticosteroid hormones and stress
2005, Techniques in the Behavioral and Neural SciencesCitation Excerpt :Regarding in vitro studies, conflicting results have been reported. One study showed that a glutamate agonist increases the amount of ACTH secretagogues but others found a decrease or no effect (Costa et al., 1992; Patchev et al., 1994; Joanny et al., 1997, 2000). Furthermore, so far little information exists regarding modulation of glutamate transmission by stress.
Dynorphin and the hypothalamo-pituitary-adrenal axis during fetal development
2003, Life SciencesCitation Excerpt :The HPA axis is controlled by a classical feedback system in which glucocorticoids interact with glucocorticoid receptors in the hypothalamus and pituitary to inhibit further ACTH release. Furthermore, the release of these hypothalamic secretagogues is influenced by a number of neurotransmitters and neuropeptides, including the endogenous opioid peptides and excitatory amino acids (Brann and Mahesh, 1992; Patchev et al., 1994). The fetal HPA axis is well-developed in late gestation in many mammalian species and has been extensively studied in the ovine fetus (Matthews and Challis, 1996).
Parts of this study have been presented in abstract form at the NIH Research Festival, September, 1991.