The Revised Edition of Korean Calendar for Allergenic Pollens

The old calendar of pollens did not reflect current pollen distribution and concentrations that can be influenced by changes of weather and environment of each region in South Korea. A new pollen calendar of allergenic pollens was made based on the data on pollen concentrations obtained in eight regions nationwide between 1997 and 2009. The distribution of pollen was assessed every day at 8 areas (Seoul, Guri, Busan, Daegu, Jeonju, Kwangju, Kangneung, and Jeju) for 12 years between July 1, 1997 and June 30, 2009. Pollens were collected by using Burkard 7-day sampler (Burkard Manufacturing Co Ltd, UK). Pollens which were stained with Calberla's fuchsin staining solution were identified and counted. Pine became the highest pollen in May, and the pollen concentrations of oak and birch also became high. Ragweed appeared in the middle of August and showed the highest pollen concentration in the middles of September. Japanese hop showed a high concentration between the middle of August and the end of September, and mugwort appeared in the middles of August and its concentration increased up until early September. In Kangneung, birch appeared earlier, pine showed a higher pollen concentration than in the other areas. In Daegu, Oriental thuja and alder produced a large concentration of pollens. Pine produced a large concentration of pollens between the middle of April and the end of May. Weeds showed higher concentrations in September and mugwort appeared earlier than ragweed. In Busan the time of flowering is relatively early, and alder and Oriental thuja appeared earliest among all areas. In Kwangju, Oriental thuja and hazelnut appeared in early February. Japanese cedar showed the highest pollen concentration in March in Jeju. In conclusion, update information on pollen calendar in South Korea should be provided for allergic patients through the website to manage and prevent the pollinosis

GABAergic-like dopamine synapses in the mouse brain

Dopaminergic neurons exist in the midbrain and their axons establish synapses throughout the whole brain. Synaptic transmission at these synapses is crucial for volitional movement and reward-related behaviors, while dysfunction of these synapses causes various psychiatric and neurological disorders. Despite this significance, the brain-wide spatial and functional features of dopamine (DA) synapses remain poorly understood due to difficulties in defining functional DA synapses at the molecular and physiological levels. Here we show that DA synapses are structured and function like GABAergic synapses in the mouse brain. DA transmission is strongly correlated with GABA co-transmission at DA synapses across the brain areas. In addition, functional DA synapses contain GABAergic postsynaptic markers in their postsynaptic membrane and are unevenly distributed throughout the brain with distinct spatial clustering. In the dorsal striatum, GABAergic-like DA synapses are uniquely clustered on the dendrites and GABA transmission at these synapses have disparate physiological properties. Remarkably, the attenuation of GABA co-transmission preceded any deficits in dopaminergic transmission or motor functions of the animal model of Parkinsonism. Our findings show distinct spatial and functional properties of GABAergic-like DA synapses in health and disease. Furthermore, the GABAergic-like features of DA synapses can be utilized to better understand the real complexity of synaptic actions at DA synapses in regulating neural circuits

GABAergic-like Dopamine Synapses in the Mouse Brain

Dopaminergic axons originate in the midbrain (substantia nigra pars compacta and ventral tegmental area) and establish widely spread synapses throughout the brain. Synaptic transmission at these synapses plays a crucial role for volitional movement and reward-related behaviors, while the dysfunction of dopamine synapses causes various psychiatric and neurological disorders. Despite this significance, the true nature of brain-wide spatial and functional features of dopamine synapses remains poorly understood due to difficulties defining functional dopamine synapses at the molecular and physiological levels. Here we show that dopamine synapses are structured and function like GABAergic synapses in the mouse brain with marked regional heterogeneity. Dopamine transmission is strongly correlated with GABA co-transmission at dopamine synapses across the brain areas. In addition, functional dopamine synapses possess GABAergic postsynaptic markers and are unevenly distributed throughout the brain with distinct spatial clustering. In the dorsal striatum, GABAergic-like dopamine synapses are uniquely clustered on the dendrites and GABA transmission at dopamine synapses has disparate physiological characteristics. Remarkably, the attenuation of GABA co-transmission precedes defects in dopaminergic transmission in animal model of Parkinsonism. Our findings unravel distinct spatial and functional nature of GABAergic-like dopamine synapses in health and disease. Furthermore, the broader implication of our results is that GABAergic-like features of dopamine synapses can be utilized to better understand the real complexity of synaptic actions at dopamine synapses in regulating neural circuits

GABAergic-like dopamine synapses in the brain

Dopaminergic axons originate in the midbrain (substantia nigra pars compacta and ventral tegmental area) and establish widely spread synapses throughout the brain. Synaptic transmission at these synapses plays a crucial role for volitional movement and reward-related behaviors, while the dysfunction of dopamine synapses causes various psychiatric and neurological disorders. Despite this significance, the true nature of brain-wide spatial and functional features of dopamine synapses remains poorly understood due to difficulties defining functional dopamine synapses at the molecular and physiological levels. Here we show that dopamine synapses are structured and function like GABAergic synapses in the mouse brain with marked regional heterogeneity. Dopamine transmission is strongly correlated with GABA co-transmission at dopamine synapses across the brain areas. In addition, functional dopamine synapses possess GABAergic postsynaptic markers and are unevenly distributed throughout the brain with distinct spatial clustering. In the dorsal striatum, GABAergic-like dopamine synapses are uniquely clustered on the dendrites and GABA transmission at dopamine synapses has disparate physiological characteristics. Remarkably, the attenuation of GABA co-transmission precedes defects in dopaminergic transmission in animal model of Parkinsonism. Our findings unravel distinct spatial and functional nature of GABAergic-like dopamine synapses in health and disease. Furthermore, the broader implication of our results is that GABAergic-like features of dopamine synapses can be utilized to better understand the real complexity of synaptic actions at dopamine synapses in regulating neural circuits

Gabaergic-like dopamine synapses in health and parkinson's disease

Dopaminergic neurons exist in the midbrain and their axons establish synapses throughout the whole brain. Synaptic transmission at these synapses is crucial for volitional movement and reward-related behaviors, while dysfunction of these synapses causes various psychiatric and neurological disorders. Despite this significance, true biological nature of dopamine synapses remains poorly understood due to difficulties defining functional dopamine synapses at the molecular and physiological levels. Here we show that GABA co-transmission co-exists with dopamine transmission across the brain and a significant portion of dopamine synapses are structured and function like GABAergic synapses with marked regional heterogeneity, which we call GABAergic-like dopamine synapses identified by triple co-localization of tyrosine hydroxylase (TH), bassoon, and neuroligin-2 (NL2). GABAergic-like dopamine synapses show higher density, but lower clustered patterns compared to conventional GABAergic synapses on the dendrites of spiny projection neurons in the dorsal striatum. Moreover, GABA transmission at dopamine synapses has physiological properties distinct from conventional GABA transmission in terms of its calcium channel dependency and quantal properties. Interestingly, 6 weeks knockdown of NL2, a key postsynaptic protein at GABAergic synapses, unexpectedly does not weaken GABA co-transmission but instead temporarily facilitates it at dopamine synapses in striatal neurons. As expected, longer periods of NL2 knockdown (12 weeks) significantly diminishes GABA co-transmission. On the other hand, dopamine transmission and GABAergic-like dopamine synapses are considerably downregulated in both 6 weeks and 12 weeks of NL2 knockdown. More importantly, the attenuation of GABA co-transmission precedes deficits in dopaminergic transmission in animal models of Parkinson???s disease. Our findings reveal unknown spatial and functional nature of GABAergic-like dopamine synapses in health and disease. Furthermore, the broader implication of our results is that GABAergic-like features of dopamine synapses can be utilized to better understand the real complexity of synaptic actions at dopamine synapses in regulating neural circuits

GABAergic-like dopamine synapses in health and Parkinsonism

Dopamine synapses play a crucial role for volitional movement and reward-related behaviors, while dysfunction of dopamine synapses causes various psychiatric and neurological disorders. Despite this significance, true biological nature of dopamine synapses remains poorly understood in the brain. Here we show that dopamine transmission is strongly correlated with GABA co-transmission across the brain and dopamine synapses are structured and function like GABAergic synapses with marked regional heterogeneity. In addition, GABAergic-like dopamine synapses are uniquely clustered on the dendrites and GABA transmission at dopamine synapses has distinct physiological properties. Interestingly, knockdown of neuroligin-2, a key postsynaptic protein at GABAergic synapses, unexpectedly does not weaken GABA co-transmission but instead facilitates it at dopamine synapses in the striatal neurons. More importantly, the attenuation of GABA co-transmission precedes deficits in dopaminergic transmission in an animal model of Parkinsonism. Our findings reveal unknown spatial and functional nature of GABAergic-like dopamine synapses in health and disease

GABAergic-like dopamine synapses in the brain and Parkinson???s disease

Dopamine synapses play a crucial role for volitional movement and reward-related behaviors, while dysfunction of dopamine synapses causes various psychiatric and neurological disorders. Despite this significance, true biological nature of dopamine synapses remains poorly understood in the brain. Here we show that dopamine transmission is strongly correlated with GABA co-transmission across the brain and dopamine synapses are structured and function like GABAergic synapses with marked regional heterogeneity. In addition, GABAergic-like dopamine synapses are uniquely clustered on the dendrites and GABA transmission at dopamine synapses has distinct physiological properties. Interestingly, knockdown of neuroligin-2, a key postsynaptic protein at GABAergic synapses, temporarily facilitates GABA co-transmission at dopamine synapses in the striatal neurons. More importantly, the attenuation of GABA co-transmission precedes deficits in dopaminergic transmission in an animal model of Parkinson???s disease. Our findings reveal unknown spatial and functional nature of GABAergic-like dopamine synapses in health and Parkinson???s disease

GABAergic-like dopamine synapses in health and Parkinsonism

Dopamine synapses play a crucial role for volitional movement and reward- related behaviors, while dysfunction of dopamine synapses causes various psychiatric and neurological disorders. Despite this significance, true biological nature of dopamine synapses remains poorly understood in the brain. Here we show that dopamine transmission is strongly correlated with GABA co-transmission across the brain and dopamine synapses are structured and function like GABAergic synapses with marked regional heterogeneity. In addition, GABAergic-like dopamine synapses are uniquely clustered on the dendrites and GABA transmission at dopamine synapses has distinct physiological properties. Interestingly, knockdown of neuroligin- 2, a key postsynaptic protein at GABAergic synapses, unexpectedly does not weaken GABA co-transmission but instead facilitates it at dopamine synapses in the striatal neurons. More importantly, the attenuation of GABA co-transmission precedes deficits in dopaminergic transmission in an animal model of Parkinsonism. Our findings reveal unknown spatial and functional nature of GABAergic-like dopamine synapses in health and disease

GABAergic-like dopamine synapses in the brain

Dopaminergic axons originate in the midbrain and establish widely spread synapses throughout the brain. Synaptic transmission at these synapses plays a crucial role for volitional movement and reward-related behaviors, while the dysfunction of dopamine synapses causes various psychiatric and neurological disorders. Despite this significance, the true nature of brain-wide spatial and functional features of dopamine synapses remains poorly understood due to difficulties defining functional dopamine synapses at the molecular and physiological levels. Here we show that dopamine synapses are structured and function like GABAergic synapses in the mouse brain with marked regional heterogeneity. Dopamine transmission is strongly correlated with GABA co-transmission at dopamine synapses across the brain areas. In addition, functional dopamine synapses possess GABAergic postsynaptic markers and are unevenly distributed throughout the brain with distinct spatial clustering. In the dorsal striatum, GABAergic-like dopamine synapses are uniquely clustered on the dendrites and GABA transmission at dopamine synapses has disparate physiological characteristics. Importantly, knockdown of the inhibitory cell adhesion molecule in the postsynaptic striatal neurons unexpectedly did not weaken but instead facilitated GABA transmission at dopamine synapses. Lastly, the attenuation of GABA co-transmission precedes defects in dopaminergic transmission in an animal model of Parkinsonism. Our findings unravel distinct spatial and functional nature of GABAergic-like dopamine synapses in health and disease. Furthermore, the broader implication of our results is that GABAergic-like features of dopamine synapses can be utilized to better understand the real complexity of synaptic actions at dopamine synapses in regulating neural circuits