Редактирование: AIDA (раздел)

==Publications==

{{medline-entry
|title=Identification of Postharvest Senescence Regulators Through Map-Based Cloning Using Detached Arabidopsis Inflorescences as a Model Tissue.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29392668
|abstract=Postharvest deterioration of fruits and vegetables can be accelerated by biological, environmental, and physiological stresses. Fully understanding tissue response to harvest will provide new opportunities for limiting postharvest losses during handling and storage. The model plant Arabidopsis thaliana (Arabidopsis) has many attributes that make it excellent for studying the underlying control of postharvest responses. It is also one of the best resourced plants with numerous web-based bioinformatic programs and large numbers of mutant collections. Here we introduce a novel assay system called [[AIDA]] (the Arabidopsis Inflorescence Degreening Assay) that we developed for understanding postharvest response of immature tissues. We also demonstrate how the high-throughput screening capability of [[AIDA]] can be used with mapping technologies (high-resolution melting [HRM] and needle in the k-stack [NIKS]) to identify regulators of postharvest senescence in ethyl methanesulfonate (EMS) mutagenized plant populations. Whether it is best to use HRM or NIKS or both technologies will depend on your laboratory facilities and computing capabilities.
|mesh-terms=* Aging
* Arabidopsis
* Biomarkers
* Chlorophyll
* Chromosome Mapping
* Genomics
* Organ Specificity
* Phenotype
* Plant Physiological Phenomena
* Polymorphism, Single Nucleotide
|keywords=* EMS
* Ethyl methanesulfonate
* HRM
* High-resolution melting
* Postharvest
* Senescence
* WGS
* Whole genome sequencing
|full-text-url=https://sci-hub.do/10.1007/978-1-4939-7672-0_17
}}
{{medline-entry
|title=Interaction of DHPG-LTD and synaptic-LTD at senescent [[CA3]]-[[CA1]] hippocampal synapses.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24390964
|abstract=The susceptibility, but not the magnitude, of long-term depression (LTD) induced by hippocampal [[CA3]]-[[CA1]] synaptic activity (synaptic-LTD) increases with advanced age. In contrast, the magnitude of LTD induced by pharmacological activation of [[CA3]]-[[CA1]] group I metabotropic glutamate receptors (mGluRs) increases during aging. This study examined the signaling pathways involved in induction of LTD and the interaction between paired-pulse low frequency stimulation-induced synaptic-LTD and group I mGluR selective agonist, (RS)-3,5-dihydroxyphenylglycine (DHPG, 100 µM)-induced DHPG-LTD in hippocampal slices obtained from aged (22-24 months) male Fischer 344 rats. Prior induction of synaptic-LTD did not affect induction of DHPG-LTD; however, prior induction of the DHPG-LTD occluded synaptic-LTD suggesting that expression of DHPG-LTD may incorporate synaptic-LTD mechanisms. Application of individual antagonist for the group I mGluR ([[AIDA]]), the N-methyl-d-aspartate receptor (NMDAR) (AP-5), or L-type voltage-dependent Ca(2 ) channel (VDCC) (nifedipine) failed to block synaptic-LTD and any two antagonists severely impaired synaptic-LTD induction, indicating that activation of any two mechanisms is sufficient to induce synaptic-LTD in aged animals. For DHPG-LTD, [[AIDA]] blocked DHPG-LTD and individually applied NMDAR or VDCC attenuated but did not block DHPG-LTD, indicating that the magnitude of DHPG-LTD depends on all three mechanisms.
|mesh-terms=* Aging
* Animals
* CA1 Region, Hippocampal
* CA3 Region, Hippocampal
* Calcium Channel Blockers
* Calcium Channels, L-Type
* Electric Stimulation
* Excitatory Amino Acid Agonists
* Excitatory Amino Acid Antagonists
* Glycine
* In Vitro Techniques
* Indans
* Long-Term Synaptic Depression
* Male
* Nifedipine
* Rats
* Rats, Inbred F344
* Receptors, Metabotropic Glutamate
* Receptors, N-Methyl-D-Aspartate
* Resorcinols
* Synapses
|keywords=* DHPG
* NMDA receptors
* VDCC
* aging
* calcium
* long-term depression
* mGluR
* synaptic plasticity
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3959216
}}
{{medline-entry
|title=Effects of mGluR5 and mGluR1 antagonists on anxiety-like behavior and learning in developing rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/19505510
|abstract=Antagonists of group I metabotropic receptors exhibit anxiolytic action in adult rats. In immature animals we demonstrated anticonvulsant action of MPEP and [[AIDA]], antagonists of group 5 and group 1, respectively. However, there are no developmental data on anxiolytic-like and learning actions of both compounds. This study investigated whether the anticonvulsant dose range of MPEP and [[AIDA]] affects anxiety-like behavior and learning ability in immature rats. Animals at 12, 18 and 25 postnatal (P) days received MPEP in doses of 10, 20 or 40 mg/kg i.p., [[AIDA]] in doses of 10 or 20 mg/kg i.p. In P18 and P25 rats anxiety-like behavior and locomotor activity were tested in the light-dark box and open-field test at 15 (1st session) and 60 (2nd session) minutes after drug administration. Learning ability of P12, P18, and P25 animals was examined in the homing response test 15 min after drug administration. Both antagonists exhibited anxiolytic-like action in the 1st session, effects in the 2nd session were less marked. In the open-field test both antagonists increased locomotion only in P18 animals. Age-dependent changes were found in the homing response test, the return latency being longer only in P12 animals. While MPEP in doses of 20- and 40-mg/kg in P12 and 40-mg/kg in P18 rats prolonged the homing response, [[AIDA]] did not affect the homing behavior. Both MPEP and [[AIDA]] exert anxiolytic-like effect also in immature rats. Except for the youngest animals no changes in learning ability in the homing response test were found.
|mesh-terms=* Aging
* Animals
* Anti-Anxiety Agents
* Anxiety
* Excitatory Amino Acid Antagonists
* Indans
* Learning
* Male
* Motor Activity
* Neuropsychological Tests
* Pyridines
* Random Allocation
* Rats
* Rats, Wistar
* Receptor, Metabotropic Glutamate 5
* Receptors, Metabotropic Glutamate
* Time Factors

|full-text-url=https://sci-hub.do/10.1016/j.bbr.2009.05.032
}}
{{medline-entry
|title=Age-dependent anticonvulsant action of antagonists of group I glutamate metabotropic receptors in rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/19097860
|abstract=Metabotropic glutamate receptors (mGluR) may represent a perspective target for anticonvulsant therapy but spectrum of their anticonvulsant effects is not sufficiently known. Our study was aimed at comparison of anticonvulsant actions of antagonists of mGluR1 and mGluR5 subtypes in immature rats. Seven-, 12-, 18- and 25-day-old animals were pretreated with mGluR1 antagonist [[AIDA]] (1-20mg/kg i.p.) or mGluR5 antagonist MTEP (5-40 mg/kg i.p.) 30 min before pentetrazol administration (100mg/kg s.c.). Two types of motor seizures were elicited: minimal, clonic seizures (mS) and generalized tonic-clonic seizures (GTCS). mS could be induced only in 18- and 25-day-old rats, and their incidence was decreased to 0-50% by nearly all doses of either drug in 18- but not in 25-day-old rats. GTCS were observed in all age groups; higher doses of both antagonists specifically suppressed the tonic phase in 7-, 12- and 18-day-old rats. The highest efficacy was found in 12-day-old rats; seizure severity was significantly decreased even by the 10-mg/kg dose of MTEP and the 2-mg/kg dose of [[AIDA]] in this age group. In addition, MTEP tended to suppress also the clonic phase in 7-day-old rats. Time course of action studied in 12-day-old animals demonstrated much longer action of MTEP (more than 4h) than of [[AIDA]] (less than 1h). Administration of [[AIDA]] but not MTEP resulted in a paradoxical shortening of latencies of seizures even at time intervals when the incidence of the tonic phase of GTCS was decreased. Both mGluR antagonists exhibit specific anticonvulsant action in rat pups during the first 3 postnatal weeks.
|mesh-terms=* Aging
* Analysis of Variance
* Animal Diseases
* Animals
* Animals, Newborn
* Anticonvulsants
* Dicarboxylic Acids
* Dose-Response Relationship, Drug
* Epilepsy
* Male
* Pentylenetetrazole
* Pyridines
* Rats
* Rats, Wistar
* Reaction Time
* Receptors, Metabotropic Glutamate
* Severity of Illness Index
* Thiazoles
* Time Factors

|full-text-url=https://sci-hub.do/10.1016/j.eplepsyres.2008.11.004
}}
{{medline-entry
|title=Age-related changes in tolerance to the marine algal excitotoxin domoic acid.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/12243765
|abstract=During an incident of toxic mussel poisoning, the epileptogenic excitotoxin domoic acid (DOM) was associated with lasting neurological deficits mainly in older patients (), suggesting supersensitivity to excitotoxins is a feature of brain aging. Here, hippocampal slices from young (3 months) and aged (26-29 months) Sprague Dawley rats were assessed by [[CA1]] field potential analysis before and after preconditioning with DOM. In naïve slices from young animals, DOM produced initial hyperexcitability followed by significant dose-dependent reductions in population spike amplitude during prolonged application. Following toxin washout, only small changes in neuronal activity were evident during a second application of DOM, suggesting that a resistance to the effects of DOM occurs in hippocampal slices which have undergone prior exposure to DOM. This inducible tolerance was not antagonized by the NMDA receptor blockers APV or MK-801, nor was it diminished by the group I, II or III mGluR blockers [[AIDA]], CPPG and EGLU. Likewise, neither the AMPA/KA blocker CNQX nor the VSCC blocker nifedipine were effective in blocking tolerance induction in young slices. Field potential analysis revealed significant age-related reductions in [[CA1]] EPSP strength, population spike amplitude and paired-pulse inhibition, but aged slices did not differ in sensitivity to DOM relative to young. However, aged [[CA1]] failed to exhibit any tolerance to DOM following preconditioning, suggesting that a loss of inducible neuroprotective mechanisms may account for increased sensitivity to excitotoxins during aging.
|mesh-terms=* Aging
* Animals
* Calcium Channel Blockers
* Drug Tolerance
* Excitatory Amino Acid Antagonists
* Hippocampus
* In Vitro Techniques
* Kainic Acid
* Male
* Neuromuscular Depolarizing Agents
* Neurons
* Rats
* Rats, Sprague-Dawley
* Receptors, Glutamate

|full-text-url=https://sci-hub.do/10.1016/s0028-3908(02)00088-6
}}