Glutamate fibres

Glutamate Decreased presynaptic markers Decreased HC AMPA and kainate receptor expression Minor changes in FC NMDA R sub-units Altered glutamate fibres in cingulate cortex NMDA receptor antagonists produce schizophrenia-like psychosis Roles of NMDA receptors in development and neurotoxicity Partial NMDA receptor agonists have some therapeutic benefits... 

These polymers, typical of polyamides with fewer than four main chain carbon atoms in the repeating unit, decompose before melting and have to be processed from solution. Several of the polymers may, however, be spun into fibres. Over thirty years ago Courtaulds produced silk-like fibres on an experimental commercial scale from poly-(L-alanine) and from poly-(a-methyl-L-glutamate). The latter material is also said to be in use as a synthetic leather in Japan. The... 

Japanese have also shown interest in poly-(L-glutamic acid) for the manufacture of silk-like fibres. 

Long-term potentiation (LTP) is a synaptic plasticity phenomenon that corresponds to an increase in the synaptic strength (increase in the post-synaptic response observed for the same stimulation of the presynaptic terminals) observed after a high frequency stimulation (tetanus) of the afferent fibres. This increased response is still observed hours and even days after the tetanus. The phenomenon is often observed at glutamatergic synapses and involves, in most cases, the activation of the V-methyl D-aspartate (NMDA) subtype of ionotropic glutamate receptors. 

Lesions in conjunction with concentration studies can also be useful. Section of dorsal roots and degeneration of afferent fibres produces a reduction in glutamate and substance P which can then be associated with sensory inputs. Temporary reduction of the blood supply to the cord causes preferential destruction of interneurons and a greater loss of asparate and glycine, compared with other amino acids and so links... 

Figure 21.5 Mechanisms of opioid analgesia at the spinal level. Action potentials in nociceptive afferent fibres invade the terminal and by opening calcium channels (L, N and P-type) cause the release of glutamate and peptides that further transmit pain subsequent to activation of their postsynaptic receptors. Presynaptic opioid receptor activation (mu- and delta-mediated effects have been most clearly shown) opens potassium channels which hyperpolarise the terminal, so reducing transmitter release and inhibiting the postsynaptic neuron...

Figure 5.5 — Flow-through biosensor for the determination of L-glutamate. (A) Flow injection manifold. (B) Sensing microzone of the probe sensor (optrode), incorporated in the flow-cell (FTC). P pump IV injection valve MC mixing chamber AD air damper BFB bifurcated fibre bimdle LS light source PMT photomultiplier R recorder GLU L-glutamate 0-Glu 2-oxoglutarate E enzyme layer I optical insulator S sensing layer PS polyester support. For details, see text. (Adapted from [6] with permission of Elsevier Science Publishers).

Lefebvre, C., Fisher, K., Cahill, C. M., Coderre, T. J. Evidence that DHPG-induced nociception depends on glutamate release from primary afferent C-fibres, Neuroreport. 2000, 11, 1631-1635. 

In the brain stem, TRPV1 receptor activation, similarly to P2X3 receptor activation (see above), facilitated spontaneous glutamate release in a tetrodotoxin- and Cd2+-insensitive manner, even though the two presynaptic receptors were located on different primary afferent fibres (Jin et al. 2004). Action potential-dependent glutamate release, in contrast, was reduced by TRPV 1 activation (Doyle et al. 2002). In paraventricular neurons, TRPV 1 receptor activation facilitated spontaneous glutamate release in a tetrodotoxin- and Cd2+-insensitive way, but in that case evoked glutamate release was enhanced too (Li et al. 2004). 

Nakatsuka T, Gu JG (2001) ATP P2X Receptor-mediated enhancement of glutamate release and evoked EPSCs in dorsal horn neurons of the rat spinal cord. J Neurosci 21 6522-31 Nakazawa K (1994) ATP-activated current and its interaction with acetylcholine-activated current in rat sympathetic neurons. J Neurosci 14 740-50 Narkiewicz K, van de Borne PJ, Hausberg M, Cooley RL, Winniford MD, Davison DE, Somers VK (1998) Cigarette smoking increases sympathetic outflow in humans. Circulation 98 528-34 Nicoll RA, Schmitz D (2005) Synaptic plasticity at hippocampal mossy fibre synapses. Nat Rev Neurosci 6 863-76... 

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