Associative learning elicits the formation of multiple-synapse boutons

The formation of new synapses has been suggested to underlie learning and memory. However, previous work from this laboratory has demonstrated that hippocampus-dependent associative learning does not induce a net gain in the total number of hippocampal synapses and, hence, a net synaptogenesis. The aim of the present work was to determine whether associative learning involves a specific synaptogenesis confined to the formation of multiple-synapse boutons (MSBs) that synapse with more than one dendritic spine. We used the behavioral paradigm of trace eyeblink conditioning, which is a hippocampus-dependent form of associative learning. Conditioned rabbits were given daily 80-trial sessions to a criterion of 80% conditioned responses in a session. During each trial, the conditioned stimulus (tone) and the unconditioned stimulus (corneal airpuff) were presented with an intervening trace interval of 500 msec. Brain tissue was taken for morphological analyses 24 hr after the last session. Unbiased stereological methods were used for obtaining estimates of the total number of MSBs in the stratum radiatum of hippocampal subfield CA1. The results showed that the total number of MSBs was significantly increased in conditioned rabbits as compared with pseudoconditioned or unstimulated controls. This conditioning-induced change, which occurs without a net synaptogenesis, reflects a specific synaptogenesis resulting in MSB formation. Models of the latter process are proposed. The models postulate that it requires spine motility and may involve the relocation of existing spines from nonactivated boutons or the outgrowth of newly formed spines for specific synaptogenesis with single-synapse boutons activated by the conditioning stimulation

Intercomparison of erythemal broadband radiometers calibrated by seven UV calibration facilities in Europe and the USA

International audienceA bi-lateral intercomparison of erythemal broadband radiometers was performed between seven UV calibration facilities. The owners calibrations were compared relative to the characterisation and calibration performed at PMOD/WRC in Davos, Switzerland. The calibration consisted in the determination of the spectral and angular response of the radiometer, followed by an absolute calibration performed outdoors relative to a spectroradiometer which provided the absolute reference. The characterization of the detectors in the respective laboratories are in good agreement: The determination of the angular responses have deviations below ±4% and the spectral responses agree within ±20%. A "blind" intercomparison of the erythemally weighted irradiances derived by the respective institutes and PMOD/WRC showed consistent measurements to within ±2% for the majority of institutes. One institute showed slightly larger deviation of 10%. The differences found between the different instrument calibrations are all within the combined uncertainty of the calibration

On the correspondence between surface UV observations and TOMS determinations of surface UV: a potential method for quality evaluating world surface UV observations

A comparison of erythemally weighted surface UV irradiance observations with similar NASA TOMS surface UV determinations is described. Comparisons are made for two observation periods: the Robertson-Berger (R-B) meter period from 1974 to the late 1980s and the current period from 1996 to the present when more sophisticated UVB-1 instruments were used. The more primitive R-B meter observations that comprised the fi rst U.S. UV network are seen to drift downward with respect to those of the TOMS. While the UVB-1 observations did not appear to drift, a substantial bias is noted to exist between the TOMS and the UVB-1 stations collecting observations; the TOMS estimations tend to be higher. A portion of the bias may be attributed to errors in calibration, total ozone, and cosine response of the surface instrumentation. Unaccounted aerosol effects, although not considered to be large in the TOMS estimations, present another source of error. Comparisons are fi rst done for all sky conditions and then for clear sky conditions. The biases typically agree for all sky conditions within the uncertainties of the surface instruments' calibrations, liberally defi ned as ± 5%, implying that the TOMS cloud correction scheme performs reasonably well. Snow cover severely impacts the TOMS observations, giving considerably higher estimations. The biases for clear sky conditions ranged from 15% to 19% with no obvious drifts between the satellite and surface observations. The variation in the biases among stations is within the calibration uncertainties of the instruments, but the absolute bias is unexpectedly large. The standard deviations of the clear sky comparisons among all stations are steady at 4.8% ± 0.7%. A plot of the TOMS/UVB-1 ratio versus TOMS cloud refl ectivity observations is noisy, but qualitatively suggestive of a possible slight increase (~ 5% or greater) over the range of clear to overcast skies. The results from these comparisons is believed to be relevant to a WMO goal of uniformly assuring the quality of UV observations made by networks in many countries. The results for clear sky comparisons suggest that a satellite observing system such as TOMS, which provides global coverage daily, might partially serve as a fi rst-order check to quality assure UV observations being made by networks worldwide. Future research should concentrate on determining the causes of the large differences seen between the UVB-1 and TOMS and the range of uncertainties, using a larger array of stations

Learning intrinsic excitability in medium spiny neurons

We present an unsupervised, local activation-dependent learning rule for intrinsic plasticity (IP) which affects the composition of ion channel conductances for single neurons in a use-dependent way. We use a single-compartment conductance-based model for medium spiny striatal neurons in order to show the effects of parametrization of individual ion channels on the neuronal activation function. We show that parameter changes within the physiological ranges are sufficient to create an ensemble of neurons with significantly different activation functions. We emphasize that the effects of intrinsic neuronal variability on spiking behavior require a distributed mode of synaptic input and can be eliminated by strongly correlated input. We show how variability and adaptivity in ion channel conductances can be utilized to store patterns without an additional contribution by synaptic plasticity (SP). The adaptation of the spike response may result in either "positive" or "negative" pattern learning. However, read-out of stored information depends on a distributed pattern of synaptic activity to let intrinsic variability determine spike response. We briefly discuss the implications of this conditional memory on learning and addiction.Comment: 20 pages, 8 figure

CAMKII Activation Is Not Required for Maintenance of Learning-Induced Enhancement of Neuronal Excitability

Pyramidal neurons in the piriform cortex from olfactory-discrimination trained rats show enhanced intrinsic neuronal excitability that lasts for several days after learning. Such enhanced intrinsic excitability is mediated by long-term reduction in the post-burst after-hyperpolarization (AHP) which is generated by repetitive spike firing. AHP reduction is due to decreased conductance of a calcium-dependent potassium current, the sIAHP. We have previously shown that learning-induced AHP reduction is maintained by persistent protein kinase C (PKC) and extracellular regulated kinase (ERK) activation. However, the molecular machinery underlying this long-lasting modulation of intrinsic excitability is yet to be fully described. Here we examine whether the CaMKII, which is known to be crucial in learning, memory and synaptic plasticity processes, is instrumental for the maintenance of learning-induced AHP reduction. KN93, that selectively blocks CaMKII autophosphorylation at Thr286, reduced the AHP in neurons from trained and control rat to the same extent. Consequently, the differences in AHP amplitude and neuronal adaptation between neurons from trained rats and controls remained. Accordingly, the level of activated CaMKII was similar in pirifrom cortex samples taken form trained and control rats. Our data show that although CaMKII modulates the amplitude of AHP of pyramidal neurons in the piriform cortex, its activation is not required for maintaining learning-induced enhancement of neuronal excitability