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Abrahamasen et al 2008 Used cre to selectively deliver diptheria tox to Nav1.8 neurons. No response to noxious mechanosensation and cold. No inflammatory hyperalgesia after complete Freunds. Neuropathic pain intact, can it be blocked using drugs shown to work previously?
Basbaum et al 2009 Review: 2 kinds of Adelta fibre - type1 responds equally, type2 has lower heat threshold. C fibres also heterogenous. Nociceptors project to laminae 1&2 of sup dorsal horn. TRPM8 & TRPV1 are in non-overlapping populations, probably labelled lines.
Schmidt et al 2005 C fibres can be heat/mechanical/both/neither, chemical injury (capsaicin/mustard oil) incr range of acceptable stimuli. Used human peroneal nerve. Isolated individual C fibres by stimulating skin while measuring, then tested response to different stimuli
Olausson et al 2008 C fibres can carry basic information on light touch (affective component?), not enough to localise. Same fibres had no heat/chemical response. 2 Patients w/o large myelinated sensory fibres, lost fibres through neuropathy as adults and feel no touch.
Molliver et al 1997 Non-peptidergic C fibres express the GDNF receptor (c-ret). A large percentage bind IB4 isolectin. CGRP+ves are separate and respond to NGF through TrkA receptors. NB from another source: Some C fibres transmit itch.
Basbaum and Jessell 2000 Nociceptors are pseudo-unipolar with ion channels roughly evenly distributed across all terminals. Also allows bidirectional transfer of information, forming the basis for neurogenic inflammation
Malmberg et al 1997 Lamina 2 contains excitatory neurons containing PKCγ. Global KO of PKCγ: normal response to acute pain, reduced neuropathic pain (partial sciatic N ligation). Markers: reduced incr in NK1 receptors and NPY + substance P was less reduced rel to controls.
Neumann et al 2008 Lamina2 of the cord (containing PKCγ) is targetted by myelinated non-nocicep afferents. Cholera tox B, selective for this type, used to mark pathways, overlapped w/ PKCγ stain. Fos incr in PKCγ neurons by rotarod, shows touch is activating PKCγ neurons
Cesare & McNaughton 1996 Shows that noxious heat causes an inward current carried by monovalent cations (nonselective), also shows bradykinin sensitisation is specific for heat and acts through PKC (activators and inhibitors to prove).
Lawson et al 2008 TRPV1 KO mice lack the population of heat-specific C-fibres but retain mech-heat polymodal fibres, tested i ex vivo preparations. Indicates TRPV1 is not the only player.
Cavanaugh et al 2009 Shows that capsaicin completely abolishes heat sensitivity, this is thought to be due to overstimulation of TRPV1+ cells causing deactivation. Shows that any other players in heat sensitivity are presumably in TRPV1+ nerves (coexpressed for redundancy).
Guler et al 2002 When transfected into xenopus oocytes or HEK cells TRPV4 creates a heat activated current stimulated by temperatures lower than those needed to activate TRPV1. It is also present in thermosensory region of the hypothalamus (medial preoptic area in rats
Bautista et al 2007 TRPM8 mutations cause cold insensitivity, channel active at <25 degrees. A small number (4%) of nerves respond only to temp <12 degrees, preserve some cold response in TRPM8 KO. Nerves shown to be sensitive by calcium imaging and extracell nerve recording
Karashima et al 2009 Used TRPA1 conditional KO regulated by tetracycline. Response to cold present but reduced, particularly at mild cold (10deg). Some behavioural differences (less jumping in TRPA1 KO at 0&10deg), longer latency to tail flick when tail placed in cold water
Noel et al 2009 PGE2 given to TREK KO mice, no incr reponse to osmotic pain. Indicates TREK is involved in incr sensitivity to this modality. Pain measured by time paw-licking post-injection. Deletion of K+ channels causes heat/mechano hyperalgesia w/o stimulus
Muraki et al 2003 Ex vivo, hypo-osmotic solution activates inward currents abolished by Ca free medium. Antisense oligodeoxynucleotides against TRPV2 reduced response to osmotic stimuli
Gevaert et al 2007 TRPV4 KO have altered bladder voiding, thought to be due to dysfunction in osmotic sensation. Also causes reduced ATP release which is normally involved. (Shown separately for P2X3 KO mice although Piezo channels now thought to be mechanotransducers)
Hinman et al 2006 Chemosensation probably due to modification of TRPA1 N-term cysteines. Less reactive ligand analogues had no effect. Produced new agonist w/o structure similarity but known to react covalently w/ cysteines, produced activation that resisted washout.
Zimmerman et al 2007 Shows Nav1.8 is reqd for cold pain, other Navs inactivated at those temps. When limb is cooled ordinary touch is less strong, pain still strong. Nav1.8 is TTX resistant so KO of Nav1.8 causes TTX to work. Noxious cold response is decr in Nav1.8 KO mice
Luo et al 2001 α2δ subunit of Cav is upreg in neuropathic pain (spinal nerve ligation). Upreg of protein (western blot) and RNA (RNAse protection assay). This is target of gabapentin used in neuropathic pain.
Caceres et al 2009 TRPA1 antagonists beneficial in asthma. Reduced levels of cytokines and reduced leukocyte migration in TRPA1-ve mouse asthma model. Might link to chemosensitivity? May be endogenous agonists released in asthma (also cold induced asthma link!)
Immke & McClesky 2003 Lower levels of Ca enable easier opening of ASICs by H ions, explains muscle pains as lactate chelates Ca. Ca competes for H binding and the channel opens as Ca dissociates
Liu et al 2008 Src interaction & enhancement of NMDA currents thought to be important in chronic pain central hyperalgesia (in cord). Src blocking fragment/KO reduced allodynia after nerve injury. Measured using paw withdrawal from mechanical stim/acetone(cold) spray.
Campbell et al 1988 Ischaemia used to abolish touch sensitivity w/o affecting warmth/cool sensation via c fibres. At the time mechanical hyperalgesia disappeared touch sense was gone but cool/warmth detection was intact, mechanical hyperalgesia is due to myelinated fibres.
Malan et al 2002 Intrathecal GABA antagonists mimic injury conditions, inducing mechanical & heat allodynia, this indicates there is basal inhibition. Agonists reverse this and are beneficial in neuropathic pain states. Withdrawal to heat/von frey used to test pain
Harvey et al 2004 Glycine receptor α3 KO prevents PGE inhibition of glycine inh currents. PKA inh also removed PGE effects on wt glycine currents. KO normal in basal conditions, indicates compensatory mechanisms (at what point is the baseline set?)
Coull et al 2003 Ionic equilibrium potentials are altered after injury (CCI), perforated patch clamp (minimal dilution). Showed using fura-2 Ca sensor that GABA agonsits could cause AP firing. KCC2 reduced on side of injury (western blot). KCC2 antagonists cause allodynia
Coull et al 2005 Intrathecal injection of activated microglia mimics neuropathic pain, causing allodynia and making GABA excitatory. Effects blocked by trkB inhibitor suggesting BDNF release is to blame. BDNF causes same effects ex vivo and when virally expressed in rats.
Kim et al 2004 TLR2 activation is thought to activate microglia, TLR2 KO mice have higher pain thresholds post injury. Staining for markers of glial activation showed that it was reduced but not gone. TNFa production also reduced. P2X4 may also be involved.
Coste et al 2010 Applied force using a piezo electrically driven probe while patch clamping the cell. Data suggests non-selective cation permeability. Systematically knocked down proteins from cells expressing the current. Transfection into cells induced mech sense.
Coste et al 2012 Mouse piezo is sensitive to ruthenium red, drosophila version is not (both in model cells with same protein background), suggests that the two encode separate channels rather than activating another protein
Waxman et al 1999 Review: BDNF has no effect on sodium currents but does affect GABA. Drugs acting at sodium channels do have some effectiveness in neuropathic pain.
Moechars et al 2006 VGLUT2 +/- mice have attenuated neuropathic pain (spared nerve injury) and less anxiety-related behaviour. Normal memory and acute pain. VGLUT2 decr in thalamus thought to be important, peripheral nerves can compensate with VGLUT1. -/- was embryolethal.
Tsuda et al 2003 Showed that P2X4 blockade reduces neuropathic pain, pain mimicked by injection of microglia activated by ATP. P2X4 upregulated after unjury on ipsilateral side of cord
Created by: Jonmassie



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