African swine fever in wild boar

The European Commission requested EFSA to compare the reliability of wild boar density estimates across the EU and to provide guidance to improve data collection methods. Currently, the only EU-wide available data are hunting data. Their collection methods should be harmonised to be comparable and to improve predictive models for wild boar density. These models could be validated by more precise density data, collected at local level e.g. by camera trapping. Based on practical and theoretical considerations, it is currently not possible to establish wild boar density thresholds that do not allow sustaining African swine fever (ASF). There are many drivers determining if ASF can be sustained or not, including heterogeneous population structures and human-mediated spread and there are still unknowns on the importance of different transmission modes in the epidemiology. Based on extensive literature reviews and observations from affected Member States, the efficacy of different wild boar population reduction and separation methods is evaluated. Different wild boar management strategies at different stages of the epidemic are suggested. Preventive measures to reduce and stabilise wild boar density, before ASF introduction, will be beneficial both in reducing the probability of exposure of the population to ASF and the efforts needed for potential emergency actions (i.e. less carcass removal) if an ASF incursion were to occur. Passive surveillance is the most effective and efficient method of surveillance for early detection of ASF in free areas. Following focal ASF introduction, the wild boar populations should be kept undisturbed for a short period (e.g. hunting ban on all species, leave crops unharvested to provide food and shelter within the affected area) and drastic reduction of the wild boar population may be performed only ahead of the ASF advance front, in the free populations. Following the decline in the epidemic, as demonstrated through passive surveillance, active population management should be reconsidered.info:eu-repo/semantics/publishedVersio

African swine fever in wild boar

The European Commission requested EFSA to compare the reliability of wild boar density estimates across the EU and to provide guidance to improve data collection methods. Currently, the only EU-wide available data are hunting data. Their collection methods should be harmonised to be comparable and to improve predictive models for wild boar density. These models could be validated by more precise density data, collected at local level e.g. by camera trapping. Based on practical and theoretical considerations, it is currently not possible to establish wild boar density thresholds that do not allow sustaining African swine fever (ASF). There are many drivers determining if ASF can be sustained or not, including heterogeneous population structures and human-mediated spread and there are still unknowns on the importance of different transmission modes in the epidemiology. Based on extensive literature reviews and observations from affected Member States, the efficacy of different wild boar population reduction and separation methods is evaluated. Different wild boar management strategies at different stages of the epidemic are suggested. Preventive measures to reduce and stabilise wild boar density, before ASF introduction, will be beneficial both in reducing the probability of exposure of the population to ASF and the efforts needed for potential emergency actions (i.e. less carcass removal) if an ASF incursion were to occur. Passive surveillance is the most effective and efficient method of surveillance for early detection of ASF in free areas. Following focal ASF introduction, the wild boar populations should be kept undisturbed for a short period (e.g. hunting ban on all species, leave crops unharvested to provide food and shelter within the affected area) and drastic reduction of the wild boar population may be performed only ahead of the ASF advance front, in the free populations. Following the decline in the epidemic, as demonstrated through passive surveillance, active population management should be reconsidered.info:eu-repo/semantics/publishedVersio

Bidirectional unitary postsynaptic responses at PV → PYR synapses are normal in Nlgn3^R451C mice.

<p>A) Simplified schematic of a PV → PYR synapse. B) Representative traces averaged from 20 consecutive sweeps (including failures). A short 20 Hz train of 5 action potentials is elicited from the presynaptic PV interneuron (in voltage clamp, top) and unitary IPSC (uIPSCs) are recorded from the postsynaptic pyramidal neuron (WT = middle; Nlgn3^R451C = bottom). Scale bars: 500 pA (PV), 25 pA (PYR); 25 ms. C) Scatter plot of uIPSC1 amplitude for each connected pair from WT (<i>n</i> = 34) and Nlgn3^R451C (<i>n</i> = 29). D) Scatter plot of uEPSC1 of connected PYR → PV pairs showing no difference in excitatory transmission onto PV interneurons between WT (<i>n</i> = 19) and Nlgn3^R451C (<i>n</i> = 12).</p

Increased inhibitory synaptic transmission at LII/III synapses from Nlgn3^R451C mice.

<p>mIPSC frequency (A), but not amplitude (B) of spontaneous inhibitory transmission in the presence of 1 μM TTX is increased Nlgn3^R451C mice (WT = 39, Nlgn3^R451C = 32). Inset: 15s raw trace from a WT (top) and Nlgn3^R451C (bottom) mouse. Scale bar: 25 pA; 0.5 s. C) The input/output (I/O) relationship of eIPSC amplitude to stimulus intensity is stronger in Nlgn3^R451C mice compared to WT controls (WT = 33, Nlgn3^R451C = 30). * <i>P</i> < 0.05, ** <i>P</i> < 0.01.</p

Firing properties of PV, SOM, and PYR neurons are not affected by the Nlgn3^R451C mutation.

<p>Raw traces of action potentials from (A) PV, (B) SOM, and (C) PYR neurons from WT (top) and Nlgn3^R451C (bottom) mice in response to a 125 pA step (represented by square pulse beneath each trace) above firing threshold. Scale bars: 25 mV; 50 ms. No difference is observed between Nlgn3^R451C and WT mice in the number of action potentials fired at 0–125 pA steps above firing threshold for PV (D), SOM (E), or PYR (F) neurons (PV: WT = 33, Nlgn3^R451C = 38; SOM: WT = 31, Nlgn3^R451C = 29; PYR: WT = 48, Nlgn3^R451C = 50). Inset: IR-DIC images taken with a 40X objective and 2X magnification of each respective cell type. Scale bar = 25 μm.</p

Number of PV and SOM interneurons is unaffected by the Nlgn3^R451C mutation.

<p>A) Representative image of DAB stained parvalbumin-positive cells with a Nissl counterstain in the somatosensory cortex. Scale bar = 50 μm. B) Representative image of DAB stained somatostatin-positive cells with a Nissl counterstain in the somatosensory cortex. Scale bar = 50 μm. C) The number of parvalbumin or somatostatin positive cells in the Nlgn3^R451C mutant somatosensory cortex counted using stereology and shown as percent of WT. WT = 10 mice, Nlgn3^R451C = 10 mice.</p

Chromatin remodeling factor Brg1 supports the early maintenance and late responsiveness of nestin-lineage adult neural stem and progenitor cells

Insights from embryonic development suggest chromatin remodeling is important in adult neural stem cells (aNSCs) maintenance and self‐renewal, but this concept has not been fully explored in the adult brain. To assess the role of chromatin remodeling in adult neurogenesis, we inducibly deleted Brg1—the core subunit of SWI/SNF‐like Brg1/Brm‐associated factor chromatin remodeling complexes—in nestin‐expressing aNSCs and their progeny in vivo and in culture. This resulted in abnormal adult neurogenesis in the hippocampus, which initially reduced hippocampal aNSCs and progenitor maintenance, and later reduced its responsiveness to physiological stimulation. Mechanistically, deletion of Brg1 appeared to impair cell cycle progression, which is partially due to elevated p53 pathway and p21 expression. Knockdown of p53 rescued the neurosphere growth defects caused by Brg1 deletion. Our results show that epigenetic chromatin remodeling (via a Brg1 and p53/p21‐dependent process) determines the aNSCs and progenitor maintenance and responsiveness of neurogenesis

Tonic endocannabinoid signaling is decreased at cortical inhibitory synapses in Nlgn3^R451C mice.

<p>Mean amplitude (A) and frequency (B) of mIPSCs recorded in the presence of 1 μM TTX and 10 μM AM 251 from pyramidal neurons of WT (<i>n</i> = 23) and Nlgn3^R451C (<i>n</i> = 23) mice. Inset: 15 s raw traces from WT (top) and Nlgn3^R451C (bottom) pyramidal neurons. Scale bar = 25 pA, 0.5 s. C) The Nlgn3^R451C-mediated increase in mIPSC frequency is occluded by bath application of AM 251 to neurons from WT mice (WT + AM 251 = 23, Nlgn3^R451C = 32). D) Input/output curves recorded in the presence of 10 μM AM 251 using the same range of stimulus intensities as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0140638#pone.0140638.g001" target="_blank">Fig 1C</a> (WT = 22, Nlgn3^R451C = 23). Mean Amplitude (E) and frequency (F) of mIPSCs recorded in the presence of CB1 receptor agonist ACEA (10 μM; WT = 24, Nlgn3^R451C = 25).* P < 0.05.</p

Chromatin remodeling factor Brg1 supports the early maintenance and late responsiveness of nestin-lineage adult neural stem and progenitor cells

Insights from embryonic development suggest chromatin remodeling is important in adult neural stem cells (aNSCs) maintenance and self‐renewal, but this concept has not been fully explored in the adult brain. To assess the role of chromatin remodeling in adult neurogenesis, we inducibly deleted Brg1—the core subunit of SWI/SNF‐like Brg1/Brm‐associated factor chromatin remodeling complexes—in nestin‐expressing aNSCs and their progeny in vivo and in culture. This resulted in abnormal adult neurogenesis in the hippocampus, which initially reduced hippocampal aNSCs and progenitor maintenance, and later reduced its responsiveness to physiological stimulation. Mechanistically, deletion of Brg1 appeared to impair cell cycle progression, which is partially due to elevated p53 pathway and p21 expression. Knockdown of p53 rescued the neurosphere growth defects caused by Brg1 deletion. Our results show that epigenetic chromatin remodeling (via a Brg1 and p53/p21‐dependent process) determines the aNSCs and progenitor maintenance and responsiveness of neurogenesis