Previous studies have reported that the surround responses of retinal ganglion cells weaken or disappear upon dark adaptation. The mechanism(s) by which this occurs is largely unknown, although changes in activity of retinal dopaminergic neurons have been implicated. In the light-adapted rabbit retina, the surround ON responses of OFF-center ganglion cells have been shown to be markedly reduced or abolished by a dopamine antagonist. This effect of a dopamine antagonist was recently shown to be reversed by the glycine antagonist strychnine and by compounds that elevate intracellular cAMP levels. The present study was conducted to determine whether strychnine and cAMP-elevating compounds could bring out the surround ON responses in OFF-center ganglion cells that are diminished upon dark adaptation. Extracellular recordings of OFF-center brisk ganglion cells were made from isolated, superfused retinal preparations. During the course of dark adaptation, the surround On responses of many cells decreased markedly.Application in both brisk-transient and brisk-sustained OFF-center ganglion cells. The center OFF responses of these cells, on the other hand, were not enhanced by strychnine. Of the cAMP-elevating compounds tested, 8-(4-chlorophenylthio) cyclic AMP was the most effective in bringing out the surround ON responses in dark-adapted OFF-center ganglion cells. The findings from this study suggest that under dark-adapted conditions glycinergic neurons inhibit the surround component of OFF-center ganglion cells. The release of glycine from these neurons is suggested to be regulated by a cAMP-dependent mechanism.

Strychnine is considered a selective competitive antagonist of glycine gated Cl− channels (Saitoh et al., 1994) and studies have used strychnine at low micromolar concentrations to study the role of glycine in rabbit retina (Linn, 1998; Protti et al., 2005). However, other studies have shown that strychnine, in the concentrations commonly used, is also a potent competitive antagonist of α7 nicotinic acetylcholine receptors (nAChRs; Matsubayashi et al., 1998). We tested the effects of low micromolar concentrations of strychnine and 3-[2′-phosphonomethyl[1,1′-biphenyl]-3-yl] alanine (PMBA), a specific glycine receptor blocker (Saitoh et al., 1994; Hosie et al., 1999) on the activation of both α7 nAChRs on retinal ganglion cells and on ganglion cell responses to a light flash. Extracellular recordings were obtained from ganglion cells in an isolated retina/choroid preparation and 500 μM choline was used as an α7 agonist (Alkondon et al., 1997). We recorded from brisk sustained and brisk transient OFF cells, many of which have been previously shown to have α7 receptors (Strang et al., 2005). Further, we tested the effect of strychnine, PMBA and α-bungarotoxin on the binding of tetramethylrhodamine α-bungarotoxin in the inner plexiform layer. Our data indicates that strychnine, at doses as low as 1.0 μM, can inhibit the α7 nAChR-mediated response to choline, but PMBA at concentrations as high as 0.4 μM does not. Binding studies show strychnine and α-bungarotoxin inhibit binding of labeled α-bungarotoxin in the IPL. Thus, the effects of strychnine application may be to inhibit glycine receptors expressed by ganglion cell or to inhibit amacrine cell α7 nAChRs, both of which would result in an increase in the ganglion cell responses. Further research will be required to disentangle the effects of strychnine previously believed to be caused by a single mechanism of glycine receptor inhibition.

Pocket gophers have long suppressed forest regeneration in clearcuts in western North America, despite the application of intensive and costly, large-scale abatement practices, which also kill non-target wildlife and may increase soil erosion. At four national forests in northern California, gophers (Thomomys bottae and T. monticola) on 50 clearcuts were baited with a 0.5% strychnine concentration on wheat or oat groats, which were presented as loose grains or in 1 × 2 cm paraffin pellets for added durability. The various baits and baiting regimes usually reduced gopher abundance by 50-100% within one month. However, gopher populations recovered too quickly to protect seedlings planted for forest regeneration, especially on plots baited with a mechanical burrow-builder. In some plots where abatement was most successful initially, gopher densities increased to levels exceeding those in control plots by 7-13 months later. As gopher populations recovered following abatement, active burrows first appeared at the plot peripheries and advanced toward the plot centres, suggesting that abated territorial residents were replaced by immigrants dispersing from the surrounding landscape.

Whereas conventional abatement practices can reduce gopher abundance in clearcuts, the small spatial and temporal scales of application encourage reinvasion of vacated ecological space. These population responses defeat the goal of forest management by increasing gopher density in clearcuts; at the same time the conifer seedlings are vulnerable to gopher predation. Predation of conifer seedlings might be reduced by not abating gophers or by using alternative harvest regimes. These alternative strategies would avoid creating the conditions under which gophers contribute to slowing forest regeneration following timber harvests, and they would avoid the widespread and possibly long-term environmental damage caused by applying acute poisons and by using the burrow-builder.

The inhibition of [3H]acetylcholine (ACh) release from cholinergic amacrine cells by glycine and GABA was studied using an in vivo eyecup preparation in anesthetized rabbits. Glycine (1 mM) had no effect on basal ACh release, but completely blocked the light-evoked release of ACh. Glycine also blocked the strong potentiating effects of picrotoxin (20 μM) normally observed on basal and light-evoked release. Strychnine (20 μM) increased basal release, albeit less than picrotoxin, but partially inhibited and altered the shape of light-evoked responses. Co-perfusion of picrotoxin and strychnine after strychnine application resulted in a larger additional basal increase. However, light-evoked responses were not restored to a control shape and magnitude, or to potentiated levels as with picrotoxin alone, but remained altered and partially inhibited. These results support the concept of a sustained GABA-mediated inhibition of the cholinergic pathway in the intact retina. In contrast, glycine-mediated inhibition of the cholinergic pathway differs, with the present results indicating a significantly smaller sustained inhibition of basal release and a temporal inhibition of light-evoked release. The lack of effect of any of these compounds on kainate-evoked responses indicates that these effects are predominately indirect, possibly on the presynaptic bipolar cell.