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. 1998 Aug 1;18(15):5603–5613. doi: 10.1523/JNEUROSCI.18-15-05603.1998

Table 2.

Mutations in eag decreased the proportion of olfactory neurons responsive to membrane-permeant cycle nucleotide analogs

Genotype Response to 3 mm 8-Br-cAMP (fold change) Response to 3 mm 8-Br-cGMP (fold change)
Increase Decrease % (n) Increase Decrease % (n)
Control lines
 CS 3.4  ± 0.7 0.55  ± 0.03 58  (36) 3.6  ± 0.7 0.52  ± 0.02 63  (40)
(n  = 17) (n  = 4) (n  = 21) (n  = 4)
 Female controls from the eagX6stock 2.7  ± 0.4 0.57  ± 0.11 69  (26) 5.0  ± 1.5 0.61  ± 0.04 64  (33)
(n  = 14) (n  = 4) (n  = 14) (n  = 7)
eag mutant lines
eagsc29 1.9 6  (16) 8.0  ± 3.1 0.41  ± 0.33 11  (46)
(n  = 1) (n  = 0) (n  = 3) (n  = 2)
eag1 2.1  ± 0.06 23  (13) 3.0  ± 1.0 23  (13)
(n  = 3) (n  = 0) (n  = 3) (n  = 0)
eagX6 2.7  ± 0.9 0.62 16  (25) 2.3  ± 0.4 0.27  ± 0.23 22  (32)
(n  = 3) (n  = 1) (n  = 5) (n  = 2)

Mutations in eag decreased the proportion of olfactory neurons responsive to membrane-permeant cyclic nucleotide analogs. Cyclic nucleotide-induced modulation of basal activity was determined in loose patch recordings during exposure of control and eagantennae to either 8-Br-cAMP (3 mm) or 8-Br-cGMP (3 mm). No significant difference in the response magnitude was observed among genotypes, when comparisons were made between each control and eag allele separately, or between combined controls and eag alleles (Student’s t test). Although the average eagsc29 response was larger than that for controls, and the average eagX6response was smaller than the control value, individual values were within the range observed for control neurons.