NACL Sensors
Ascorbate (AA)
Legend. Schematic representation of an implantable CPE constructed from Teflon-coated wire. After soldering a gold clip to facilitate later connection to the potentiostat, a small cavity (~0.5 mm long) is made by drawing the insulation over the metal wire (usually Ag or Pt-Ir). The carbon paste should be packed carefully into a cavity using a sleeved plunger of the same wire. If the paste is too loose or the cavity too short, the extracellular fluid may penetrate to the metal producing large background currents after a few days. If packed too tightly, the Teflon may crack, again allowing electrolyte into the cavity. These CPEs have been used in voltammetric experiments to monitor brain ascorbate, urate, 5HIAA and HVA, and to monitor ascorbate  amperometrically at low applied potentials.

References:

  • O'Neill R.D., Grunewald R.A., Fillenz M. and Albery W.J. (1982) Linear sweep voltammetry with carbon paste electrodes in the rat striatum. Neuroscience, 7, 1945-1954.
  • Lyne P.D. and O'Neill R.D. (1990) Stearate-modified carbon paste electrodes for detecting dopamine in vivo: decrease in selectivity caused by lipids and other surface-active agents. Anal. Chem., 62, 2347-2351.
  • Kane D.A. and O'Neill R.D. (1998) Major differences in the behaviour of carbon paste and carbon fibre electrodes in a protein-lipid matrix: implications for voltammetry in vivo. Analyst, 123, 2899-2903.

Legend: Schematic representation of the heteroexchange model proposed to explain changes in ascorbate (AA) concentration in brain ECF. Glutamate (G), released by nerve terminals following the arrival of an action potential (AP), acts at a variety of receptor sites (R) associated with its neurotransmission function. Inactivation of the chemical signal occurs by removal through a number of G uptake systems (U) that can be distinguished on the basis of their kinetic parameters, localisation, ionic dependence, substrate specificity, and susceptibility to inhibitors. The uptake of G into both neurons and glia involves heteroexchange with intracellular AA.
References:
  • Fillenz M., O'Neill R.D. and Grunewald R.A. (1986) Changes in extracellular brain ascorbate concentration as an index of excitatory amino acid release. In Monitoring Neurotransmitter Release During Behaviour (edited by Joseph M.H., et al.), Ellis Horwood, Chichester , pp. 144-163.
  • O'Neill R.D. (1995) The measurement of brain ascorbate in vivo and its link with excitatory amino acid neurotransmission. In Voltammetric Methods in Brain Systems (edited by Boulton A.A., et al.), Humana Press , New Jersey , pp. 221-268.

Legend: Example of diurnal changes in the AA signal recorded using CPEs implanted bilaterally in rat striatum, with a unilateral lesion of the descending cortico-striatal pathway (top), and simultaneously monitored motor activity (bottom) over 72 h at 12-min intervals.  These observations form part of the body of evidence for the hypothesis that changes in the concentration of AA in brain ECF reflect the activity of local glutamatergic terminals (see above). Bars indicate 12-h periods of darkness.

References:

  • O'Neill R.D., Grunewald R.A., Fillenz M. and Albery W.J. (1983) The effect of unilateral cortical lesions on the circadian changes in rat striatal ascorbate and homovanillic acid levels measured in vivo using voltammetry. Neurosci. Lett., 42, 105-110.
  • Fillenz M. and O'Neill R.D. (1986) Effects of light reversal on the circadian pattern of motor activity and voltammetric signals recorded in rat forebrain. J. Physiol. ( London ), 374, 91-101.

Legend. Effect of electrical stimulation of the perforant pathway (10 V, 200 Hz, 2.5 s duration) on the AA signal recorded at 6-min intervals with a CPE implanted in the dentate gyrus of the hippocampus over a 36-h period.  The anesthetic (chloral hydrate, 7 mL/kg 5% solution i.p.) reversibly blocked the increase normally observed in hippocampal AA. These observations form part of the body of evidence for the hypothesis that changes in the concentration of AA in brain ECF reflect the activity of local glutamatergic terminals (see above).

References:

  • O'Neill R.D., Fillenz M., Sundstrom L. and Rawlins J.N.P. (1984) Voltammetrically monitored brain ascorbate as an index of excitatory amino acid release in the unrestrained rat. Neurosci. Lett., 52, 227-233.