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1

Divergent effects of bicuculline and picrotoxin on ketamine-induced apneustic breathing

100%

Budzinska K.

Journal of Physiology and Pharmacology. Supplement

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2005

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tom 56

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nr 4

39-46

This study tested the potential role of inhibitory neurotransmission in the mechanism of apneustic respiration evoked by ketamine, an NMDA receptors antagonist. In the experiments performed in anesthetized, paralyzed, and ventilated cats, ketamine, in a dose of 0.5 mg/kg, was administered before and after GABAA receptor blockade with picrotoxin or bicuculline; all agents were given intravenously. Ketamine elicited a transient, hourlong apneustic respiration consisting of an increase in inspiratory duration and a decrease in inspiratory neural amplitude. After prior administration of picrotoxin, but not bicuculline, the maximum apneustic-like prolongation of inspiration evoked by ketamine was considerably reduced. The results suggest that the GABA receptor subunits specifically sensitive to picrotoxin play a role in shaping the ketamine-induced apneustic breathing.

2

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Role of 5-hydroxytryptamine 1B receptors and 5-hydroxytryptamine uptake inhibition in the cocaine-evoked discriminative stimulus effects in rats

100%

Filip M., Nowak E., Papla I., Przegalinski E.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 2

3

Cytoprotective effect of lithium against spontaneous and induced apoptosis of lymphoid cell line MOLT-4

84%

Pietruczuk K., Jozwik A., Ruckemann-Dziurdzinska K., Bryl E., Witkowski J. M.

Folia Histochemica et Cytobiologica

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2009

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tom 47

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nr 4

4

Alteration of sphingolipid biostat in experimental model of oxidative stress evoked by 1-methyl-4-phenylpyridinium (MPPplus)

84%

Pyszko J., Strosznajder J. B.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

Bioactive sphingolipids are important molecules that control wide spectrum of neuronal processes including neurotransmission, synaptic function, cells proliferation and death. Sphingosine kinases (SK1/2) are conserved enzymes that phosphorylate sphingosine to sphingosine-1-phosphate (S1P), which acts as a primary and secondary messenger. S1P binds to 5 receptors and plays essential role in neural signal transduction under physiological and various pathological conditions. Although growing evidence suggests important role of SK1/2 and S1P in neurodegenerative disorders including ischemia, inflammation and Alzheimer’s Disease, till now disturbances of sphingolipids homeostasis in Parkinson’s Disease (PD) remain unknown. Our study try to explain the role of SK1/2 and S1P in molecular mechanism of cell survival and death in model of oxidative stress evoked by neurotoxin 1-methyl-4-phenylpyridinium (MPP+), compound widely used in experimental model of PD. Our data presented that MPP+, comparable to SK inhibition evoked death of human neuroblastoma cells SH-SY5Y in time and concentration dependent manner. These changes are accompanied by increased free radicals concentration in these cells. Reduced level of SK1 protein was detected in SH-SY5Y cells after 24h exposure to MPP+ comparing to control. Moreover S1P pretreatment enhanced survival of these cells and protein level of SK1 comparing to MPP+ treated cells. Our data indicated that MPP+ evoked neuronal death is mediated by SK1/2 inhibition and altered sphingolipids signaling. These molecular events lead to caspase dependent apoptotic cells death and poly(ADP-ribose) polymerase-1 (PARP-1) degradation. All above results presented the alteration of sphingolipid biostat in experimental model of PD and suggested that S1P can offer novel, protective strategy.Supported by NCN Grant 5870/B/PO1/2011/40

5

Short-term depression of inspiratory activity following tonic vagal stimulation

84%

Budzinska K., Ilasz R.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 4

55-61

This study tested the role of inhibitory neurotransmission in the glutaminergic control of short-term depression (STD) of the inspiratory activity initiated by sustained stimulation of the vagus nerve in anesthetized and vagotomized cats. STD, calculated from the integrated phrenic nerve signal, lasted longer when glutaminergic neurotransmission was inhibited by ketamine, a NMDA receptor antagonist. Application of picrotoxin, a GABAA receptor antagonist, reversed the effect of ketamine and shortened the STD duration below that present in the control condition. The results showed that alternation of the neural excitability by antagonists of excitatory and inhibitory neurotransmission modulates the STD of inspiratory activity, evoked by vagal stimulation. The STD depends on the state of neural excitability and is easier accomplished when the excitability is on the high side.

6

Pathofunctional roles of glutamine transporters in neurotransmission, insulin secretion and pH regulation

84%

Chaudhry F. A.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

Glutamine is involved in many metabolic pathways such as generation of amino acids, nucleotides and glutathione. Glutamine also serves in pH homeostasis, urea formation, immune response and wound healing. In addition, glutamine is considered to be the primary precursor of the fast neurotransmitters glutamate and GABA in the central nervous system (CNS). The prevailing hypothesis of a glutamate/GABA-glutamine cycle suggests that a large amount of released glutamate and GABA are translocated into perisynaptic astroglial cells, converted into glutamine, and subsequently shuttled back to neurons for regeneration of the neurotransmitters. This mechanistic view is supported by differential localization of glutamate and GABA transporters on perisynaptic glial processes, and demonstration of the key glutamine metabolizing enzymes glutamine synthetase (GS) and phosphate-activated glutaminase (PAG) in glial cells and nerve terminals, respectively. However, the molecular mechanisms involved in glutamine extrusion from glial cells and its transport into neurons have until recently eluded characterization. We have molecularly identified a family of amino acid transporters (Slc38) with isoform specific characteristics. We show that the system A transporters (SATs) mediate neuronal transport of glutamine. SAT1 is enriched in GAD67 expressing GABAergic neurons suggesting a role in GABA formation. SAT2 expression is pronounced in the somatodendritic domains of glutamatergic neurons where it sustains formation of glutamate and is intrinsic for retrograde signaling. Activity of the homologous system N transporter SN1 – expressed exclusively on astroglial cell membranes – is dynamically regulated by intracellular protein kinases and may fine-tune extracellular levels of glutamine accessible for neuronal uptake. SN2 – also expressed in the astroglial cells, but with differential subcellular localization – mediates glutamine release for neurotransmitter synthesis and glycine release to regulate NMDA receptors. Finally, we have shown that these transporters also contribute to pH restoration during chronic metabolic acidosis and regulation of insulin secretion. Recently, I have also contributed to the investigation of a child with congenital glutamine synthetase deficiency, who developed generalized hypotonia and hyperreflexia and treatment-resistant seizures postpartum and had very low serum and cerebrospinal fluid concentrations of glutamine and glutamate (Häberle et al. 2012). Glutamine supplementation restored serum levels of glutamine and glutamate, while corresponding values in the CNS approached normal. Ammonia toxicity was also prevented. The frequency of seizures abated and EEG showed significant improvement. Altogether, our data show the importance of glutamine and glutamine transporters in normal physiology and pathophysiology and bolster existence of a glutamate/GABA-glutamine cycle.

7

Actions of sodium valproate on the central nervous system

84%

Tunnicliff G.

Journal of Physiology and Pharmacology

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1999

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tom 50

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nr 3

8

Effects of acute and chronic triazolam treatments on brain GABA levels in albino rats

84%

Aburawi S. M., Elhuwuegi A. S., Ahmed S. S., Saad S. F., Attia A. S.

Acta Neurobiologiae Experimentalis

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2000

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tom 60

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nr 4

The present study investigated the effects of acute and chronic intraperitoneal administration of Triazolam on g-aminobutyric acid (GABA) levels in different brain areas of albino rats. Three experiments were conducted. In the first, five groups of rats were acutely treated with different doses of Triazolam (0.25 mg/kg-4.0 mg/kg). In the second experiment, rats were treated chronically with a single daily dose of Triazolam (started with 0.25 mg/kg and increased by time to 1.0 mg/kg) for 5 weeks, simulating clinical use. In the third, rats were treated chronically with three daily doses of Triazolam (started with 0.25 mg/kg and increased by time to 0.5 mg/kg) for 20 days, representing a form of drug abuse. Brain levels of GABA and plasma levels of Triazolam were measured using high performance liquid chromatography (HPLC). The acute Triazolam administration produced an increase in GABA levels in all brain areas studied. The chronic administration of single daily dose of Triazolam produced normal GABA levels in all brain areas except brain stem where the levels were significantly decreased; this indicates the development of tolerance to Triazolam action on increasing GABA content. The chronic administration of three daily doses of Triazolam produced a decrease in GABA levels in all brain regions studied. In conclusion, chronic single daily dose treatment (representing normal use) produces tolerance to Triazolam effects on brain GABA levels, while chronic three daily doses administration (akin to drug abuse) causes a fall in GABA levels.

9

Biphasic enhacement of nitric oxide synthase activity and cGMP level following brain ischemia in gerbils

84%

Strosznajder J., Chalimoniuk M.

Acta Neurobiologiae Experimentalis

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1996

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tom 56

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nr 1

10

Extracellular ATP as a neurotransmitter: its role in synaptic plasticity in the hippocampus

84%

Wieraszko A.

Acta Neurobiologiae Experimentalis

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1996

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tom 56

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nr 2

11

Non-neural acetylcholinesterase in developing cysticercoids of Hymenolepis diminuta

84%

Moczon T., Swietlikowska A.

Wiadomości Parazytologiczne. Suplement

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2001

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tom 47

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nr 2

12

Alterations of GABA B binding caused by acute and chronic lead administration

84%

Waskiewicz J.

Acta Neurobiologiae Experimentalis

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1996

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tom 56

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nr 1

13

Is lead toxicosis a reflection of altered energy metabolism in brain synaptosomes ?

84%

Rafalowska U., Struzynska L., Dabrowska-Bouta B., Lenkiewicz A.

Acta Neurobiologiae Experimentalis

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1996

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tom 56

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nr 2

14

Interstitial cells of Cajal: is their role in gastrointestinal function in view of therapeutic perspectives underestimated or exaggerated?

84%

Timmermans J. P.

Folia Morphologica

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2001

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tom 60

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nr 1

This manuscript reviews the current views on morphology and function of the distinct subpopulations of interstitial cells of Cajal (ICC) in the digestive tract and their interrelationships with surrounding cells. Three different functions have been postulated so far, i.e. a pacemaker role, a mediator in enteric excitatory and inhibitory neurotransmission and a mechanosensor. Attention will also be paid to the interstitial cells of Cajal and their possible involvement in pathophysiological conditions. Finally, perspectives for interstitial cells of Cajal as targets for therapeutic intervention will be discussed.

15

Effect of repeated treatment with mirtazapine on the central alpha1-adrenergic receptors

84%

Rogoz Z., Wrobel A., Dlaboga D., Maj J., Dziedzicka-Wasylewska M.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 1

Mirtazapine (MIR)is an antidepressant which enhances noradrenergic and serotonergic 5-HT1A neurotransmission via antagomism of central alpha2 - adrenergic autoreceptors and heteroreceptors.The drugs does not inhibit noradrenaline and serotonin reuptake but blocks the 5-HT2 and 5-HT3 receptors and has high affinity only for central and peripheral histamine H1 receptors.The present study was aimed at determining whether repeated MIR treatment induced adaptive changes in the alpha1 - adrenergic receptors,similar to those reported by us early for tricyclic antidepressants,The experiments were carried out on male mice and rats.MIR was administered at a dose of 10 mg/kg once or repeatedly (twice daily for 14 days).The obtained results showed that MIR administrated repeatedly potentiated the methoxamine-induced exploratory hyperactivity in rats and clonidine- induced aggressiveness in mice,those effects being mediated by alpha1 - adrenergic receptors. MIR given repeatedly (but not acutely)increased the binding (Bmax )of [3H ]prazosin to alpha1 - adrenergic receptors in cerebral cortex,however,the ability of the alpha1 - adrenoceptor agonist phenylephrine to compete for the these sites was not significantly changed.The above results indicate that repeated MIR administration increases the responsiveness of alpha1 - adrenergic system (behavioural and biochemical changes),as tricyclics do.However, the question whether the increased functional responsiveness found in the present study is important for the clinical antidepressant efficacy,remains open.

16

Different distribution of c-kit positive interstitial cells of Cajal-like in children’s urinary bladders

67%

Piaseczna-Piotrowska A. M., Dzieniecka M., Kulig A., Danilewicz M., Chilarski A.

Folia Histochemica et Cytobiologica

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2011

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tom 49

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nr 3

17

The decrease in JNK- and p38-MAP kinase activity is accompanied by the enhancement of PP2A phosphatase level in the brain of prenatally stressed rats

67%

Budziszewska B., Szymanska M., Leskiewicz M., Basta-Kaim A., Jaworska-Feil L., Kubera M., Jantas D., Lason W.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 2

Our previous study suggests that in prenatal stress model of depression glucocorticoid receptor (GR) function in adult rats is enhanced. However, the long-term consequences of stress, a causal factor in depression, on intracellular elements involved into the regulation of GR function is poorly examined. Mitogen-activated protein kinases (MAPKs), activity of which is disturbed in depression, are important regulators of GR action, so they can mediate the effect of stress on GR function. Therefore, the aim of the present study was to investigate the levels of active phosphorylated forms of extracellular signal-regulated kinases (ERK), Jun N-terminal kinases (JNK) and the p38 kinase in the hippocampus and frontal cortex in rats subjected to prenatal stress. The concentration of MAP kinase phosphatase (MKP-1, MKP-2) and protein phosphatase-2A (PP2A), which dephosphorylate all forms of MAP kinases, were also determined. During verification of the applied model of depression, we found that prenatally stressed rats displayed high level of immobility in the Porsolt test and that the administration of imipramine, fluoxetine, mirtazapine and tianeptine for 21 days normalized this parameter. Western blot study revealed that rats subjected to prenatal stress had decreased levels of p-JNK1 and p-JNK2 in the hippocampus and p-p38 in the frontal cortex, but the concentrations of p-ERK1 and p-ERK2 were not changed. Chronic treatment with imipramine inhibited the stress-induced decrease in p-JNK1/2, while imipramine, fluoxetine and mirtazapine blocked changes in p-p38. PP2A phosphatase level was higher in the hippocampus and frontal cortex in prenatally stressed animals than in control rats. Chronic treatment with antidepressant drugs attenuated the stress-induced increase in the level of this phosphatase, but had no effect on its concentration in control animals. There was no significant difference in MKP-1 and in MKP-2 levels in both brain structures between control and prenatally stressed rats. The obtained results showed that prenatal stress decreased the levels of active form of JNK and p38, but enhanced PP2A phosphatase expression and most of these changes were reversed by antidepressant drugs. Since p-JNK and p-p38 are known to inhibit GR function their lowered levels may enhance glucocorticoid action. Furthermore, the increased PP2A concentration may intensify GR action not only by inhibition of JNK and p38 phosphorylation, but also by a direct influence on the process of GR translocation.

18

Administration of Greek Royal Jelly produces fast response in neurotransmission of aged Wistar male rats

67%

Pyrzanowska J., Piechal A., Blecharz-Klin K., Joniec-Maciejak I., Graikou K., Chinou J., Widy-Tyszkiewicz E.

Journal of Pre-Clinical and Clinical Research

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2015

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tom 09

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nr 2

Introduction. Royal Jelly (RJ) is a popular bee-derived product used widely in European and Asian traditional medicine. RJ has some pharmacological activities to support health and longevity as well as prevent ageing. Objectives. To evaluate whether a short-term 6-day Royal Jelly administration is able to induce behavioural and neurochemical effects in aged rats. Materials and method. RJ (previously chemically characterized by GC-FID and GC–MS) was given to 18-month-old male Wistar rats (100 and 500mg of powder/kg b.w./day) in subcutaneous injection for 6 days. Spatial memory was assessed in a water maze. Afterwards, the level of neurotransmitters, their metabolites and turnover in the selected brain regions were estimated by HPLC. Results. Short-term RJ administration did not change spatial memory in aged rats in the water maze, although it was sufficiently active to modify most of all the serotonergic and dopaminergic transmission in the prefrontal cortex and hippocampus. Conclusion. The obtained results indicate that Royal Jelly is able to affect very quickly the neurotransmission in the brain structures responsible for cognitive performance; however, short-term administration is not sufficient to exert behavioural consequences.

19

Glycine enhances extracellular 45Ca2 response to NMDA application investigated with microdialysis of rabbit hippocampus in vivo

67%

Lazarewicz J. W., Salinska E., Puka M.

Acta Neurobiologiae Experimentalis

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1992

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tom 52

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nr 2

20

The effects of cholecystokinin A and B receptor antagonists, devazepide and L 365260, on citalopram-induced decrease of exploratory behaviour in rat

67%

Matto V., Harro J., Allikmets L.

Journal of Physiology and Pharmacology

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1996

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tom 47

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nr 4

Ograniczanie wyników

Divergent effects of bicuculline and picrotoxin on ketamine-induced apneustic breathing

Role of 5-hydroxytryptamine 1B receptors and 5-hydroxytryptamine uptake inhibition in the cocaine-evoked discriminative stimulus effects in rats

Cytoprotective effect of lithium against spontaneous and induced apoptosis of lymphoid cell line MOLT-4

Alteration of sphingolipid biostat in experimental model of oxidative stress evoked by 1-methyl-4-phenylpyridinium (MPPplus)

Short-term depression of inspiratory activity following tonic vagal stimulation

Pathofunctional roles of glutamine transporters in neurotransmission, insulin secretion and pH regulation

Actions of sodium valproate on the central nervous system

Effects of acute and chronic triazolam treatments on brain GABA levels in albino rats

Biphasic enhacement of nitric oxide synthase activity and cGMP level following brain ischemia in gerbils

Extracellular ATP as a neurotransmitter: its role in synaptic plasticity in the hippocampus

Non-neural acetylcholinesterase in developing cysticercoids of Hymenolepis diminuta

Alterations of GABA B binding caused by acute and chronic lead administration

Is lead toxicosis a reflection of altered energy metabolism in brain synaptosomes ?

Interstitial cells of Cajal: is their role in gastrointestinal function in view of therapeutic perspectives underestimated or exaggerated?

Effect of repeated treatment with mirtazapine on the central alpha1-adrenergic receptors

Different distribution of c-kit positive interstitial cells of Cajal-like in children’s urinary bladders

The decrease in JNK- and p38-MAP kinase activity is accompanied by the enhancement of PP2A phosphatase level in the brain of prenatally stressed rats

Administration of Greek Royal Jelly produces fast response in neurotransmission of aged Wistar male rats

Glycine enhances extracellular 45Ca2 response to NMDA application investigated with microdialysis of rabbit hippocampus in vivo

The effects of cholecystokinin A and B receptor antagonists, devazepide and L 365260, on citalopram-induced decrease of exploratory behaviour in rat