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. Author manuscript; available in PMC: 2012 Jun 14.
Published in final edited form as: Epilepsia. 2011 Dec 9;53(1):157–167. doi: 10.1111/j.1528-1167.2011.03345.x

Table 3.

Electrochemistry comparisons between kindled animals and surgical controls measured in hippocampal subfields after a 30-day latent period following amygdalar kindling

Measure Region Ipsilateral
Contralateral
Kindled Control Kindled Control
Tonic glutamate level DG 5.77 ± 1.80 (12) 2.26 ± 0.60 (11) 1.84 ± 0.27 (8) 2.81 ± 0.91 (5)
CA3 3.48 ± 0.94 (10) 2.24 ± 0.55 (6) 1.57 ± 0.41 (4) 1.87 ± 0.72 (5)
CA1 3.20 ± 0.94 (9) 3.07 ± 1.18 (6) 3.20 ± 0.94 (9) 2.87 ± 1.24 (6)
K+-evoked peak amplitude DG 5.40 ± 1.85 (11) 6.22 ± 0.94 (11) 4.70 ± 1.10 (8) 4.11 ± 0.97 (8)
CA3 5.09 ± 1.13 (10) 6.60 ± 1.73 (10) 4.38 ± 1.58 (6) 8.51 ± 3.44 (6)
CA1 5.97 ± 1.38 (9) 9.91 ± 3.37 (9) 5.67 ± 1.63 (7) 4.72 ± 1.36 (6)
K+-evoked peak area DG 22.11 ± 9.62 (12) 28.22 ± 10.62 (11) 25.21 ± 7.25 (7) 11.93 ± 5.71 (5)
CA3 18.20 ± 4.01 (10) 61.35 ± 21.09 (10) 29.26 ± 9.08 (6) 10.36 ± 2.80 (5)
CA1 25.75 ± 4.30 (9) 30.69 ± 8.57 (7) 16.93 ± 6.58 (7) 21.18 ± 5.89 (6)

Microelectrode arrays were used to detect resting (tonic) glutamate levels and (phasic) K+-evoked release of glutamate in hippocampal subfields of kindled and control animals as described in Methods. Quantities expressed are micromolar; (n) = number of animals. There were no differences in a region across hemispheres and between kindled and control.