AII amacrine cells, which are the third-order neurons in the rod pathway, can be differentially labelled in rabbit retina by injecting Nuclear Yellow into the posterior chamber. Under ultraviolet excitation, the labelled retina appears strongly metachromatic, with the AII nuclei fluorescing silvery-yellow and the nuclei of other amacrine cells fluorescing blue. Labelled AII cells were injected with Lucifer Yellow under direct microscopic control in a superfused retinal preparation, and the dye was later photoconverted to an opaque reaction product. Rabbit AII amacrines, which number about 525,000 cells, reach a maximum density of 2,500-3,000 cells/mm2 on the peak visual streak, dropping to 400-500 cells/mm2 at the superior margin. These narrow-field amacrines have a bistratified dendritic morphology, with distinctive "lobular appendages" in sublamina a of the inner plexiform layer and wider ranging "arboreal dendrites" in sublamina b. Although the lobular field area increases 10-fold from the visual streak to the far periphery, the lobular field coverage is almost uniform across the retina, averaging 1.0 in inferior retina and 0.8 in superior retina. The dendritic field area of the arboreal dendrites also increases with eccentricity from the visual streak, but there are pronounced differences between inferior and superior retina. The arboreal fields are 2 to 3 times larger than the lobular fields throughout the inferior retina but up to 15 times larger in the superior retina. The arboreal field overlap is only 1.8 at the peak visual streak, increasing slightly to about 2.4 over most of the inferior retina; the overlap increases sharply in the superior retina, however, reaching values of 10 or more in the far periphery. Both the lobular and arboreal fields of AII cells are spaced more regularly than the somata, thus covering apparent gaps in the somatic array. An analysis of the potential convergence and divergence between rod bipolar cells and AII amacrine cells in the rabbit retina indicates that the neuronal architecture of the rod circuit is not organized in a uniform module that is simply scaled-up from central to peripheral retina. Moreover, peripheral fields in the superior and inferior retina that have equivalent densities of interneurons show markedly different rod bipolar----AII amacrine convergence ratios, with the result that many more rod photoreceptors converge on an AII amacrine cell in the superior retina than in the inferior retina.(ABSTRACT TRUNCATED AT 400 WORDS)

Mammalian retinae have a well-defined neuronal pathway that serves rod vision. In rabbit retina, the different populations of interneurons in the rod pathway can be selectively labeled, either separately or in combination. The rod bipolar cells show protein kinase C immunoreactivity; the rod (AII) amacrine cells can be distinguished in nuclear-yellow labeled retina; the rod reciprocal (S1 & S2) amacrine cells accumulate serotonin; and the dopaminergic amacrine cells show tyrosine-hydroxylase immunoreactivity. Furthermore, intracellular dye injection of the microscopically identified interneurons enables whole-population and single-cell studies to be combined in the same tissue. Using this approach, we have been able to analyze systematically the neuronal architecture of the rod circuit across the rabbit retina and compare its organization with that of the rod circuit in central cat retina. In rabbit retina, the rod interneurons are not organized in a uniform neuronal module that is simply scaled up from central to peripheral retina. Moreover, peripheral fields in superior and inferior retina that have equivalent densities of each neuronal type show markedly different rod bipolar to AII amacrine convergence ratios, with the result that many more rod photoreceptors converge on an AII amacrine cell in superior retina. In rabbit retina, much of the convergence in the rod circuit occurs in the outer retina whereas, in central cat retina, it is more evenly distributed between the inner and outer retina.

Aims Sea-level rise is one of the most certain consequences of global warming and is predicted to exert significant adverse effects on wildlife in coastal habitats worldwide. Terrestrial fauna inhabiting low-lying islands are likely to suffer the greatest loss to habitat from sea-level rise and other oceanographic impacts stemming from anthropogenic climate change. Bramble Cay (Maizab Kaur), an ~4ha, low elevation sand cay located in Torres Strait, Australia, supports the only known population of the endangered Bramble Cay melomys Melomys rubicola Thomas, 1924. As a result of a decline in this population noted during previous monitoring to 2004, habitat loss due to erosion of the cay and direct mortality from storm surges were implicated as major threats to this species. This study aimed to confirm the current conservation status of the species, to seek information about the key factor or factors responsible for the population decline and to recover any remaining individuals for a captive insurance population. Methods During three survey periods (December 2011, March 2014 and August–September 2014), a total of 1170 small mammal trap-nights, 60 camera trap-nights, 5h of nocturnal searches and 5h of diurnal searches were undertaken on Bramble Cay. Key results All three survey periods failed to detect any Bramble Cay melomys. The island had experienced a recent, severe reduction in vegetation, which is the primary food resource for the Bramble Cay melomys. Herbaceous cover on the cay decreased from 2.16ha in 2004 to 0.065ha in March 2014 before recovering somewhat to 0.19ha in August–September 2014. Conclusions These results demonstrate that this rodent species has now been extirpated on Bramble Cay. The vegetation decline was probably due to ocean inundation resulting from an increased frequency and intensity of weather events producing extreme high water levels and storm surges, in turn caused by anthropogenic climate change. Implications The loss of the Bramble Cay melomys from Bramble Cay probably represents the first documented mammalian extinction due to human-induced climate change. This event highlights the immediate need to mitigate predicted impacts of sea-level rise and ocean inundation on other vulnerable species occurring on low lying islands and in susceptible coastal zones through captive breeding and reintroduction or other targeted measures.

The water mouse is a small and vulnerable rodent present in coastal areas of south-west Papua New Guinea, and eastern Queensland and the Northern Territory of Australia. Current knowledge regarding the distribution of the water mouse is incomplete and the loss of one local population has been documented in southeast Queensland, a region where pressures from urban and industrial development are increasing. Water mouse populations have not been studied intensively enough to enable the primary factors responsible for the local decline to be identified. We surveyed the distribution and density of the water mouse along the Maroochy River of southeast Queensland, near the southern extent of the species’ range, to gather baseline data that may prove valuable for detecting any future decline in this population’s size or health. All areas of suitable habitat were surveyed on foot or by kayak or boat over a three-year period. We found 180 water mouse nests, of which ~94% were active. Permanent camera monitoring of one nest and limited supplementary live trapping suggested that up to three individual mice occupied active nests. Water mouse density was estimated to be 0.44 per hectare of suitable habitat along the Maroochy River. Should future monitoring reveal an adverse change in the water mouse population on the Maroochy River, a concerted effort should be made to identify contributing factors and address proximate reasons for the decline.

1. We have used intracellular recording and staining techniques to examine the importance of certain identified interneurons within the system responsible for triggering kicks and jumps in the locust, Locusta migratoria. In particular, our study focused on a pair of metathoracic interneurons called the M-neurons. These cells make strong inhibitory connections to hind-leg flexor motoneurons and are thought to play a key role in the termination of flexor activity which causes kicks and jumps to be triggered (8, 20, 24). 2. Simultaneous recordings from M-neurons and flexor motoneurons during bilateral hindleg kicks revealed that in most cases the onset of the M-neuron's high-frequency discharge coincided precisely with the start of the flexor's rapid repolarization. This result demonstrated that M's activity had the correct timing to be involved in the triggering process and so confirmed suggestions made in previous studies. At times, however, the flexor motoneurons began to repolarize slowly prior to the first spike in the M-neuron, indicating that triggering must involve other neurons and perhaps also an additional mechanism such as a reduction of flexor excitation. 3. The sufficiency and necessity of the M-neurons for triggering kicks were tested by experiments involving intracellular current injections. The application of a brief pulse of depolarizing current to an M-neuron, in order to evoke a burst of spikes in the cell prior to the time it would normally have become active, caused extension of the ipsilateral leg to be triggered prematurely but did not influence the motor program in the contralateral leg. This effect was only observed when the discharge frequency evoked artificially in the M-neuron was greater than that seen during natural performance of the behavior. Even then, the repolarization produced in the flexor motoneurons by the current pulses was not the same as occurs normally. We conclude that under natural circumstances the M-neurons, by themselves, are not sufficient to trigger kicks. 4. When the usual discharge in an M-neuron was prevented by the injection of hyperpolarizing current, both legs were still able to kick. This lack of necessity of the M-neurons confirms that additional neurons must be involved in the triggering process. The rate of repolarization of the flexor motoneurons during kicks in which M activity had been abolished was slower and more variable than is seen in normal kicks but this did not appear to alter the timing of leg extension.(ABSTRACT TRUNCATED AT 400 WORDS)