Functions of ionotropic and metabotropic glutamate receptors in sensory transmission in the mammalian thalamus

Acute Shift in Glutamate Concentrations Following Experimentally Induced Panic with Cholecystokinin Tetrapeptide—A 3T-MRS Study in Healthy Subjects

“…In similarly designed studies using the CCK-4 paradigm, an immediate shift of GABA A -receptor modulating neuroactive steroids after experimentally induced panic was observed in patients with PD (Strohle et al, 2003) and healthy volunteers (Eser et al, 2005), with the latter study suggesting that the significant increase of 3a-5a-tetrahydrodeoxycorticosterone (3a,5a-THDOC) as a positive allosteric modulator of the GABA A -receptor might contribute to the termination of the anxiety response to CCK-4 (Eser et al, 2005). According to Salt and Eaton (1996), GABAergic and glutamatergic neurotransmission seems to be modulated by presynaptic metabotropic glutamate (mGlu) autoreceptors. Moreover, it has also been suggested that neurosteroids, synthesized in cortical glutamatergic neurons, may exert GABAergic activity through autocrine (targeting postsynaptic receptors at the same neuron) and/or paracrine (targeting receptors at distal neurons) mechanisms (Rupprecht et al, 2010).…”

Pharmacological dissection of the paradoxical pain induced by a thermal grill

“…In particular, the role of glutamate and NMDA receptors in spinal and supraspinal transmission, integration and modulation of both nociceptive and non nociceptive somatosensory signals is extensively documented (e.g. Dougherty et al 1992;Salt and Eaton, 1996). The reduction of paradoxical pain induced by ketamine may be a consequence of its action in the spinal dorsal horn and/or in the brain, particularly in the thalamus where there are numerous glutamate receptors, including the NMDA subtype (Salt, 2002).…”

“…The corticofugal inputs to the thalamic sensory relay nuclei also involve glutamate and NMDA receptors (Salt and and Eaton, 1996;Salt, 2002). Thus, the reduction of paradoxical pain by ketamine may be the results of its action on the transmission of somatosensory signals and/or on the cortico-thalamic (top-down) modulation of sensory processes.…”

“…We tested the possible involvement of the glutamatergic and endogenous opioid systems, because these neurotransmitter systems are widely expressed throughout the somatosensory systems and are involved in the transmission and modulation of pain signals (Salt and Eaton, 1996;Bodnar and Klein, 2003;Fundytus, 2001). We analyzed the effects of two treatments on paradoxical burning pain, normal (physiological) thermal pain and non painful thermal sensations induced by a thermal grill: the treatments were the N-methyl-D-aspartate (NMDA) receptor antagonist, ketamine, and the opioid receptor antagonist, naloxone, administered intravenously according to a randomized, double-blind, placebocontrolled, cross-over design.…”

Serotonin as a Modulator of Glutamate- and GABA-Mediated Neurotransmission: Implications in Physiological Functions and in Pathology

“…Glutamate-and GABA-mediated effects can also be modulated by 5-HT at a post-synaptic site; the mechanisms of interaction have been elucidated in some cases and include: 1) recruitment of receptors on the post-synaptic membrane [104]; 2) modulation of receptor function by promoting its phosphorylation [49,103,191]; 3) effects converging on a common signaling pathway, such as a G protein [6,144], adenylate cyclase [169] or phospholipase C [147]; 4) modulation of a common membrane ion channel [54,169]; 5) effects on distinct ion channels, reciprocally influencing membrane potential and neuronal excitability [2,46,154,155,161].…”