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The results show that non-competitive AMPA receptor antagonists can profoundly block anxiety-like behavior in rodents independently from their motor depressant activity. However, the sedative properties at higher doses might limit their therapeutic utility as new anxiolytic drugs.

BackgroundIngestion of sulphonamide-derived drugs has been reported to possibly have ocular side-effects. Authors aimed to present a rare case of indapamide-induced transient myopia with ciliary body edema and supraciliary effusion.Case presentationA 39 years old caucasian female patient presented at the Department of Neurology with headache and sudden bilateral loss of distant vision. Neurological assessment and cranial CT scans were unremarkable. For her hypertension, twice a day bisoprolol 2.5 mg and once a day indapamide 1.5 mg tablets were prescribed several days before. At her presenting, ophthalmic findings were as follows: visual acuity 0.08-7.25Dsph = 1.0 and 0.06-7.25Dsph = 1.0; IOP 25 mmHg and 24 mmHg, anterior chamber depth (ACD) 2.32 mm and 2.49 mm, lens thickness (L) 4.02 mm and 4.09 mm in the right and the left eye, respectively. By means of ultrasound biomicroscopy (UBM), thickened (720 / 700 micron) and detached ciliary body, its forward movement (ciliary body-cornea angle 108′ / 114′) and forward rotated ciliary processes were seen. Angle opening distance (AOD500) were 300 / 314 microns. By the following days, the myopia gradually diminished, and a week after her first symptoms, her uncorrected visual acuity was 1.0 in both eyes, IOP 13 mmHg and 17 mmHg, ACD 3.68 mm and 3.66 mm, L 3.78 mm and 3.81 mm in the right and the left eye, respectively. Ciliary body edema and detachment disappeared (ciliary body thickness 225 / 230 micron), both of the ciliary body-cornea angle 134′ / 140′ and the AOD500 (650 / 640 microns) increased. At this point, the patient admitted that she had stopped taking indapamide two days before.ConclusionsOur case report is the third one in the literature to present indapamide-induced transient myopia, and the first to employ UBM for describing the characteristics of this rare condition. According to the findings, authors suggest that both ciliary muscle contraction and ciliary body edema may play role in the pathomechanism. UBM seems to be a useful tool in the differential diagnosis of acute myopia. Further, authors wish to draw attention to one of the potential adverse effects of this drug which was not listed by its package insert.

Energy charge controls intermediary metabolism and cellular regulation. Here we show that inhibition of energy conservation at the level of glucose uptake, glycolysis, citric acid cycle, and oxidative phosphorylation induces cell death, leading to fragmentation of DNA into an oligonucleosomal ladder and morphological changes typical for apoptosis. Bcl-2, the prototype of oncogenes that suppress cell death, efficiently inhibits apoptosis induced by metabolic inhibitors. Bcl-2 does not antagonize the inhibitory potential of mitochondrial inhibitors, and cannot prevent or delay the decrease of the cellular ATP level subsequent to metabolic inhibition. Thus, we propose that Bcl-2 blocks apoptosis at a point downstream of the collapse of the cellular-energy homeostasis.Keywords : apoptosis ; ATP; energy conservation ; Bcl-2 ; metabolic regulation.Apoptosis, a common form of cell death, can be induced by mic reticulum (ER) membranes [15]. The mechanism of action of Bcl-2 is largely unknown. It has been shown that Bcl-2 a wide array of physiological and pathological stimuli [1,2]. This form of cell death is characterized by morphological retards diminution of the mitochondrial membrane potential (∆ψ) and reactive oxygen species (ROS) generation in T-cell changes of cellular structures, such as cell shrinkage, chromatin condensation, and membrane blebbing [1]. Molecular-biological hybridomas in response to dexamethasone and ceramide [10], protects against lipid peroxidation in IL-3Ϫdependent lymphoid studies on cell death have identified a number of genetic factors implicated in induction or suppression of apoptosis [2].progenitor cells [16] and regulates intracellular calcium repartitioning [17,18]. The biochemical mechanism of apoptosis remains elusive. The common theme emerging from most of the studies is mitoIn the present study we report that inhibition of energy conservation at the level of glycolysis, citric acid cycle or oxidachondrial dysfunction [3]. It has been shown that alterations in mitochondrial structure and function are early events in tive phosphorylation results in cell death showing oligonucleosomal DNA degradation, chromosomal condensation and apoptosis induced by tumor-necrosis factor [4,5], dexamethasone [6], oxygen radicals [7], nitric oxide [8] and activation of fragmentation, characteristics of apoptosis. Bcl-2 inhibited cell death induced by blockage of energy metabolism. However, exp53 [9]. The first signs of mitochondrial instability, reduced transmembrane potential and generation of reactive oxygen radi-pression of Bcl-2 neither blocks the activity of electron-transport-chain inhibitors, nor does it rescue cellular ATP levels. Apcals, both precede oligonucleosomal DNA fragmentation [10], a characteristic feature of apoptosis. Extensive DNA damage by parently, Bcl-2 orchestrates a protective response to depletion of cellular ATP. oxygen radicals induces activation of poly-(ADP-ribose) polymerase, leading to depletion of its substrate, NAD ϩ , and subsequently the cellular ATP pool [11]. An...