scholarly journals GABAB receptor modulation of synaptic function

2011 ◽  
Vol 21 (2) ◽  
pp. 339-344 ◽  
Author(s):  
Jason R Chalifoux ◽  
Adam G Carter
Keyword(s):  
Gabab Receptor ◽  
Synaptic Function ◽  
Receptor Modulation

Effects of μ-Opioid Receptor Modulation on GABAB Receptor Synaptic Function in Hippocampal CA1

2007 ◽  
Vol 97 (3) ◽  
pp. 2301-2311 ◽  
Author(s):  
A. Rory McQuiston
Keyword(s):  
Gabab Receptor ◽  
Gaba Release ◽  
Excitatory Input ◽  
Synaptic Function ◽  
Stratum Radiatum ◽  
Stratum Pyramidale ◽  
Receptor Modulation ◽  
Excitatory Activity ◽  
Hippocampal Ca1 ◽  
Cgp 55845

Activation of μ-opioid receptors (MORs) alters information coding, synaptic plasticity, and spatial memory in hippocampal CA1. In CA1, MORs act by inhibiting GABA release onto both GABAA and GABAB receptors exclusively. MOR activation can facilitate excitatory inputs in CA1 dendritic layers by inhibiting synaptic activation of GABAA receptors. In this study, we use voltage-sensitive dye imaging to show that MOR activation by the MOR agonist DAMGO suppressed GABAB inhibitory postsynaptic potentials in all layers of CA1. When stimulating excitatory input in stratum oriens (SO), stratum radiatum (SR), or stratum lacunosum-moleculare (SLM) with five pulses at 20 Hz in the presence of bicuculline (50 μM), DAMGO (1 μM) was most effective at increasing the amplitude of the last excitatory event. This effect was reversed by the MOR antagonist CTOP (1 μM) and occluded by the GABAB receptor agonist CGP 55845 (10 μM). DAMGO was less effective at increasing the amplitude of later excitatory events compared with the effect of CGP 55845. DAMGO was relatively ineffective at increasing the amplitude of excitatory inputs in SLM but had significantly greater effects on excitatory events as they propagated to stratum pyramidale (SP). When stimulating in SR, DAMGO was least effective at increasing excitatory amplitudes in SLM and most effective in SP and SO. Finally, DAMGO was equally effective at increasing excitatory activity amplitudes in all layers of CA1 after stimulating in SO. Therefore MOR suppresses GABAB synaptic hyperpolarizations in all layers of CA1 and most effectively facilitates excitatory activity in CA1 output layers.

In vivo andin vitro ethanol exposure in prenatal rat brain: GABAB receptor modulation on dopamine D1 receptor and protein kinase A

Synapse ◽  
2008 ◽  
Vol 62 (7) ◽  
pp. 534-543 ◽  
Author(s):  
H.Y. Lee ◽  
N. Naha ◽  
S.P. Li ◽  
M.J. Jo ◽  
M.L. Naseer ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Rat Brain ◽  
Gabab Receptor ◽  
Ethanol Exposure ◽  
Dopamine D1 Receptor ◽  
D1 Receptor ◽  
Receptor Modulation ◽  
Kinase A

Nitric oxide and cGMP modulate retinal glutamate receptors

1996 ◽  
Vol 76 (4) ◽  
pp. 2307-2315 ◽  
Author(s):  
D. G. McMahon ◽  
L. V. Ponomareva
Keyword(s):  
Nitric Oxide ◽  
Glutamate Receptors ◽  
Horizontal Cell ◽  
Synaptic Function ◽  
Horizontal Cells ◽  
Glutamate Excitotoxicity ◽  
No Donors ◽  
Receptor Modulation ◽  
Cell Recording ◽  
Endogenous Nitric Oxide

1. In the retina, as in other regions of the vertebrate central nervous system, glutamate receptors mediate excitatory chemical synaptic transmission and are a critical site for the regulation of cellular communication. In this study, retinal horizontal cells from the hybrid less were dissociated in cell culture, voltage clamped by the whole cell recording technique, and the currents evoked by application of excitatory amino acids recorded. 2. Responses to glutamate and its agonist kainate were reduced by approximately 50% in the presence of the nitric oxide (NO) donors sodium nitroprusside and S-nitroso-N-acetylpenicillamine. The effect of these compounds was blocked by the NO scavenger hemoglobin. 3. This effect of NO donors on kainate currents could be mimicked by the application of a membrane permeable guanosine 3',5'-cyclic monophosphate (cGMP) analogue, 8-Br-cGMP. The NO effect was also blocked by application of the guanylate cyclase inhibitor LY-83583, and by a protein kinase G inhibitor peptide. 4. In H1-type horizontal cells, stimulation of endogenous nitric oxide synthase with L-arginine reduced kainate responses, whereas application of D-arginine had no effect. 5. This receptor modulation mechanism may act in concert with other pre- and postsynaptic mechanisms to modify horizontal cell synaptic function according to the adaptational state of the retina and also may protect horizontal cells from glutamate excitotoxicity.

GABAB receptor modulation of serotonin neurons in the dorsal raphe nucleus escalates aggression in mice

2010 ◽  
Vol 68 ◽  
pp. e104 ◽  
Author(s):  
Aki Takahashi ◽  
Akiko Shimamoto ◽  
Christopher O. Boyson ◽  
Tsuyoshi Koide ◽  
Joseph F. DeBold ◽  
...  
Keyword(s):  
Dorsal Raphe Nucleus ◽  
Gabab Receptor ◽  
Dorsal Raphe ◽  
Raphe Nucleus ◽  
Receptor Modulation ◽  
Serotonin Neurons ◽  
Dorsal Raphé

GABAB Receptor Modulation of Rapid Inhibitory and Excitatory Neurotransmission From Subfornical Organ and Other Afferents to Median Preoptic Nucleus Neurons

2004 ◽  
Vol 92 (1) ◽  
pp. 111-122 ◽  
Author(s):  
Miloslav Kolaj ◽  
Donglin Bai ◽  
Leo P. Renaud
Keyword(s):  
Gabab Receptor ◽  
Potassium Conductance ◽  
Subfornical Organ ◽  
Receptor Subtypes ◽  
Preoptic Nucleus ◽  
Paired Pulse ◽  
Median Preoptic Nucleus ◽  
Postsynaptic Currents ◽  
Receptor Modulation ◽  
Rat Brain Slice

Cardiovascular and behavioral responses to circulating angiotensin require intact connectivity along the upper lamina terminalis joining the subfornical organ (SFO) with the median preoptic nucleus (MnPO). Whole cell patch-clamp recordings in sagittal rat brain slice preparations revealed that 28/40 MnPO neurons responded to electrical stimulation of SFO efferents with bicuculline-sensitive GABAA receptor-mediated inhibition and glutamate-mediated postsynaptic excitation involving AMPA and N-methyl-d-aspartate (NMDA) receptor subtypes, blockable with 2,3-dioxo-6nitro-1, 2,3,4-tetrahydrobenzo [f] quinoxaline-7-sulfoamide disodium (NBQX) and d-2-amino-4-phosphonovaleric acid (d-APV), respectively. Bath applications of baclofen induced a concentration-dependent (0.3–10 μM) reduction in these SFO-evoked postsynaptic currents, attenuation of SFO-evoked paired-pulse depression, and reduction in frequency (but not amplitude) of miniature postsynaptic currents, consistent with an action at presynaptic GABAB receptors. Baclofen's effects on miniature currents lacked sensitivity to barium, ω-conotoxin GVIA, and cadmium. Acting at postsynaptic GABAB receptors, baclofen hyperpolarized a majority of MnPO neurons by increasing a G protein–coupled inwardly rectifying potassium conductance and suppressing an N-type high-voltage–activated calcium conductance. The latter contributed to reduction in action potential afterhyperpolarization and enhanced cell firing and spike frequency adaptation when tested with a depolarizing stimulus. All baclofen-induced effects were blockable with CGP52432 . CGP52432 alone had no significant effect on SFO-evoked postsynaptic current amplitudes or paired-pulse ratios, but did induce an increase in miniature inhibitory postsynaptic current (mIPSC) frequency in 2/4 cells tested, indicating that ambient levels of GABA could activate presynaptic GABAB receptors on undefined inputs. These observations indicate that MnPO neurons receive both a GABAergic and glutamatergic innervation from SFO. Both forms of rapid neurotransmission are subject to modulation via pre- and postsynaptic GABAB receptors.

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