@article {1985, title = {Intraglomerular inhibition: signaling mechanisms of an olfactory microcircuit.}, journal = {Nature Neuroscience}, volume = {8}, year = {2005}, month = {2005 Mar}, pages = {354-64}, abstract = {

Microcircuits composed of principal neuron and interneuron dendrites have an important role in shaping the representation of sensory information in the olfactory bulb. Here we establish the physiological features governing synaptic signaling in dendrodendritic microcircuits of olfactory bulb glomeruli. We show that dendritic gamma-aminobutyric acid (GABA) release from periglomerular neurons mediates inhibition of principal tufted cells, retrograde inhibition of sensory input and lateral signaling onto neighboring periglomerular cells. We find that L-type dendritic Ca(2+) spikes in periglomerular cells underlie dendrodendritic transmission by depolarizing periglomerular dendrites and activating P/Q type channels that trigger GABA release. Ca(2+) spikes in periglomerular cells are evoked by powerful excitatory inputs from a single principal cell, and glutamate release from the dendrites of single principal neurons activates a large ensemble of periglomerular cells.

}, keywords = {1, 3-Pyridinecarboxylic acid, 4-dihydro-2, 6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Animals, Bicuculline, Cadmium, Calcium, Calcium Channel Agonists, Calcium Channel Blockers, Calcium Signaling, Chelating Agents, Dendrites, Diagnostic Imaging, Dihydropyridines, Dose-Response Relationship, Drug, Drug Interactions, Egtazic Acid, Electric Stimulation, GABA Antagonists, gamma-Aminobutyric Acid, Membrane Potentials, Methyl ester, Neural Conduction, Neural Inhibition, Neural Networks (Computer), Neurons, Newborn, Nickel, Nimodipine, Olfactory Bulb, Patch-Clamp Techniques, Phosphinic Acids, Potassium, Propanolamines, Pyrimidines, Rats, Signal Transduction, Sprague-Dawley, Synapses, Synaptic Transmission, Tetrodotoxin, Time Factors, Valine}, issn = {1097-6256}, doi = {10.1038/nn1403}, author = {Murphy, Gabe J and Darcy, Daniel P and Isaacson, Jeffry S} } @article {1986, title = {Sensory neuron signaling to the brain: properties of transmitter release from olfactory nerve terminals.}, journal = {The Journal of Neuroscience: The Official Journal of the Society for Neuroscience}, volume = {24}, year = {2004}, month = {2004 Mar 24}, pages = {3023-30}, abstract = {

Olfactory receptor neurons (ORNs) convey sensory information directly to the CNS via conventional glutamatergic synaptic contacts in olfactory bulb glomeruli. To better understand the process by which information contained in the odorant-evoked firing of ORNs is transmitted to the brain, we examined the properties of glutamate release from olfactory nerve (ON) terminals in slices of the rat olfactory bulb. We show that marked paired pulse depression is the same in simultaneously recorded periglomerular and tufted neurons, and that this form of short-term plasticity is attributable to a reduction of glutamate release from ON terminals. We used the progressive blockade of NMDA receptor (NMDAR) EPSCs by MK-801 [(5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5-10-imine hydrogen maleate] and stationary fluctuation analysis of AMPA receptor (AMPAR) EPSCs to determine the probability of release (P(r)) of ON terminals; both approaches indicated that P(r) is unusually high (\>/=0.8). The low-affinity glutamate receptor antagonists gamma-d-glutamylglycine and l-amino-5-phosphonovaleric acid blocked ON-evoked AMPAR- and NMDAR-mediated EPSCs, respectively, to the same extent under conditions of low and high P(r), suggesting that multivesicular release is not a feature of ON terminals. Although release from most synapses exhibits a highly nonlinear dependence on extracellular Ca(2+), we find that the relationship between glutamate release and extracellular Ca(2+) at ON terminals is nearly linear. Our results suggest that ON terminals have specialized features that may contribute to the reliable transmission of sensory information from nose to brain.

}, keywords = {Afferent, AMPA, Animals, Brain, Calcium, Electric Stimulation, Excitatory Amino Acid Antagonists, Excitatory Postsynaptic Potentials, Glutamate, Glutamic Acid, N-Methyl-D-Aspartate, Neuronal Plasticity, Neurons, Neurotransmitter Agents, Olfactory Bulb, Olfactory Nerve, Presynaptic Terminals, Rats, Receptors, Sprague-Dawley, Synaptic Transmission}, issn = {1529-2401}, doi = {10.1523/JNEUROSCI.5745-03.2004}, author = {Murphy, Gabe J and Glickfeld, Lindsey L and Balsen, Zev and Isaacson, Jeffry S} } @article {1987, title = {Presynaptic cyclic nucleotide-gated ion channels modulate neurotransmission in the mammalian olfactory bulb.}, journal = {Neuron}, volume = {37}, year = {2003}, month = {2003 Feb 20}, pages = {639-47}, abstract = {

Cyclic nucleotide-gated channels (CNGCs) on the dendritic cilia of olfactory receptor neurons (ORNs) are critical for sensory transduction in the olfactory system. Do CNGCs also play a role in the axons and/or nerve terminals of ORNs? We find that the cyclic nucleotides cAMP and cGMP can both facilitate and depress synaptic transmission between olfactory nerve fibers and their targets in olfactory bulb glomeruli. Cyclic nucleotides increase intracellular Ca(2+) in ORN terminals and enhance spontaneous transmitter release; at higher concentrations, cyclic nucleotides depress evoked transmission by altering olfactory nerve excitability. Cyclic nucleotides have no effect on transmission or nerve excitability, however, in mice lacking olfactory CNGCs. Taken together, our results identify a novel role for presynaptic CNGCs in modulating neurotransmission.

}, keywords = {Animals, Calcium, Cyclic, Cyclic GMP, Electric Stimulation, Enzyme Inhibitors, Excitatory Postsynaptic Potentials, Forskolin, GABA Agonists, Inbred C57BL, Ion Channel Gating, Ion Channels, Mice, Nucleotides, Olfactory Bulb, Patch-Clamp Techniques, Presynaptic Terminals, Rats, Sprague-Dawley, Synaptic Transmission}, issn = {0896-6273}, author = {Murphy, Gabe J and Isaacson, Jeffry S} }