Chronic nicotine exposure influences learning and memory in the honey bee.

In insects, nicotine activates nicotinic acetylcholine receptors, which are expressed throughout the central nervous system. However, little work has been done to investigate the effects of chronic nicotine treatment on learning or other behaviors in non-herbivorous insects. To examine the effects of long term nicotine consumption on learning and memory, honey bees were fed nicotine containing solutions over four days. Bees were able to detect nicotine at 0.1 mM in sucrose solutions, and in a no choice assay, bees reduced food intake when nicotine was 1 mM or higher. Treatment with a low dose of nicotine decreased the proportion of bees able to form an associative memory when bees were conditioned with either a massed or spaced appetitive olfactory training paradigm. On the other hand, higher doses of nicotine increased memory retention and the proportion of bees responding to the odor during 10 min and 24 h recall tests. The reduction in nicotine containing food consumed may also impact response levels during learning and recall tests. These data suggest that long term exposure to nicotine has complex effects on learning and memory.

The impact of temporal modulations in irradiance under light adapted conditions on the mouse suprachiasmatic nuclei (SCN).

Electrophysiological responses of SCN neurons to light steps are well established, but responses to more natural modulations in irradiance have been much less studied. We address this deficit first by showing that variations in irradiance for human subjects are biased towards low temporal frequencies and small magnitudes. Using extracellular recordings we show that neurons in the mouse SCN are responsive to stimuli with these characteristics, tracking sinusoidal modulations in irradiance best at lower temporal frequencies and responding to abrupt changes in irradiance over a range of commonly encountered contrasts. The spectral sensitivity of these light adapted responses indicates that they are driven primarily by cones, but with melanopsin (and/or rods) contributing under more gradual changes. Higher frequency modulations in irradiance increased time averaged firing of SCN neurons (typically considered to encode background light intensity) modestly over that encountered during steady exposure, but did not have a detectable effect on the circadian phase resetting efficiency of light. Our findings highlight the SCN's ability to encode naturalistic temporal modulations in irradiance, while revealing that the circadian system can effectively integrate such signals over time such that phase-resetting responses remain proportional to the mean light exposure.