Biomedical subjects

Halina Sienkiewicz-Jarosz

Publications and source records attributed to Halina Sienkiewicz-Jarosz.

7 recordsLinked to original sources

PubMed2004

Depressive symptoms and taste reactivity in humans.

Animal studies suggest that induction of depression-like states may alter preference for sweet tastants. A major goal of the present study was to search for correlations between depressive symptoms measured by the Beck Depression Inventory (BDI) and taste responses to sweet and bitter substances. Thirty-three nonclinical volunteers rated intensity and pleasantness of chocolate and vanilla milk as well as of sucrose- and quinine-soaked filter paper disks. Reactivity to citric acid (sour) and sodium chloride (salty) was also tested with the paper disk methodology. Taste detection thresholds were assessed by means of electrogustometry. A weak inverse relationship was found between the BDI scores (range: 3-33) and rated intensity of paper disks soaked in 60% sucrose. No correlations were found between depressive symptoms and intensity, pleasantness or identification of the other samples. Similarly, there was no relationship between the BDI scores and responses to chocolate and vanilla milk. BDI scores were not associated with electrogustometric thresholds. These data suggest that depressive symptoms may not influence taste reactivity in nonclinical population.

Aconitic Acid↗

PubMed2002

SPECT as a diagnostic test in the investigation of dementia.

Single photon emission tomography (SPECT) permits the assessment of the decrease of regional cerebral blood flow (rCBF). The aim of this study was to assess the relationship between the different types of dementia (Alzheimer's disease (AD), vascular dementia (VaD) and frontotemporal dementia (FTD)) and the rCBF in the SPECT examination. In patients with AD, the SPECT examination showed hypoperfusion in temporoparietal regions, contrary to patients with frontotemporal dementia, where hypoperfusion was limited to the frontal area, and compared to patients with VaD, where "patchy" rCBF changes were observed in different regions. In mild cases of AD, perfusion deficits were observed in the frontal regions equal to those in VaD. The study shows that the SPECT examination may be useful in distinguishing between AD, VaD, and FTD; however, for proper diagnosis in the early stages of AD, additional factors must be taken into consideration.

Age of Onset↗

PubMed2002

Effects of pentylenetetrazol-induced kindling of seizures on rat emotional behavior and brain monoaminergic systems.

The influence of pentylenetetrazol (PTZ)-induced kindling of seizures on the rat emotional behavior, the brain monoamine turnover rate measured in vitro, and correlation between behavioral and biochemical parameters, were examined in rats. The repeated administration of PTZ (35 mg/kg, ip) evoked kindled seizures in rats (Stage 4 or 5 of clonic-tonic convulsions-maximum). PTZ kindling caused selective changes in the rat emotional behavior, present in some models of anxiety only (a decreased freezing time in the conditioned freezing test and a decreased spontaneous and aversively conditioned ultrasonic vocalization). Simultaneously, PTZ kindling decreased the concentration of homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) in the prefrontal cortex, decreased the DA (HVA/DA ratio) turnover rate in the striatum, and inhibited the serotonin (5-HT) metabolism (5-HIAA/5-HT ratio) in the hippocampus and the prefrontal cortex. Correlations between dopamine (DA) or 5-HT regional metabolic rates in brain structures and animal behavior were either abolished or reversed in PTZ-kindled animals. It is concluded that both DA and 5-HT systems contribute to the emotional effects of PTZ-induced kindling of seizures. The hypothesis is put forward that PTZ kindling-induced inhibition of the serotonergic innervation may lead to the compensatory increase in 5-HT(1A) receptors in the dentate gyrus of the hippocampus, thus evoking the anxiolytic-like changes in animal behavior.

Animals↗

PubMedDate not supplied

Exploratory activity and a conditioned fear response: correlation with cortical and subcortical binding of the alpha4beta2 nicotinic receptor agonist [3H]-epibatidine.

Rat behavior in the open field and the conditioned fear response test was correlated with specific binding of the alpha4beta2 nicotinic acetylcholine receptor (nAChR) agonist, [3H]-pibatidine, assayed in different brain structures by autoradiography. A significant positive correlation was found between the ligand binding in the frontal cortex (r = 0.529, p < 0.011), the entorhinal cortex (r = 0.603, p < 0.003), and CA1 layer of the hippocampus (r = 0.465, p < 0.029), and the conditioned freezing reaction in the contextual fear conditioning test. In the frontal cortex, there was also a significant positive correlation between [3H]-epibatidine binding and preconditioned freezing reaction (r = 0.469, p < 0.028), and a negative correlation with rat motility (r = -0.452, p < 0.035). Rat motor activity correlated in a negative way with preconditioned freezing reaction (r = -0.436, p < 0.043), and in a positive way with the number of entries into the central sector of the open field (r = 0.690, p < 0.001). The neophobia-related parameter of the open field behavior (the number of central entries) did not correlate with the [3H]-epibatidine binding. Factor analysis confirmed these findings and showed that rat behavioral parameters measured in the tests of neophobia and conditioned freezing were loading on different factors, thus, pointing to separate central mechanisms operating in both behavioral models of anxiety. Furthermore, factor analysis showed that rat conditioned freezing behavior and [3H]-epibatidine binding in the CA1 layer of the hippocampus and enorhinal cortex, represented similar central processes. These findings suggest that rat emotional reactions evoked by different stressors (neophobia vs. conditioned fear) are differently regulated by the central cholinergic system. The presented data indicate also a significant, structure dependent correlation between rat conditioned emotional reaction and the alpha4beta2 nAChR ligand binding, in the rat cortical forebrain structures.

Animals↗

PubMedDate not supplied

Lack of changes in cortical [3H]-muscimol binding in rats sensitized to nicotine-induced enhancement of dopamine metabolism.

It was proposed that chronic nicotine treatment may induce adaptive changes in GABAA receptors, thus leading to the attenuation of a GABAergic inhibition of dopaminergic neurons. This putative mechanism might underlie the sensitization to nicotine-induced increase in locomotor activity and dopamine metabolism; i.e. phenomena highly significant to the dependence-producing effects of this psychostimulant. To test this hypothesis, in the present study we have analyzed the influence of acute and repeated treatment of rats with nicotine on the binding of a highly selective and competitive GABAA receptor agonist, [3H]-muscimol. The binding was investigated by autoradiography in different brain cortical structures. It was found that nicotine given at the dose stimulating locomotor activity (0.6 mg/kg, sc), markedly increased striatal HVA concentration in the group of animals chronically pretreated (for 6 days) with this psychostimulant. Neither acute nor repeated nicotine administration changed in a significant way the [3H]-muscimol binding to brain cortical structures. Thus, the hypothesis about the role of adaptive changes in GABAA receptors in the enhancement of the biochemical and behavioral effects of nicotine was not confirmed.

Animals↗

PubMedDate not supplied

[Diagnostic difficulties in Creutzfeldt-Jakob disease--case report].

The Creutzfeldt-Jakob disease (CJD) is rare spongiform encephalopathy. Its main symptoms are rapidly progressing dementia, myoclonic jerks, visual disturbances, ataxia, and pyramidal and extrapyramidal signs. A case of sporadic form of the CJD is reported, with blurred vision as one of the first symptoms. This symptom occurred shortly after vaccination against influenza, and was accompanied by other signs suggesting postvaccinal encephalitis. However, at a later stage of the disease typical changes were found in EEG recording and in magnetic resonance imaging (MRI). The presence of the 14-3-3 protein was detected in the patient's cerebrospinal fluid. The diagnosis of sporadic Creutzfeldt-Jakob disease was verified neuropathologically.

Brain↗

PubMedDate not supplied

[The effect of rivastigmine on cognitive functions and regional cerebral blood flow in Alzheimer's disease and vascular dementia: follow-up for 2 years].

BACKGROUND AND PURPOSE: The aim of the work was to investigate the effect of treatment with rivastigmine, one of the inhibitors of acetylcholinesterase (AChE-I) on the regional cerebral perfusion (rCBF) and the cognitive functions of the brain in patients with Alzheimer's Disease (AD) and Vascular Dementia (VaD). MATERIAL AND METHODS: The investigations of rCBF were carried out using SPECT (Single Photon Emission Computed Tomography). The results given concern investigations of patients carried out at the onset of the investigation, after 12 months, and 24 months of rivastigmine treatment. RESULTS: In patients with AD it was found that treatment with rivastigmine increases rCBF by 5-7% in the temporal areas during the first 12 months. In the frontal areas the increase was by 3-5%. During the next 12 months rCBF with an accuracy of 2% returned to the initial level, with the exception of the motor cortex, where it remained on the level increased by 5-6%. However, the cognitive functions remained constant during the first 12 months of treatment and decreased significantly during the next 12 months. In patients with VaD rCBF increased in all the regions of the brain except for the temporal posterior regions, and remained at an elevated level for the next 12 months. The cognitive functions deteriorated slowly, but to a much lesser degree than in the case of AD. CONCLUSIONS: From the investigations carried out it follows that treatment with rivastigmine during 24 months prevents a decrease of rCBF in patients with AD. However, the cognitive functions deteriorate after 24 months.

Aged↗