The Experts below are selected from a list of 49713 Experts worldwide ranked by ideXlab platform
E A Thomas - One of the best experts on this subject based on the ideXlab platform.
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multiple levels of sensory integration in the intrinsic sensory neurons of the enteric nervous system
Clinical and Experimental Pharmacology and Physiology, 2004Co-Authors: Paul P Bertrand, E A ThomasAbstract:SUMMARY 1. The enteric nervous system (ENS) is present in the wall of the gastrointestinal tract and contains all the functional classes of neuron required for complete reflex arcs. One of the most important and intriguing classes of neuron is that responsive to sensory stimuli: sensory neurons with cell bodies intrinsic to the ENS. 2. These neurons have three outstanding and interrelated features: (i) reciprocal connections with each other; (ii) a slow excitatory post-Synaptic Potential (EPSP) resulting from high-speed firing in other sensory neurons; and (iii) a large after-hyperpolarizing Potential (AHP) at the soma. Slow EPSP depolarize the cell body, generate action Potentials (APs) and reduce the AHP. Conversely, the AHP limits the firing rate and, hence, reduces transmission of slow EPSP. 3. Processing of sensory information starts at the input terminals as different patterns of APs depending on the sensory modality and recent sensory history. At the soma, the ability to fire APs and, hence, drive outputs is also strongly determined by the recent firing history of the neuron (through the AHP) and network activity (through the slow EPSP). Positive feedback within the population of intrinsic sensory neurons means that the network is able to drive outputs well beyond the duration of the stimuli that triggered them. 4. Thus, sensory input and subsequent reflex generation are integrated over several hierarchical levels within the network on intrinsic sensory neurons.
Aidas Alaburda - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of motoneurons during the cutaneous silent period in the spinal cord of the turtle
Experimental Brain Research, 2012Co-Authors: Robertas Guzulaitis, Jorn Hounsgaard, Aidas AlaburdaAbstract:The transient suppression of motor activity in the spinal cord after a cutaneous stimulus is termed the cutaneous silent period (CSP). It is not known if CSP is due to suppression of the premotor network or direct inhibition of motoneurons. This issue was examined by intracellular recordings from motoneurons in the isolated carapace-spinal cord preparation from adult turtles during rhythmic scratch-like reflex. Electrical stimulation of cutaneous nerves induced CSP-like suppression of motor nerve firing during rhythmic network activity. The stimulus that generated the CSP-like suppression of motor activity evokes a polySynaptic compound Synaptic Potential in motoneurons and suppressed their firing. This compound Synaptic Potential was hyperpolarizing near threshold for action Potentials and was associated with a substantial increase in conductance during the CSP in the motor pool. These results show that direct postSynaptic inhibition of motoneurons contributes to the CSP.
Andrew J Delaney - One of the best experts on this subject based on the ideXlab platform.
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sk channels regulate excitatory Synaptic transmission and plasticity in the lateral amygdala
Nature Neuroscience, 2005Co-Authors: E Louise S Faber, Andrew J DelaneyAbstract:At glutamatergic synapses, calcium influx through NMDA receptors (NMDARs) is required for long-term potentiation (LTP); this is a proposed cellular mechanism underlying memory and learning. Here we show that in lateral amygdala pyramidal neurons, SK channels are also activated by calcium influx through Synaptically activated NMDARs, resulting in depression of the Synaptic Potential. Thus, blockade of SK channels by apamin potentiates fast glutamatergic Synaptic Potentials. This potentiation is blocked by the NMDAR antagonist AP5 (D(-)-2-amino-5-phosphono-valeric acid) or by buffering cytosolic calcium with BAPTA. Blockade of SK channels greatly enhances LTP of cortical inputs to lateral amygdala pyramidal neurons. These results show that NMDARs and SK channels are colocalized at glutamatergic synapses in the lateral amygdala. Calcium influx through NMDARs activates SK channels and shunts the resultant excitatory postSynaptic Potential. These results demonstrate a new role for SK channels as postSynaptic regulators of Synaptic efficacy.
Paul P Bertrand - One of the best experts on this subject based on the ideXlab platform.
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multiple levels of sensory integration in the intrinsic sensory neurons of the enteric nervous system
Clinical and Experimental Pharmacology and Physiology, 2004Co-Authors: Paul P Bertrand, E A ThomasAbstract:SUMMARY 1. The enteric nervous system (ENS) is present in the wall of the gastrointestinal tract and contains all the functional classes of neuron required for complete reflex arcs. One of the most important and intriguing classes of neuron is that responsive to sensory stimuli: sensory neurons with cell bodies intrinsic to the ENS. 2. These neurons have three outstanding and interrelated features: (i) reciprocal connections with each other; (ii) a slow excitatory post-Synaptic Potential (EPSP) resulting from high-speed firing in other sensory neurons; and (iii) a large after-hyperpolarizing Potential (AHP) at the soma. Slow EPSP depolarize the cell body, generate action Potentials (APs) and reduce the AHP. Conversely, the AHP limits the firing rate and, hence, reduces transmission of slow EPSP. 3. Processing of sensory information starts at the input terminals as different patterns of APs depending on the sensory modality and recent sensory history. At the soma, the ability to fire APs and, hence, drive outputs is also strongly determined by the recent firing history of the neuron (through the AHP) and network activity (through the slow EPSP). Positive feedback within the population of intrinsic sensory neurons means that the network is able to drive outputs well beyond the duration of the stimuli that triggered them. 4. Thus, sensory input and subsequent reflex generation are integrated over several hierarchical levels within the network on intrinsic sensory neurons.
Mala M Shah - One of the best experts on this subject based on the ideXlab platform.
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neuronal hcn channel function and plasticity
Current Opinion in Physiology, 2018Co-Authors: Mala M ShahAbstract:The hyperpolarization-activated cyclic nucleotide-gated (HCN) ion channel is a voltage-gated cation channel that is activated with hyperpolarization. Four subunits, HCN1–4, have thus far been identified. All four subunits are expressed in the central nervous system (CNS), though their expression pattern varies considerably. In many CNS neurons, HCN channels are localised to somato-dendritic compartments where they regulate the resting membrane Potential and membrane resistance, and thereby affect Synaptic Potential shapes and integration and neuronal firing patterns. Emerging evidence suggests that HCN channels are also present within certain axons and Synaptic terminals. Modulation of preSynaptic HCN channel activity leads to altered Synaptic release in a synapse-specific manner. Given that HCN channel function can be modified by activity-dependent and neurotransmitter receptor activation, HCN channels may diversely affect neuronal and network excitability, thereby affecting physiological states such as learning and memory as well as pathophysiological conditions such as epilepsy and depression.
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Cortical HCN channels: function, trafficking and plasticity
The Journal of Physiology, 2014Co-Authors: Mala M ShahAbstract:The hyperpolarization-activated cyclic nucleotide-gated (HCN) channels belong to the superfamily of voltage-gated potassium ion channels. They are, however, activated by hyperpolarizing Potentials and are permeable to cations. Four HCN subunits have been cloned, of which HCN1 and HCN2 subunits are predominantly expressed in the cortex. These subunits are principally located in pyramidal cell dendrites, although they are also found at lower concentrations in the somata of pyramidal neurons as well as other neuron subtypes. HCN channels are actively trafficked to dendrites by binding to the chaperone protein TRIP8b. Somato-dendritic HCN channels in pyramidal neurons modulate spike firing and Synaptic Potential integration by influencing the membrane resistance and resting membrane Potential. Intriguingly, HCN channels are present in certain cortical axons and Synaptic terminals too. Here, they regulate Synaptic transmission but the underlying mechanisms appear to vary considerably amongst different Synaptic terminals. In conclusion, HCN channels are expressed in multiple neuronal subcellular compartments in the cortex, where they have a diverse and complex effect on neuronal excitability.
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PreSynaptic HCN1 channels regulate Ca_V3.2 activity and neurotransmission at select cortical synapses
Nature Neuroscience, 2011Co-Authors: Zhuo Huang, Rafael Lujan, Ivan Kadurin, Victor N Uebele, John J Renger, Annette C. Dolphin, Mala M ShahAbstract:The authors find that hyperpolarization-activated cyclic nucleotide–gated 1 (HCN1) channel subunits are localized to the active zone of asymmetric Synaptic terminals targeting mouse entorhinal cortical layer III pyramidal neurons. The preSynaptic HCN channels inhibit Synaptic glutamate release by suppressing the activity of low-threshold voltage-gated T-type (Ca_V3.2) calcium channels. The hyperpolarization-activated cyclic nucleotide–gated (HCN) channels are subthreshold, voltage-gated ion channels that are highly expressed in hippocampal and cortical pyramidal cell dendrites, where they are important for regulating Synaptic Potential integration and plasticity. We found that HCN1 subunits are also localized to the active zone of mature asymmetric Synaptic terminals targeting mouse entorhinal cortical layer III pyramidal neurons. HCN channels inhibited glutamate Synaptic release by suppressing the activity of low-threshold voltage-gated T-type (Ca_V3.2) Ca^2+ channels. Consistent with this, electron microscopy revealed colocalization of preSynaptic HCN1 and Ca_V3.2 subunit. This represents a previously unknown mechanism by which HCN channels regulate Synaptic strength and thereby neural information processing and network excitability.
