Although the phenomenon of adhesion in geckos has been intensively studied for over 200 years, our understanding of how the morphological apparatus associated with this arose is less clear. Indeed, whether or not all of the intricate morphological hierarchy that is implicated in the attachment and removal of the adhesive setae originated at the same time is unknown. To explore whether setae may have arisen prior to the other parts of this structural hierarchy, we undertook morphological observations of Gonatodes, an ancestrally padless, sphaerodatyline genus known to exhibit the expression of incipient subdigital pads in some species. Focusing on this geographically and morphologically well-circumscribed genus, for which intraspecific relationships are adequately known and ecology is quite well documented, allowed us to deduce trends in digit proportions, shape, scalation, and skeletal structure, and associate these with the micro-ornamentation of the subdigital surfaces. Our findings indicate that in Gonatodes, setae capable of inducing adhesion are present without the modifications of the digital musculotendinous, circulatory and skeletal systems that are generally considered to be necessary for the operation of a functional adhesive apparatus. The acquisition of these latter characteristics (independently in many lineages of gekkotans, and incipiently so in Anolis) may have been preceded by a suite of modifications of the digits that enhanced static clinging in relation to sit-and-wait predation and the ability to take refuge on surfaces unavailable to other taxa. These possibilities await further testing.

Daily exposure to light synchronizes the circadian clock, located in the suprachiasmatic nucleus (SCN), to external day/night cycles. These responses to light can be modified by serotonergic drugs, such as serotonin 5HT1B receptor agonists. Triptans are specific 5HT1B agonists prescribed to treat migraines. Here, we examined the effects of two triptans (zolmitriptan and sumatriptan) on photic phase resetting in Syrian hamsters. Pre-treatment with intra-SCN sumatriptan significantly attenuates, and at higher doses completely blocks, phase advances to light during the late night. Pre-treatment with systemic zolmitriptan significantly attenuates both light-induced phase advances and phase delays. Neither of these drugs, nor their vehicles, causes phase shifts on their own. Pre-treatment with zolmitriptan also significantly reduces the expression of light-induced c-fos in the SCN. Neither zolmitriptan nor vehicle alone induces significant c-fos expression in the SCN. Finally, pre-treatment with zolmitriptan does not attenuate phase shifts to intra-SCN N-methyl-d-aspartate injections, indicating that the mechanism of action for zolmitriptan is likely to be through activation of presynaptic 5HT1B receptors on retinal terminals, thereby decreasing light-induced neurotransmitter release. As triptans are commercially available medications, there is potential for their use in blocking unwanted photic phase shifting during shift-work or jet-lag. Additionally, triptans may also affect the circadian clock in patients receiving them regularly for migraines. Finally, our results may hint at the mechanism by which triptans can alleviate the photophobia that frequently accompanies migraines, namely by activating 5HT1B receptors on retinal terminals elsewhere in the brain, and thereby diminishing visually-evoked neurotransmitter signalling in those areas.