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Control of spinal nociception by the midbrain periaqueductal grey matterWaters, Alexander Juergen January 1999 (has links)
No description available.
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Cutaneous afferent evoked activity in the postnatal rat spinal cordJennings, Ernest Albert January 1999 (has links)
No description available.
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Sensory processing in the isolated in vitro rat spinal cord with particular emphasis on opioid-related peptides, excitatory and inhibitory amino acidsMaile, Rebecca Ann January 2002 (has links)
No description available.
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Dorsal horn neurones in the sacral spinal cord of the rat : receptive field and encoding propertiesLaird, Jennifer Marie Ann January 1989 (has links)
No description available.
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Endomorphin-Like Immunoreactivity in the Rat Dorsal Horn and Inhibition of Substantia Gelatinosa Neurons in VitroWu, S. Y., Dun, S. L., Wright, M. T., Chang, J. K., Dun, N. J. 01 March 1999 (has links)
Endomorphin 1 and 2 are two tetrapeptides recently isolated from bovine as well as human brains and proposed to be the endogenous ligand for the μ- opiate receptor Opioid compounds expressing μ-receptor preference are generally potent analgesics. The spinal cord dorsal horn is considered to be an important site for the processing of sensory information including pain. The discovery that endomorphins produced greater analgesia in mice upon intrathecal as compared to intracerebroventricular injections raises the possibility that dorsal horn neurons may represent the anatomic site upon which endomorphins exert their analgesic effects. We report here the detection of endomorphin 2-immunoreactive fiber-like elements in superficial layers of the rat dorsal horn by immunohistochemical techniques. Whole-cell patch recordings from substantia gelatinosa neurons of cervical spinal cord slices revealed two conspicuous effects of exogenously applied endomorphin 1 and 2: (i) depression of excitatory postsynaptic potentials evoked by stimulation of dorsal root entry zone, and (ii) hyperpolarization of substantia gelatinosa neurons. These effects were reversed by the selective μ-opiate receptor antagonist β-funaltrexamine. Collectively, the detection of endomorphin-like immunoreactivity in nerve fibers of the superficial layers and the inhibitory action of endomorphins on substantia gelatinosa neurons provide further support for a potential role of these two peptides in spinal nociception.
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Nociceptin-Like Immunoreactivity in the Rat Dorsal Horn and Inhibition of Substantia Gelatinosa NeuronsLai, C. C., Wu, S. Y., Dun, S. L., Dun, N. J. 10 October 1997 (has links)
Nociceptin, also referred to as orphanin FQ, is believed to be the endogenous ligand for the ORL1. Nociceptin, when injected intracerebroventricularly to mice, produced hyperalgesia in behavioral tests. Recent studies have demonstrated the presence of ORL1 transcript in the spinal cord, and ORL1-like immunoreactivity has been localized to nerve fibers and somata throughout the spinal cord. Here, we report the localization of nociceptin-like immunoreactivity to fiber-like elements of the superficial layers of the rat dorsal horn by immunohistochemical techniques. Whole-cell recordings from substantia gelatinosa neurons in transverse lumbar spinal cord slices of 22-26-day-old rats showed that exogenous nociceptin at low concentrations (100-300 nM) depressed excitatory postsynaptic potentials evoked by stimulation of dorsal rootlets without causing an appreciable change of resting membrane potentials and glutamate- evoked depolarizations. At a concentration of 1 μM, nociceptin hyperpolarized substantia gelatinosa neurons and suppressed spike discharges. The hyperpolarizing and synaptic depressant action of nociceptin was not reversed by the known opioid receptor antagonist naloxone (1 μM). Our result provides evidence that nociceptin-like peptide is concentrated in nerve fibers of the rat dorsal horn and that it may serve as an inhibitory transmitter within the substantia gelatinosa.
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Effects of Endomorphin on Substantia Gelatinosa Neurons in Rat Spinal Cord SlicesWu, Su Ying, Ohtubo, Yoshitaka, Brailoiu, G. Cristina, Dun, Nae J. 01 November 2003 (has links)
1. Whole-cell patch recordings were made from substantia gelatinosa (SG) neurons in transverse lumbar spinal cord slices of 15- to 30-day-old rats. 2. Endomorphin 1 (EM-1) or EM-2 (≤ 10 μM) hyperpolarized or induced an outward current in 26 of the 66 SG neurons. The I-V relationship showed that the peptide activates an inwardly rectifying K + current. 3. EM-1 or EM-2 (0.3-10 μM) suppressed short-latency excitatory postsynaptic currents (EPSCs) and long-latency inhibitory postsynaptic currents (IPSCs) in nearly all SG neurons tested or short-latency IPSCs in six of the 10 SG neurons. [Met 5] enkephalin or [D-Ala 2, N-Me-Phe 4, Gly 5-ol]-enkephalin (DAMGO) (1-10 μM) depressed EPSCs and IPSCs. EM-1 or EM-2 depressed synaptic responses without causing a significant change in holding currents or inward currents induced by glutamate. 4. Glutamate also evoked a short-latency outward current in five SG neurons or a biphasic current in two neurons; the outward current was blocked by tetrodotoxin (TTX, 0.3 μM) or bicuculline (10 μM). EM-1 or DAMGO (1 or 5 μM) attenuated the glutamate-evoked outward or biphasic currents in four of the seven SG neurons. 5. EM-1 (1 μM) reduced the frequency, but not the amplitude of miniature EPSCs or miniature IPSCs. 6. Naloxone (1 μM) or the selective μ-opioid receptor antagonist β-funaltrexamine (β-FNA, 25 μM) antagonized the action of EM; EM-induced hyperpolarizations persisted in the presence of the κ-opioid receptor antagonist (nor-binaltorphimine dihydrochloride, 1 μM) and/or σ-opioid receptor antagonist (naltrindole hydrochloride, 1 μM). 7. It may be concluded that EM acting on μ-opioid receptors hyperpolarizes a population of SG neurons by activating an inwardly rectifying K + current, and attenuates excitatory and inhibitory synaptic currents evoked in a population of SG neurons, probably by a presynaptic site of action.
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Distribution of substance P (SP), samostatin (SOM) and methionine-enkephalin immunoreactivities in the spinal cord of the domestic fowl, Gallus domesticusLaValley, Antoinette January 1980 (has links)
No description available.
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Mechanisms of rapid receptive field reorganization in rat spinal cordVu, Hung 08 1900 (has links)
Rapid receptive field (RF) reorganization of somatosensory neurons in the rat dorsal horn was examined using extracellular single unit recording. Subcutaneous injection of lidocaine into RFs of dorsal horn neurons results in expansion of their RFs within minutes. The expanded RFs appear adjacent to or/and proximal to original RFs. Out of 63 neurons tested, 36 (58%) show RF reorganization. The data suggest that dorsal horn of spinal cord is one of the initial sites for RF reorganization. The neural mechanisms of this effect are not well understood. We propose that changes in biophysical properties (membrane conductance, length constant) of the neurons resulting from lidocaine injection contribute to RF reorganization. Iontophoretic application of glutamate onto dorsal horn neurons that show lidocaine induced RF's expansion were used to test the model. Application of glutamate produced reduction of reorganized RFs in 9 of 20 (45%) tested cells. Application of NBQX produced no effect on either original or expanded RFs indicate that RF shrinkage effects of glutamate involve NMDA receptors. The results are consistent with the prediction of the proposed model. Subcutaneous injection of capsaicin into tactile RFs of low threshold mechanoreceptive dorsal horn neurons produced no effect on the RF sizes that are consistent with other studies. Following the injection, the original RFs were completely silenced (46%) or remained responsive (54%).
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The Regulation of Neuronal Excitability and Nociception by Tonic GABAergic InhibitionBonin, Robert 23 July 2013 (has links)
The mammalian central nervous system maintains a delicate balance between neuronal excitation and inhibition. Conventional synaptic inhibition is mediated through the transient activity of postsynaptic γ-aminobutyric acid (GABA) at type A GABA (GABAA) receptors. A subset of GABAA receptors is also located outside of inhibitory synapses. These extrasynaptic receptors generate a tonic inhibitory conductance in response to low concentrations of extracellular GABA. Tonic inhibition broadly suppresses neuronal activity and regulates many vital processes such as sleep, consciousness and memory formation.
This thesis examines the physiological effects of tonic inhibition at the cellular level and in the behaving animal. This thesis also explores whether gabapentin, a commonly used sedative, anxiolytic, and analgesic drug, enhances tonic GABAergic inhibition. I hypothesize that: (1) tonic GABAA receptor activity reduces the intrinsic excitability of neurons; (2) the activity of tonically active GABAA receptors in spinal pain pathways attenuates nociception; and (3) tonic inhibition can be upregulated by gabapentin.
The results show that a tonic inhibitory current generated by α5 subunit-containing GABAA (α5GABAA) receptors reduces the excitability of hippocampal pyramidal neurons excitability by increasing the rheobase, but does not change the gain of action potential firing. A similar shunting inhibition is present in spinal cord lamina II neurons that is generated by δ subunit-containing GABAA receptors. The activity of these receptors in spinal nociceptive pathways reduces acute thermal nociception and may constrain central sensitization in a behavioural model of persistent pain. Finally, gabapentin increases a tonic inhibitory current in cultured hippocampal neurons independent from changes in the expression of α5GABAA receptors or in the concentration of GABAA receptor ligands.
The results of this thesis demonstrate that tonically active GABAA receptors play an important role in the regulation of neuronal activity and nociception, and that tonic inhibition represents a novel target of therapeutic drugs.
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