Journal articles: 'Brain – Effect of drugs on'

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Toth, Miklos. "Epigenetic Neuropharmacology: Drugs Affecting the Epigenome in the Brain." Annual Review of Pharmacology and Toxicology 61, no. 1 (January 6, 2021): 181–201. http://dx.doi.org/10.1146/annurev-pharmtox-030220-022920.

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This review explores how different classes of drugs, including those with therapeutic and abuse potential, alter brain functions and behavior via the epigenome. Epigenetics, in its simplest interpretation, is the study of the regulation of a genes’ transcriptional potential. The epigenome is established during development but is malleable throughout life by a wide variety of drugs, with both clinical utility and abuse potential. An epigenetic effect can be central to the drug's therapeutic or abuse potential, or it can be independent from the main effect but nevertheless produce beneficial or adverse side effects. Here, I discuss the various epigenetic effects of main pharmacological drug classes, including antidepressants, antiepileptics, and drugs of abuse.

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AHMED, SAIMA, MUHAMMAD ASADULLAH, and ATA-UR REHMAN. "EFFECT OF DRUGS;." Professional Medical Journal 20, no. 01 (December 10, 2012): 103–13. http://dx.doi.org/10.29309/tpmj/2013.20.01.586.

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ABSTRACT... Objective: The aim of this study was to determine head-dipping exploratory test parameter as a measure of strongmodulating effect on brain and behavior. Design: It was an observational animal study. Setting: University of Karachi. Period: Jan 2004 toJuly 2006. Material & methods: In this present study, drugs used reserpine, nux- vomica; anacardium and chlorpromazine were widerange of pharmacological actions. We evaluate the effectiveness of these drugs as agents with modulating effect on brain and behavioraccessed by head dipping parameter. In this study, 25 mice were included belonging to both sexes. The study animals were divided intofive groups of five animals each. Four groups were given drugs and one group was kept as control. Mice (20-35g) of either sex were usedin this study. One group was kept as control for drugs. Mice were kept under room temperature. Tap-water was allowed ad-Libitum.30minutes after giving drugs, animals were observed for 10 minutes with two minutes of interval. Tablet crushed in 10ml of water, 1cc wasgiven. Screening method used was head dipping. Results: Strychnos Nux-Vomica when used in a dose of 0.07mg has strong action oncholinergic system, CNS activity and frequent head dipping (39.8±28.8) was observed. Rauwolfia serpentine is an active alkaloidparticularly present in reserpine (62.2±43.4) no significant head dipping effect was observed. Anacardium (37.2±28.6) &Chlorpromazine (39.4±32.4), show decrease effects. Keeping in view, the medicinal importance of these herbs, our present study wasdesigned to screen these drugs for CNS activity on albino mice.

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Crespo-Facorro, Benedicto, Roberto Roiz-Santiáñez, Rocío Pérez-Iglesias, José M. Pelayo-Terán, José M. Rodríguez-Sánchez, Diana Tordesillas-Gutiérrez, MariLuz Ramírez, et al. "Effect of antipsychotic drugs on brain morphometry." Progress in Neuro-Psychopharmacology and Biological Psychiatry 32, no. 8 (December 2008): 1936–43. http://dx.doi.org/10.1016/j.pnpbp.2008.09.020.

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Jaddoa, Estabraq, Jinit Masania, Eva Masiero, Tiziana Sgamma, Randolph Arroo, Daniel Sillence, and Tyra Zetterström. "Effect of antidepressant drugs on the brain sphingolipid system." Journal of Psychopharmacology 34, no. 7 (May 14, 2020): 716–25. http://dx.doi.org/10.1177/0269881120915412.

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Background: Major depression is a common mood disorder and the central sphingolipid system has been identified as a possible drug target of this condition. Here we investigated the action of antidepressant drugs on sphingolipid levels in rat brain regions, plasma and in cultured mouse macrophages. Methods: Two antidepressant drugs were tested: the serotonin reuptake inhibitor paroxetine and the noradrenaline reuptake inhibitor desipramine, either following acute or chronic treatments. Content of sphingosine and ceramide were analysed using LC-MS or HPLC-UV, respectively. This was from samples of brain, plasma and cultured mouse macrophages. Antidepressant-induced effects on mRNA expression for two key genes of the sphingolipid pathway, SMPD1 and ASAH1, were also measured by using quantitative real-time PCR. Results: Chronic but not acute administration of paroxetine or desipramine reduced sphingosine levels in the prefrontal cortex and hippocampus (only paroxetine) but not in the striatum. Ceramide levels were also measured in the hippocampus following chronic paroxetine and likewise to sphingosine this treatment reduced its levels. The corresponding collected plasma samples from chronically treated animals did not show any decrease of sphingosine compared to the corresponding controls. Both drugs failed to reduce sphingosine levels from cultured mouse macrophages. The drug-induced decrease of sphingolipids coincided with reduced mRNA expression of two enzymes of the central sphingolipid pathway, i.e. acid sphingomyelinase ( SMPD1) and acid ceramidase ( ASAH1). Conclusions: This study supports the involvement of brain sphingolipids in the mechanism of action by antidepressant drugs and for the first time highlights their differential effects on brain versus plasma levels.

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Wahab Alahmari, Abdul. "The Neuroimaging Documentation of Psychedelic Drugs’ Effect on the Brain: dmt, lsd, Psilocybin, and Ibogaine as Examples: A Mini Review." Brain and Neurological Disorders 5, no. 2 (June 21, 2022): 01–09. http://dx.doi.org/10.31579/2692-9422/027.

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Many psychedelics drugs are praised on social media platforms like YouTube by non-experts or bias documentaries claiming that these drugs have therapeutic effects on addicted patients or clarity of the mind. The aim of this paper is to collect a neuroimaging documentation of these psychedelics’ drugs and their effect on the brain. That can be documented on MRI, CT, or any other imaging modalities.

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Paulus, Walter, Guntram Schwarz, and Bernhard J. Steinhoff. "The effect of anti–epileptic drugs on visual perception in patients with epilepsy." Brain 119, no. 2 (1996): 539–49. http://dx.doi.org/10.1093/brain/119.2.539.

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Grøndahl, Tor Ø., and Iver A. Langmoen. "Epileptogenic effect of antibiotic drugs." Journal of Neurosurgery 78, no. 6 (June 1993): 938–43. http://dx.doi.org/10.3171/jns.1993.78.6.0938.

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✓ The epileptogenicity of antibiotic drugs represents a clinical problem, and it is well known that the use of penicillin and certain other preparations can induce seizures. In the present study, the authors investigated the epileptogenic properties of different concentrations of 12 commonly used antibiotic medications belonging to seven separate groups. The drugs were tested in the hippocampus, which has a low threshold for the development of epileptiform activity. The hippocampal slice technique, using rat tissue, was employed since absence of the blood-brain barrier allows administration of the drugs in known concentrations. The preparation was exposed to antibiotics in known concentrations and the amplitude and number of population spikes were recorded. Penicillin G was used as a reference substance. Cloxacillin (≥ 1 gm/liter), cephalothin (≥ 1 gm/liter), gentamicin (≥ 80 mg/liter), chloramphenicol (≥ 1 gm/liter), ciprofloxacin (≥ 50 mg/liter), erythromycin (≥ 1 gm/liter), and ampicillin (≥ 1 gm/liter) showed moderate to marked epileptogenic effects, whereas cefuroxime, clindamycin, cefotaxime, vancomycin, and tobramycin had no epileptogenic effects.

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Breggin, Peter R. "Intoxication Anosognosia: The Spellbinding Effect of Psychiatric Drugs." Ethical Human Psychology and Psychiatry 8, no. 3 (December 2006): 201–16. http://dx.doi.org/10.1891/ehppij-v8i3a003.

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Why do so many individuals persist in taking psychoactive substances, including psychiatric drugs, after adverse mental and behavioral effects have become severe and even disabling? The author has previously proposed the brain-disabling principle of psychiatric treatment that all somatic psychiatric treatments impair the function of the brain and mind. Intoxication anosognosia (medication spellbinding) is an expression of this drug-induced mental disability. Intoxication anosognosia causes the victim to underestimate the degree of drug-induced mental impairment, to deny the harmful role that the drug plays in the person’s altered state, and in many cases compel the individual to mistakenly believe that he or she is functioning better. In the extreme, the individual displays out-of-character compulsively destructive behaviors, including violence toward self and others.

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Levin, Aaron. "Brain Imaging, Other Advances Reveal Drugs’ Effects on Brain." Psychiatric News 48, no. 12 (June 12, 2013): 1. http://dx.doi.org/10.1176/appi.pn.2013.6b36.

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Roy, Ranadhir, Daniel N. Riahi, and Jorge Cisneros. "Effect of Combined Anticancer Drugs Treatment on Heterogeneous Brain Tumors." International Journal of Applied and Computational Mathematics 3, no. 4 (April 6, 2017): 3877–96. http://dx.doi.org/10.1007/s40819-017-0331-7.

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Maisov, N. I., T. D. Baimanov, and Yu V. Burov. "Adrenalin uptake by rat brain synaptosomes: Effect of psychotropic drugs." Bulletin of Experimental Biology and Medicine 112, no. 2 (August 1991): 1126–30. http://dx.doi.org/10.1007/bf00839557.

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Fokin, Yu V., M. M. Borisova, and S. Yu Kharitonov. "Neuroimaging of the Intracentral Brain of Cats by Normalization of Electrograms under the Action of Semax." Journal Biomed 17, no. 3 (September 16, 2021): 74–78. http://dx.doi.org/10.33647/2074-5982-17-3-74-78.

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Normalization of FFT-transformed brain electrograms under the action of Semax was performed. The adequacy of the approach to assessing the pharmacodynamics of nootropic drugs exhibiting an activating effect on intracentral relations of the brain was shown. The high-frequency components of encephalograms (the γ-range in particular) were confirmed to be the most important indicators of the effects of psychotropic drugs.

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Hunter, R., D. J. Wyper, J. Patterson, M. T. Hansen, and G. M. Goodwin. "Cerebral Pharmacodynamics of Physostigmine in Alzheimer's Disease Investigated Using Single-Photon Computerised Tomography." British Journal of Psychiatry 158, no. 3 (March 1991): 351–57. http://dx.doi.org/10.1192/bjp.158.3.351.

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The effects of physostigmine on patterns of rCBF in patients with pre-senile Alzheimer's disease were studied using 99mTc-labelled HMPAO SPECT. Regional CBF increased in the left cortex relative to right, with the most significant effect in left frontal and higher frontal regions. Measures of regional brain function, such as SPECT, are an important complement to psychological test batteries in understanding the effects in brain of putative antidementia drugs. SPECT brain imaging could extend our understanding of the action of psychotropic drugs in other major psychiatric illnesses.

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Kawabata, Shinji, Hideki Kashiwagi, Kohei Yoshimura, Yusuke Fukuo, Ryo Hiramatsu, Naosuke Nonoguchi, Motomasa Furuse, Shin-Ichi Miyatake, and Masahiko Wanibuchi. "ET-5 Biological effects of simultaneous use of multiple drugs in neutron capture therapy using rat brain tumor model." Neuro-Oncology Advances 3, Supplement_6 (December 1, 2021): vi4. http://dx.doi.org/10.1093/noajnl/vdab159.015.

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Abstract The world’s first clinical trial of boron neutron capture therapy (BNCT), which treats malignant brain tumors with a single dose of neutron irradiation using multiple boron drugs simultaneously, was performed at our institution, and its excellent results have stimulated BNCT research around the world. BNCT is a particle irradiation therapy that biologically targets cancer cells, and is expected to be a “new option for cancer treatment” because it can deliver a dose of radiation at the cellular level. In the case of BNCT using a combination of multiple drugs, a method to appropriately consider the biological effects of the combination in the dose calculation has not been established. At present, BNCT based on an accelerator-based irradiation system and a boron drug (BPA) based on essential amino acids has been approved by the regulatory approval for head and neck cancer and has shown good results in brain tumors. As basic research, we have continued to develop new boron drugs, which will be essential in the future, and have explored the interpretation of the biological effects of multiple boron drugs in combination and the optimal conditions required for drug development. The survival curve of BNCT in a rat brain tumor model showed that the effect of the new drug alone was comparable to that of BPA, and the effect of the combination was improved, but the effect of the combination did not match the prediction of the combined biological effect derived from each drug. However, it has been found that the effect of the combination does not match the prediction based on the combination of biological effects derived from each drug. In other words, even if the equivalent X-ray equivalent dose (Gy-Eq) is calculated, the combined effect of some drugs exceeds the prediction, while the combined effect of other drugs is poor.

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Mobilio, Daniel, Agata Kieliszek, Shawn Chafe, Chitra Venugopal, and Sheila Singh. "BSCI-22 DETERMINING THE EFFECT OF NOVEL SMALL MOLECULE DRUGS AGAINST THE MIGRATION OF BRAIN METASTASIS INITIATING CELLS (BMICS)." Neuro-Oncology Advances 4, Supplement_1 (August 1, 2022): i5. http://dx.doi.org/10.1093/noajnl/vdac078.020.

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Abstract BACKGROUND Brain metastases are secondary tumors that predominantly arise from the spread of lung, skin, and breast cancers. The current standard of care for brain metastases is complete surgical resection, with a median survival of four months. Therefore, there is a dire need to discover new therapies that effectively target brain metastases. To do this, we have identified anti-brain metastasis drugs that specifically target brain metastasis initiating cells (BMICs), a cancer stem cell population that is thought to escape standard therapies and has the ability to leave their primary tumor, seed the brain, and form a secondary brain tumor. Since the migration of the BMICs is essential to the development of brain metastases in patients, the main goal of this study was to determine the effect our anti-brain metastasis drugs have against the migration of lung, skin, and breast BMICs. METHODS This migration assay utilizes a bi-well silicone structure which effectively establishes a ‘wound’ healing-like migration assay. BMICs are plated in optimized equal concentrations in each silicone bi-well structure to successfully form two cellular mono-layers that are separated by a middle silicone wall. Once cells adhere to the plate the silicone structure is removed and the area between the two cell populations is imaged over time with an in vitro imaging system. RESULTS This optimized assay has been used to screen our anti-brain metastasis drugs against the migration of lung, breast, and skin BMICs. Thus far our drugs have been tested against lung and skin BMICs which resulted in a significant decrease in BMIC migration. SIGNIFICANCE Since brain metastasis arises from the migration of cancer cells to a secondary organ, it is crucial to discover the effect of anti-brain metastasis drugs on BMIC migration prior to the initiation of preclinical animal trials.

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Navari, S., and P. Dazzan. "Do antipsychotic drugs affect brain structure? A systematic and critical review of MRI findings." Psychological Medicine 39, no. 11 (April 2, 2009): 1763–77. http://dx.doi.org/10.1017/s0033291709005315.

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BackgroundThe potential effects of antipsychotic drugs on brain structure represent a key factor in understanding neuroanatomical changes in psychosis. This review addresses two issues: (1) do antipsychotic medications induce changes in total or regional human brain volumes and (2) do such effects depend on antipsychotic type?MethodA systematic review of studies reporting structural brain magnetic resonance imaging (MRI) measures: (1) directly in association with antipsychotic use; and (2) in patients receiving lifetime treatment with antipsychotics in comparison with drug-naive patients or healthy controls. We searched Medline and EMBASE databases using the medical subject heading terms: ‘antipsychotics’ AND ‘brain’ AND (MRI NOT functional). The search included studies published up to 31 January 2007. Wherever possible, we reported the effect size of the difference observed.ResultsThirty-three studies met our inclusion criteria. The results suggest that antipsychotics act regionally rather than globally on the brain. These volumetric changes are of a greater magnitude in association with typical than with atypical antipsychotic use. Indeed, there is evidence of a specific effect of antipsychotic type on the basal ganglia, with typicals specifically increasing the volume of these structures. Differential effects of antipsychotic type may also be present on the thalamus and the cortex, but data on these and other brain areas are more equivocal.ConclusionsAntipsychotic treatment potentially contributes to the brain structural changes observed in psychosis. Future research should take into account these potential effects, and use adequate sample sizes, to allow improved interpretation of neuroimaging findings in these disorders.

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Kumar, Bhumika, Mukesh Pandey, Faheem H. Pottoo, Faizana Fayaz, Anjali Sharma, and P. K. Sahoo. "Liposomes: Novel Drug Delivery Approach for Targeting Parkinson’s Disease." Current Pharmaceutical Design 26, no. 37 (October 26, 2020): 4721–37. http://dx.doi.org/10.2174/1381612826666200128145124.

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Parkinson’s disease is one of the most severe progressive neurodegenerative disorders, having a mortifying effect on the health of millions of people around the globe. The neural cells producing dopamine in the substantia nigra of the brain die out. This leads to symptoms like hypokinesia, rigidity, bradykinesia, and rest tremor. Parkinsonism cannot be cured, but the symptoms can be reduced with the intervention of medicinal drugs, surgical treatments, and physical therapies. Delivering drugs to the brain for treating Parkinson’s disease is very challenging. The blood-brain barrier acts as a highly selective semi-permeable barrier, which refrains the drug from reaching the brain. Conventional drug delivery systems used for Parkinson’s disease do not readily cross the blood barrier and further lead to several side-effects. Recent advancements in drug delivery technologies have facilitated drug delivery to the brain without flooding the bloodstream and by directly targeting the neurons. In the era of Nanotherapeutics, liposomes are an efficient drug delivery option for brain targeting. Liposomes facilitate the passage of drugs across the blood-brain barrier, enhances the efficacy of the drugs, and minimize the side effects related to it. The review aims at providing a broad updated view of the liposomes, which can be used for targeting Parkinson’s disease.

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Boussadia, B., C. Ghosh, C. Plaud, J. M. Pascussi, F. de Bock, M. C. Rousset, D. Janigro, and N. Marchi. "Effect of status epilepticus and antiepileptic drugs on CYP2E1 brain expression." Neuroscience 281 (December 2014): 124–34. http://dx.doi.org/10.1016/j.neuroscience.2014.09.055.

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Raseroka, B. H., and W. E. Ormerod. "The trypanocidal effect of drugs in different parts of the brain." Transactions of the Royal Society of Tropical Medicine and Hygiene 80, no. 4 (January 1986): 634–41. http://dx.doi.org/10.1016/0035-9203(86)90162-8.

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Moret, C. "Effect of antidepressant drugs on monoamine synthesis in brain in vivo." Neuropharmacology 31, no. 7 (July 1992): 679–84. http://dx.doi.org/10.1016/0028-3908(92)90146-g.

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Saleh, Mohammed A. A., Chi Fong Loo, Jeroen Elassaiss-Schaap, and Elizabeth C. M. De Lange. "Lumbar cerebrospinal fluid-to-brain extracellular fluid surrogacy is context-specific: insights from LeiCNS-PK3.0 simulations." Journal of Pharmacokinetics and Pharmacodynamics 48, no. 5 (June 17, 2021): 725–41. http://dx.doi.org/10.1007/s10928-021-09768-7.

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AbstractPredicting brain pharmacokinetics is critical for central nervous system (CNS) drug development yet difficult due to ethical restrictions of human brain sampling. CNS pharmacokinetic (PK) profiles are often altered in CNS diseases due to disease-specific pathophysiology. We previously published a comprehensive CNS physiologically-based PK (PBPK) model that predicted the PK profiles of small drugs at brain and cerebrospinal fluid compartments. Here, we improved this model with brain non-specific binding and pH effect on drug ionization and passive transport. We refer to this improved model as Leiden CNS PBPK predictor V3.0 (LeiCNS-PK3.0). LeiCNS-PK3.0 predicted the unbound drug concentrations of brain ECF and CSF compartments in rats and humans with less than two-fold error. We then applied LeiCNS-PK3.0 to study the effect of altered cerebrospinal fluid (CSF) dynamics, CSF volume and flow, on brain extracellular fluid (ECF) pharmacokinetics. The effect of altered CSF dynamics was simulated using LeiCNS-PK3.0 for six drugs and the resulting drug exposure at brain ECF and lumbar CSF were compared. Simulation results showed that altered CSF dynamics changed the CSF PK profiles, but not the brain ECF profiles, irrespective of the drug’s physicochemical properties. Our analysis supports the notion that lumbar CSF drug concentration is not an accurate surrogate of brain ECF, particularly in CNS diseases. Systems approaches account for multiple levels of CNS complexity and are better suited to predict brain PK.

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Larsson, Markus K., Lilly Schwieler, Michel Goiny, Sophie Erhardt, and Göran Engberg. "Chronic Antipsychotic Treatment in the Rat – Effects on Brain Interleukin-8 and Kynurenic Acid." International Journal of Tryptophan Research 8 (January 2015): IJTR.S25915. http://dx.doi.org/10.4137/ijtr.s25915.

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Schizophrenia is associated with activation of the brain immune system as reflected by increased brain levels of kynurenic acid (KYNA) and proinflammatory cytokines. Although antipsychotic drugs have been used for decades in the treatment of the disease, potential effects of these drugs on brain immune signaling are not fully known. The aim of the present study is to investigate the effects of chronic treatment with antipsychotic drugs on brain levels of cytokines and KYNA. Rats were treated daily by intraperitoneally administered haloperidol (1.5 mg/kg, n = 6), olanzapine (2 mg/kg, n = 6), and clozapine (20 mg/kg, n = 6) or saline ( n = 6) for 30 days. Clozapine, but not haloperidol or olanzapine-treated rats displayed significantly lower cerebrospinal fluid (CSF) levels of interleukin-8 compared to controls. Whole brain levels of KYNA were not changed in any group. Our data suggest that the superior therapeutic effect of clozapine may be a result of its presently shown immunosuppressive action. Further, our data do not support the possibility that elevated brain KYNA found in patients with schizophrenia is a result of antipsychotic treatment.

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Borowicz-Reutt, Kinga K. "How Antidepressant Drugs Affect the Antielectroshock Action of Antiseizure Drugs in Mice: A Critical Review." International Journal of Molecular Sciences 22, no. 5 (March 3, 2021): 2521. http://dx.doi.org/10.3390/ijms22052521.

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Depression coexists with epilepsy, worsening its course. Treatment of the two diseases enables the possibility of interactions between antidepressant and antiepileptic drugs. The aim of this review was to analyze such interactions in one animal seizure model—the maximal electroshock (MES) in mice. Although numerous antidepressants showed an anticonvulsant action, mianserin exhibited a proconvulsant effect against electroconvulsions. In most cases, antidepressants potentiated or remained ineffective in relation to the antielectroshock action of classical antiepileptic drugs. However, mianserin and trazodone reduced the action of valproate, phenytoin, and carbamazepine against the MES test. Antiseizure drug effects were potentiated by all groups of antidepressants independently of their mechanisms of action. Therefore, other factors, including brain-derived neurotrophic factor (BDNF) and glial-derived neurotrophic factor (GDNF) modulation, should be considered as the background for the effect of drug combinations.

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Schlagal, Caitlin R., and Ping Wu. "Alcohol and Cocaine Combined Substance Use on Adult Hypothalamic Neural Stem Cells and Neurogenesis." Brain Plasticity 6, no. 1 (December 29, 2020): 41–46. http://dx.doi.org/10.3233/bpl-190091.

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Many advancements have been made over the years looking at the individual and combined effects of drugs of abuse on the brain, with one key area of research focusing on the effects on neurogenesis. An integral part of fetal brain development and, later, maintenance in the adult brain, neurogenesis occurs in three main regions: subventricularzone of the lateral ventricles (SVZ), subgranularzone of the dentate gyrus (SGZ), and the tanycyte layer in the hypothalamus (TL). We will review current literature on combined drugs of abuse and their effect on adult neurogenesis. More specifically, this review will focus on the effect of combining cocaine and alcohol. Additionally, the tanycyte layer will be explored in more depth and probed to look at the neurogenic properties of tanycytes and their role in neurogenesis.

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Boström, Emma, Margareta Hammarlund-Udenaes, and Ulrika S. H. Simonsson. "Blood–Brain Barrier Transport Helps to Explain Discrepancies in In Vivo Potency between Oxycodone and Morphine." Anesthesiology 108, no. 3 (March 1, 2008): 495–505. http://dx.doi.org/10.1097/aln.0b013e318164cf9e.

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Background The objective of this study was to evaluate the brain pharmacokinetic-pharmacodynamic relations of unbound oxycodone and morphine to investigate the influence of blood-brain barrier transport on differences in potency between these drugs. Methods Microdialysis was used to obtain unbound concentrations in brain and blood. The antinociceptive effect of each drug was assessed using the hot water tail-flick method. Population pharmacokinetic modeling was used to describe the blood-brain barrier transport of morphine as the rate (CLin) and extent (Kp,uu) of equilibration, where CLin is the influx clearance across the blood-brain barrier and Kp,uu is the ratio of the unbound concentration in brain to that in blood at steady state. Results The six-fold difference in Kp,uu between oxycodone and morphine implies that, for the same unbound concentration in blood, the concentrations of unbound oxycodone in brain will be six times higher than those of morphine. A joint pharmacokinetic-pharmacodynamic model of oxycodone and morphine based on unbound brain concentrations was developed and used as a statistical tool to evaluate differences in the pharmacodynamic parameters of the drugs. A power model using Effect = Baseline + Slope . C best described the data. Drug-specific slope and gamma parameters made the relative potency of the drugs concentration dependent. Conclusions For centrally acting drugs such as opioids, pharmacokinetic-pharmacodynamic relations describing the interaction with the receptor are better obtained by correlating the effects to concentrations of unbound drug in the tissue of interest rather than to blood concentrations.

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Saganuwan, Saganuwan Alhaji. "Chemistry and Effects of Brainstem Acting Drugs." Central Nervous System Agents in Medicinal Chemistry 19, no. 3 (October 31, 2019): 180–86. http://dx.doi.org/10.2174/1871524919666190620164355.

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Background: Brain is the most sensitive organ, whereas brainstem is the most important part of Central Nervous System (CNS). It connects the brain and the spinal cord. However, a myriad of drugs and chemicals affects CNS with severe resultant effects on the brainstem. Methods: In view of this, a number of literature were assessed for information on the most sensitive part of brain, drugs and chemicals that act on the brainstem and clinical benefit and risk assessment of such drugs and chemicals. Results: Findings have shown that brainstem regulates heartbeat, respiration and because it connects the brain and spinal cord, all the drugs that act on the spinal cord may overall affect the systems controlled by the spinal cord and brain. The message is sent and received by temporal lobe, occipital lobe, frontal lobe, parietal lobe and cerebellum. Conclusion: Hence, the chemical functional groups of the brainstem and drugs acting on brainstem are complementary, and may produce either stimulation or depression of CNS.

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Robinson, P. J., and S. I. Rapoport. "Binding Effect of Albumin on Uptake of Bilirubin by Brain." Pediatrics 79, no. 4 (April 1, 1987): 553–58. http://dx.doi.org/10.1542/peds.79.4.553.

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A mathematical model is presented to describe quantitatively the uptake of bilirubin into the brain from blood, under conditions of extensive binding to plasma proteins. The model relates bilirubin uptake to the rate constants for dissociation and association of the albumin/bilirubin complex and to the transit time of blood through brain capillaries. A rational basis is given for deciding between the total or the free bilirubin concentration as an appropriate indicator of brain exposure to the toxic effects of bilirubin. The effect of competition for binding sites by drugs such as sulfonamides on the brain uptake of bilirubin is also described quantitatively.

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Bergen, Donna C. "Prophylactic Antiepileptic Drugs in Patients with Brain Tumors." Epilepsy Currents 5, no. 5 (September 2005): 182–83. http://dx.doi.org/10.1111/j.1535-7511.2005.00057.x.

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Seizure Prophylaxis in Patients with Brain Tumors: A Meta-analysis Sirven JI, Wingerchuk DM, Drazkowski JF, Lyons MK, Zimmerman RS Mayo Clin Proc 2004;79:1489–1494 Purpose To assess whether antiepileptic drugs (AEDs) should be prescribed to patients with brain tumors who have no history of seizures. Methods We performed a meta-analysis of randomized controlled trials (1966 to 2004) that evaluated the efficacy of AED prophylaxis versus no treatment or placebo to prevent seizures in patients with brain tumors who had no history of epilepsy. Summary odds ratios were calculated by using a random-effects model. Three subanalyses were performed to assess pooled odds ratios (ORs) of seizures in patients with primary glial tumors, cerebral metastases, and meningiomas. Results Of 474 articles found in the initial search, 17 were identified as primary studies. Five trials met inclusion criteria: patients with a neoplasm (primary glial tumors, cerebral metastases, and meningiomas) but no history of epilepsy who were randomized to either an AED or placebo. The three AEDs studied were phenobarbital, phenytoin, and valproic acid. Of the five trials, four showed no statistical benefit of seizure prophylaxis with an AED. Meta-analysis confirmed the lack of AED benefit at 1 week (OR, 0.91; 95% confidence interval [CI], 0.45–1.83) and at 6 months (OR, 1.01; 95% CI, 0.51–1.98) of follow-up. The AEDs had no effect on seizure prevention for specific tumor pathology, including primary glial tumors (OR, 3.46; 95% CI, 0.32–37.47), cerebral metastases (OR, 2.50; 95% CI, 0.25–24.72), and meningiomas (OR, 0.62; 95% CI, 0.10–3.85). Conclusions No evidence supports AED prophylaxis with phenobarbital, phenytoin, or valproic acid in patients with brain tumors and no history of seizures, regardless of neoplastic type. Subspecialists who treat patients with brain tumors need more education on this issue. Future randomized controlled trials should address whether any of the newer AEDs are useful for seizure prophylaxis.

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Srivastava, Rohit K., and Pratibha Singh. "Stem cell therapies as a therapeutic option to counter chemo brain: a negative effect of cancer treatment." Regenerative Medicine 15, no. 6 (June 2020): 1789–800. http://dx.doi.org/10.2217/rme-2020-0060.

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Chemo brain, a constellation of cognitive deficiencies followed by chemotherapy drugs, used to treat different types of cancers and adversely impacts the quality of life of a cancer survivor. The underlying mechanism of chemo brain remains vague, thus delaying the advancement of efficient treatments. Unfortunately, there is no US FDA approved medicine for chemo brain and often medicines considered for chemo brain are already the ones approved for other diseases. Nevertheless, researches exploring stem cell transplantation in different neurodegenerative diseases demonstrate that cellular transplantation could reverse chemotherapy-induced chemo brain. This review talks about the mechanism behind the cognitive impairments instigated by different chemotherapy drugs used in cancer treatment, and how stem cell therapy could be advantageous to overcome this disease.

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Scaini, Giselli, Natália Rochi, Meline O. S. Morais, Débora D. Maggi, Bruna T. De-Nês, João Quevedo, and Emilio L. Streck. "In vitro effect of antipsychotics on brain energy metabolism parameters in the brain of rats." Acta Neuropsychiatrica 25, no. 1 (February 2013): 18–26. http://dx.doi.org/10.1111/j.1601-5215.2012.00650.x.

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ObjectiveTypical and atypical antipsychotic drugs have been shown to have different clinical, biochemical and behavioural profiles. It is well described that impairment of metabolism, especially in the mitochondria, leads to oxidative stress and neuronal death and has been implicated in the pathogenesis of a number of diseases in the brain. In this context, we investigated the in vitro effect of antipsychotic drugs on energy metabolism parameters in the brain of rats.MethodsClozapine (0.1, 0.5 and 1.0 mg/ml), olanzapine (0.1, 0.5 and 1.0 mg/ml) and aripiprazole (0.05, 0.15 and 0.3 mg/ml) were suspended in buffer and added to the reaction medium containing rat tissue homogenates and the respiratory chain complexes, succinate dehydrogenase and creatine kinase (CK) activities were evaluated.ResultsOur results showed that olanzapine and aripriprazole increased the activities of respiratory chain complexes. On the other hand, complex IV activity was inhibited by clozapine, olanzapine and aripriprazole. CK activity was increased by clozapine at 0.5 and 1.0 mg/ml in prefrontal cortex, cerebellum, striatum, hippocampus and posterior cortex of rats. Moreover, olanzapine and aripiprazole did not affect CK activity.ConclusionIn this context, if the hypothesis that metabolism impairment is involved in the pathophysiology of neuropsychiatric disorders is correct and these results also occur in vivo, we suggest that olanzapine may reverse a possible diminution of metabolism.

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Kita, Hideki, Hirotami Matsuo, Hitomi Takanaga, Junichi Kawakami, Koujirou Yamamoto, Tatsuji Iga, Mikihiko Naito, et al. "In Vivo and In Vitro Toxicodynamic Analyses of New Quinolone-and Nonsteroidal Anti-Inflammatory Drug-Induced Effects on the Central Nervous System." Antimicrobial Agents and Chemotherapy 43, no. 5 (May 1, 1999): 1091–97. http://dx.doi.org/10.1128/aac.43.5.1091.

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ABSTRACT We investigated the correlation between an in vivo isobologram based on the concentrations of new quinolones (NQs) in brain tissue and the administration of nonsteroidal anti-inflammatory drugs (NSAIDs) for the occurrence of convulsions in mice and an in vitro isobologram based on the concentrations of both drugs for changes in the γ-aminobutyric acid (GABA)-induced current response in Xenopus oocytes injected with mRNA from mouse brains in the presence of NQs and/or NSAIDs. After the administration of enoxacin (ENX) in the presence or absence of felbinac (FLB), ketoprofen (KTP), or flurbiprofen (FRP), a synergistic effect was observed in the isobologram based on the threshold concentration in brain tissue between mice with convulsions and those without convulsions. The three NSAIDs did not affect the pharmacokinetic behavior of ENX in the brain. However, the ENX-induced inhibition of the GABA response in the GABAA receptor expressed in Xenopus oocytes was enhanced in the presence of the three NSAIDs. The inhibition ratio profiles of the GABA responses for both drugs were analyzed with a newly developed toxicodynamic model. The inhibitory profiles for ENX in the presence of NSAIDs followed the order KTP (1.2 μM) > FRP (0.3 μM) > FLB (0.2 μM). These were 50- to 280-fold smaller than those observed in the absence of NSAIDs. The inhibition ratio (0.01 to 0.02) of the GABAA receptor in the presence of both drugs was well-fitted to the isobologram based on threshold concentrations of both drugs in brain tissue between mice with convulsions and those without convulsions, despite the presence of NSAIDs. In mice with convulsions, the inhibitory profiles of the threshold concentrations of both drugs in brain tissue of mice with convulsions and those without convulsions can be predicted quantitatively by using in vitro GABA response data and toxicodynamic model.

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Vega Rasgado, Lourdes A., Guillermo Ceballos Reyes, and Fernando Vega-Díaz. "Anticonvulsant Drugs, Brain Glutamate Dehydrogenase Activity and Oxygen Consumption." ISRN Pharmacology 2012 (March 8, 2012): 1–8. http://dx.doi.org/10.5402/2012/295853.

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Glutamate dehydrogenase (GDH, E.C. 1.4.1.3.) is a key enzyme for the biosynthesis and modulation of glutamate (GLU) metabolism and an indirect γ-aminobutyric acid (GABA) source, here we studied the effect of anticonvulsants such as pyridoxal phosphate (PPAL), aminooxyacetic acid (AAOA), and hydroxylamine (OHAMINE) on GDH activity in mouse brain. Moreover, since GLU is a glucogenic molecule and anoxia is a primary cause of convulsions, we explore the effect of these drugs on oxygen consumption. Experiments were performed in vitro as well as in vivo for both oxidative deamination of GLU and reductive amination of α-ketoglutarate (αK). Results in vitro showed that PPAL decreased oxidative deamination of GLU and oxygen consumption, whereas AAOA and OHAMINE inhibited GDH activity competitively and also inhibited oxygen consumption when αK reductive amination was carried out. In contrast, results showed that in vivo, all anticonvulsants enhanced GLU utilization by GDH and also decreased oxygen consumption. Together, results suggest that GDH activity has repercussions on oxygen consumption, which may indicate that the enzyme activity is highly regulated by energy requirements for metabolic activity. Besides, GDH may participate in regulation of GLU and, indirectly GABA levels, hence in neuronal excitability, becoming a key enzyme in seizures mechanism.

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Amato, Maria Pia, Mattia Fonderico, Emilio Portaccio, Luisa Pastò, Lorenzo Razzolini, Elio Prestipino, Angelo Bellinvia, et al. "Disease-modifying drugs can reduce disability progression in relapsing multiple sclerosis." Brain 143, no. 10 (September 16, 2020): 3013–24. http://dx.doi.org/10.1093/brain/awaa251.

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Abstract An ever-expanding number of disease-modifying drugs for multiple sclerosis have become available in recent years, after demonstrating efficacy in clinical trials. In the real-world setting, however, disease-modifying drugs are prescribed in patient populations that differ from those included in pivotal studies, where extreme age patients are usually excluded or under-represented. In this multicentre, observational, retrospective Italian cohort study, we evaluated treatment exposure in three cohorts of patients with relapsing-remitting multiple sclerosis defined by age at onset: paediatric-onset (≤18 years), adult-onset (18–49 years) and late-onset multiple sclerosis (≥50 years). We included patients with a relapsing-remitting phenotype, ≥5 years follow-up, ≥3 Expanded Disability Status Scale (EDSS) evaluations and a first neurological evaluation within 3 years from the first demyelinating event. Multivariate Cox regression models (adjusted hazard ratio with 95% conﬁdence intervals) were used to assess the risk of reaching a first 12-month confirmed disability worsening and the risk of reaching a sustained EDSS of 4.0. The effect of disease-modifying drugs was assessed as quartiles of time exposure. We found that disease-modifying drugs reduced the risk of 12-month confirmed disability worsening, with a progressive risk reduction in different quartiles of exposure in paediatric-onset and adult-onset patients [adjusted hazard ratios in non-exposed versus exposed >62% of the follow-up time: 8.0 (3.5–17.9) for paediatric-onset and 6.3 (4.9–8.0) for adult-onset, P < 0.0001] showing a trend in late-onset patients [adjusted hazard ratio = 1.9 (0.9–4.1), P = 0.07]. These results were confirmed for a sustained EDSS score of 4.0. We also found that relapses were a risk factor for 12-month confirmed disability worsening in all three cohorts, and female sex exerted a protective role in the late-onset cohort. This study provides evidence that sustained exposure to disease-modifying drugs decreases the risk of disability accumulation, seemingly in a dose-dependent manner. It confirms that the effectiveness of disease-modifying drugs is lower in late-onset patients, although still detectable.

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Niesters, Marieke, Najmeh Khalili-Mahani, Christian Martini, Leon Aarts, Joop van Gerven, Mark A. van Buchem, Albert Dahan, and Serge Rombouts. "Effect of Subanesthetic Ketamine on Intrinsic Functional Brain Connectivity." Anesthesiology 117, no. 4 (October 1, 2012): 868–77. http://dx.doi.org/10.1097/aln.0b013e31826a0db3.

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Background The influence of psychoactive drugs on the central nervous system has been investigated with positron emission tomography and task-related functional magnetic resonance imaging. However, it is not known how these drugs affect the intrinsic large-scale interactions of the brain (resting-state functional magnetic resonance imaging connectivity). In this study, the effect of low-dose S(+)-ketamine on intrinsic brain connectivity was investigated. Methods Twelve healthy, male volunteers received a 2-h intravenous S(+)-ketamine infusion (first hour 20 mg/70 kg, second hour 40 mg/70 kg). Before, during, and after S(+)-ketamine administration, resting-state brain connectivity was measured. In addition, heat pain tests were performed between imaging sessions to determine ketamine-induced analgesia. A mixed-effects general linear model was used to determine drug and pain effects on resting-state brain connectivity. Results Ketamine increased the connectivity most importantly in the cerebellum and visual cortex in relation to the medial visual network. A decrease in connectivity was observed in the auditory and somatosensory network in relation to regions responsible for pain sensing and the affective processing of pain, which included the amygdala, insula, and anterior cingulate cortex. Connectivity variations related to fluctuations in pain scores were observed in the anterior cingulate cortex, insula, orbitofrontal cortex, and the brainstem, regions involved in descending inhibition of pain. Conclusions Changes in connectivity were observed in the areas that explain ketamine's pharmacodynamic profile with respect to analgesia and psychedelic and other side effects. In addition, pain and ketamine changed brain connectivity in areas involved in endogenous pain modulation.

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KOLOSOVA, N. G., and S. I. SHATALINA. "ANTITUSSIVE DRUGS IN CHILDREN’S PRACTICE." Medical Council, no. 9 (July 18, 2017): 76–79. http://dx.doi.org/10.21518/2079-701x-2017-9-76-79.

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Adequate choice and use of antitussive therapy in pediatrics presupposes knowing at least the two key aspects: causes of cough and the specific mechanism of the cough reflex in children, as well as the mechanisms of action of antitussive drugs used. The need for the treatment of cough as such, that is, prescription of the so-called antitussive drugs, arises mainly in children with nonproductive, dry, persistent cough. Central antitussives suppress the function of the cough center in the medulla oblongata or other associated nerve centers of the brain. The antitussive drug butamirate, often used in children, selectively affects the cough center, does not cause respiratory depression, has an extremely low incidence of side effects, remains effective in prolonged therapy, and starts to exert its maximum effect after the first application

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Banach, Monika, Monika Rudkowska, Agata Sumara, and Kinga Borowicz-Reutt. "Amiodarone Enhances Anticonvulsive Effect of Oxcarbazepine and Pregabalin in the Mouse Maximal Electroshock Model." International Journal of Molecular Sciences 22, no. 3 (January 21, 2021): 1041. http://dx.doi.org/10.3390/ijms22031041.

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Accumulating experimental studies show that antiarrhythmic and antiepileptic drugs share some molecular mechanisms of action and can interact with each other. In this study, the influence of amiodarone (a class III antiarrhythmic drug) on the antiseizure action of four second-generation antiepileptic drugs was evaluated in the maximal electroshock model in mice. Amiodarone, although ineffective in the electroconvulsive threshold test, significantly potentiated the antielectroshock activity of oxcarbazepine and pregabalin. Amiodarone, given alone or in combination with oxcarbazepine, lamotrigine, or topiramate, significantly disturbed long-term memory in the passive-avoidance task in mice. Brain concentrations of antiepileptic drugs were not affected by amiodarone. However, the brain concentration of amiodarone was significantly elevated by oxcarbazepine, topiramate, and pregabalin. Additionally, oxcarbazepine and pregabalin elevated the brain concentration of desethylamiodarone, the main metabolite of amiodarone. In conclusion, potentially beneficial action of amiodarone in epilepsy patients seems to be limited by neurotoxic effects of amiodarone. Although results of this study should still be confirmed in chronic protocols of treatment, special precautions are recommended in clinical conditions. Coadministration of amiodarone, even at low therapeutic doses, with antiepileptic drugs should be carefully monitored to exclude undesired effects related to accumulation of the antiarrhythmic drug and its main metabolite, desethylamiodarone.

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Lensu, S., G. DeSiena, P. Malmberg-Aiello, and L. Tuomisto. "Effect of some antiepileptic drugs on brain histaminergic systems in the rat." Inflammation Research 51, S1 (April 2002): 51–52. http://dx.doi.org/10.1007/pl00022444.

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Mintzer, Scott. "This is Your Brain on Drugs: Predicting Anticonvulsant Effect Using Transcranial Stimulation." Epilepsy Currents 11, no. 1 (January 2011): 19–20. http://dx.doi.org/10.5698/1535-7511-11.1.19.

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Gołembiowska, Krystyna, Alexandra Jurczak, Katarzyna Kamińska, Karolina Noworyta-Sokołowska, and Anna Górska. "Effect of Some Psychoactive Drugs Used as ‘Legal Highs’ on Brain Neurotransmitters." Neurotoxicity Research 29, no. 3 (October 26, 2015): 394–407. http://dx.doi.org/10.1007/s12640-015-9569-1.

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Corazzi, Lanfranco, Gian Luigi Piccinin, Rita Roberti, Ndok Marku, Luciano Binaglia, Giuseppe Porcellati, and Giuseppe Arienti. "Effect of various drugs producing convulsive seizures on rat brain glycerolipid metabolism." Neurochemical Research 10, no. 7 (July 1985): 879–85. http://dx.doi.org/10.1007/bf00964625.

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Moncrieff, J., and J. Leo. "A systematic review of the effects of antipsychotic drugs on brain volume." Psychological Medicine 40, no. 9 (January 20, 2010): 1409–22. http://dx.doi.org/10.1017/s0033291709992297.

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BackgroundPeople with schizophrenia are often found to have smaller brains and larger brain ventricles than normal, but the role of antipsychotic medication remains unclear.MethodWe conducted a systematic review of magnetic resonance imaging (MRI) studies. We included longitudinal studies of brain changes in patients taking antipsychotic drugs and we examined studies of antipsychotic-naive patients for comparison purposes.ResultsFourteen out of 26 longitudinal studies showed a decline in global brain or grey-matter volume or an increase in ventricular or cerebrospinal fluid (CSF) volume during the course of drug treatment, including the largest studies conducted. The frontal lobe was most consistently affected, but overall changes were diffuse. One large study found different degrees of volume loss with different antipsychotics, and another found that volume changes were associated with taking medication compared with taking none. Analyses of linear associations between drug exposure and brain volume changes produced mixed results. Five out of 21 studies of patients who were drug naive, or had only minimal prior treatment, showed some differences from controls in volumes of interest. No global differences were reported in three studies of drug-naive patients with long-term illness. Studies of high-risk groups have not demonstrated differences from controls in global or lobar brain volumes.ConclusionsSome evidence points towards the possibility that antipsychotic drugs reduce the volume of brain matter and increase ventricular or fluid volume. Antipsychotics may contribute to the genesis of some of the abnormalities usually attributed to schizophrenia.

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Hayes, Ronald L., Bruce G. Lyeth, Larry W. Jenkins, Richard Zimmerman, Tracy K. McIntosh, Guy L. Clifton, and Harold F. Young. "Possible protective effect of endogenous opioids in traumatic brain injury." Journal of Neurosurgery 72, no. 2 (February 1990): 252–61. http://dx.doi.org/10.3171/jns.1990.72.2.0252.

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✓ Naloxone (0.1, 1.0, or 20.0 mg/kg), morphine (1.0 or 10.0 mg/kg), or saline was administered systemically intraperitoneally to rats 15 minutes prior to moderate fluid-percussion brain injury. The effects of the drugs were measured on systemic physiological, neurological, and body-weight responses to injury. The animals were trained prior to injury and were assessed for 10 days after injury on body-weight responses and neurological endpoints. Low doses of naloxone (0.1 or 1.0 mg/kg) significantly exacerbated neurological deficits associated with injury. Morphine (10.0 mg/kg) significantly reduced neurological deficits associated with injury. The drugs had no effect on neurological measures or body weight in sham-injured animals. Drug treatments did not significantly alter systemic physiological responses to injury. Data from these experiments suggest the involvement of endogenous opioids in at least some components of neurological deficits following traumatic brain injury and suggest the possibility that at least some classes of endogenous opioids may protect against long-term neurological deficits produced by fluid-percussion injury to the rat.

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Berríos-Cárcamo, Pablo, Mauricio Quezada, María Elena Quintanilla, Paola Morales, Marcelo Ezquer, Mario Herrera-Marschitz, Yedy Israel, and Fernando Ezquer. "Oxidative Stress and Neuroinflammation as a Pivot in Drug Abuse. A Focus on the Therapeutic Potential of Antioxidant and Anti-Inflammatory Agents and Biomolecules." Antioxidants 9, no. 9 (September 4, 2020): 830. http://dx.doi.org/10.3390/antiox9090830.

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Drug abuse is a major global health and economic problem. However, there are no pharmacological treatments to effectively reduce the compulsive use of most drugs of abuse. Despite exerting different mechanisms of action, all drugs of abuse promote the activation of the brain reward system, with lasting neurobiological consequences that potentiate subsequent consumption. Recent evidence shows that the brain displays marked oxidative stress and neuroinflammation following chronic drug consumption. Brain oxidative stress and neuroinflammation disrupt glutamate homeostasis by impairing synaptic and extra-synaptic glutamate transport, reducing GLT-1, and system Xc− activities respectively, which increases glutamatergic neurotransmission. This effect consolidates the relapse-promoting effect of drug-related cues, thus sustaining drug craving and subsequent drug consumption. Recently, promising results as experimental treatments to reduce drug consumption and relapse have been shown by (i) antioxidant and anti-inflammatory synthetic molecules whose effects reach the brain; (ii) natural biomolecules secreted by mesenchymal stem cells that excel in antioxidant and anti-inflammatory properties, delivered via non-invasive intranasal administration to animal models of drug abuse and (iii) potent anti-inflammatory microRNAs and anti-miRNAs which target the microglia and reduce neuroinflammation and drug craving. In this review, we address the neurobiological consequences of brain oxidative stress and neuroinflammation that follow the chronic consumption of most drugs of abuse, and the current and potential therapeutic effects of antioxidants and anti-inflammatory agents and biomolecules to reduce these drug-induced alterations and to prevent relapse.

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Ayala, Maria. "Brain Serotonin, Psychoactive Drugs, and Effects on Reproduction." Central Nervous System Agents in Medicinal Chemistry 9, no. 4 (December 1, 2009): 258–76. http://dx.doi.org/10.2174/187152409789630389.

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Schulz, Ellina, Almuth F. Kessler, Ellaine Salvador, Dominik Domröse, Malgorzata Burek, Catherine Tempel Brami, Tali Voloshin Sela, et al. "EXTH-02. THE BLOOD BRAIN BARRIER (BBB) PERMEABILITY IS ALTERED BY TUMOR TREATING FIELDS (TTFIELDS) IN VIVO." Neuro-Oncology 21, Supplement_6 (November 2019): vi82. http://dx.doi.org/10.1093/neuonc/noz175.336.

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Abstract OBJECTIVE For glioblastoma patients Tumor Treating Fields (TTFields) have been established as adjuvant therapy. The blood brain barrier (BBB) tightly controls the influx of the majority of compounds from blood to brain. Therefore, the BBB may block delivery of drugs for treatment of brain tumors. Here, the influence of TTFields on BBB permeability was assessed in vivo. METHODS Rats were treated with 100 kHz TTFields for 72 h and thereupon i.v. injected with Evan’s Blue (EB) which directly binds to Albumin. To evaluate effects on BBB, EB was extracted after brain homogenization and quantified. In addition, cryosections of rat brains were prepared following TTFields application. The sections were stained for tight junction proteins Claudin-5 and Occludin and for immunoglobulin G (IgG) to assess vessel structure. Furthermore, serial dynamic contrast-enhanced DCE-MRI with Gadolinium contrast agent was performed before and after TTFields application. RESULTS TTFields application significantly increased the EB accumulation in the rat brain. In TTFields-treated rats, the vessel structure became diffuse compared to control cryosections of rat brains; Claudin 5 and Occludin were delocalized and IgG was found throughout the brain tissue. Serial DCE-MRI demonstrated significantly increased accumulation of Gadolinium in the brain, observed directly after 72 h of TTFields application. The effect of TTFields on the BBB disappeared 96 h after end of treatment and no difference in contrast enhancement between controls and TTFields treated animals was detectable. CONCLUSION By altering BBB integrity and permeability, application of TTFields at 100 kHz may have the potential to deliver drugs to the brain, which are unable to cross the BBB. Utilizing TTFields to open the BBB and its subsequent recovery could be a clinical approach of drug delivery for treatment of brain tumors and other diseases of the central nervous system. These results will be further validated in clinical Trials.

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Tataranno, Maria Luisa, Serafina Perrone, Mariangela Longini, and Giuseppe Buonocore. "New Antioxidant Drugs for Neonatal Brain Injury." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/108251.

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The brain injury concept covers a lot of heterogeneity in terms of aetiology involving multiple factors, genetic, hemodynamic, metabolic, nutritional, endocrinological, toxic, and infectious mechanisms, acting in antenatal or postnatal period. Increased vulnerability of the immature brain to oxidative stress is documented because of the limited capacity of antioxidant enzymes and the high free radicals (FRs) generation in rapidly growing tissue. FRs impair transmembrane enzyme Na+/K+-ATPase activity resulting in persistent membrane depolarization and excessive release of FR and excitatory aminoacid glutamate. Besides being neurotoxic, glutamate is also toxic to oligodendroglia, via FR effects. Neuronal cells die of oxidative stress. Excess of free iron and deficient iron/binding metabolising capacity are additional features favouring oxidative stress in newborn. Each step in the oxidative injury cascade has become a potential target for neuroprotective intervention. The administration of antioxidants for suspected or proven brain injury is still not accepted for clinical use due to uncertain beneficial effects when treatments are started after resuscitation of an asphyxiated newborn. The challenge for the future is the early identification of high-risk babies to target a safe and not toxic antioxidant therapy in combination with standard therapies to prevent brain injury and long-term neurodevelopmental impairment.

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Tărăboanţă, Ionuţ, Andra Claudia Tărăboanţă-Gamen, Stefan Lucian Burlea, Liliana Luca, Angela Cristina Ghiorghe, and Sorin Andrian. "Evaluation of the Salivary Flow in Patients with Schizophrenia. A Literature Review." BRAIN. Broad Research in Artificial Intelligence and Neuroscience 13, no. 1Sup1 (March 23, 2022): 175–87. http://dx.doi.org/10.18662/brain/13.1sup1/311.

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Schizophrenia is a chronic psychiatric disease that affects approximately 1% of the global population. Schizophrenia is characterised by positive, negative and cognitive symptoms. The etiological factors of this psychiatric illness are not fully deciphered, but the most incriminated are genetic factors and environmental risk factors. The treatment of schizophrenia has the role of reduction the duration and intensity of episodes and consists in the administration of typical or atypical antipsychotic drugs, antiparkinsonian, anxiolytic, sedatives or antidepressants. Of these, some of the drugs may have side effects that modify patients' salivary flow rates. Xerostomy is a subjective sign characterized by a dry mouth sensation and is caused by hypofunction of the salivary glands. According to a series of studies, xerostomia can be an adverse effect of typical antipsychotic medication as well as antiparkinsonian medication. Sialorrhea is caused by hyperfunction of the salivary glands and is characterized by an increased secretion of saliva. This side effect is especially noticeable during the night sleep. Alteration of salivary function creates increased discomfort to the schizophrenic patient, which causes him to give up regular medication. The aim of this study is to review the literature on the link between schizophrenia, the treatment of schizophrenia and impaired salivary function.

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Chadwick, David. "Does withdrawal of different antiepileptic drugs have different effects on seizure recurrence?" Brain 122, no. 3 (March 1999): 441–48. http://dx.doi.org/10.1093/brain/122.3.441.

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Barańczyk-Kuźma, Anna, Magdalena Kuźma, Marzena Gutowicz, Beata Kaźmierczak, and Jacek Sawicki. "Glutathione S-transferase pi as a target for tricyclic antidepressants in human brain." Acta Biochimica Polonica 51, no. 1 (March 31, 2004): 207–12. http://dx.doi.org/10.18388/abp.2004_3612.

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GST pi, the main glutathione S-transferase isoform present in the human brain, was isolated from various regions of the brain and the in vitro effect of tricyclic antidepressants on its activity was studied. The results indicated that amitripyline and doxepin--derivatives of dibenzcycloheptadiene, as well as imipramine and clomipramine--derivatives of dibenzazepine, inhibit the activity of GST pi from frontal and parietal cortex, hippocampus and brain stem. All these tricyclics are noncompetitive inhibitors of the enzyme with respect to reduced glutathione and noncompetitive (amitripyline, doxepin) or uncompetitive (imipramine, clomipramine) with respect to the electrophilic substrate. Their inhibitory effect is reversible and it depends on the chemical structure of the tricyclic antidepressants rather than on the brain localization of the enzyme. We conclude that the interaction between GST pi and the drugs may reduce their availability in the brain and thus affect their therapeutic activity. On the other hand, tricyclic antidepressants may decrease the efficiency of the enzymatic barrier formed by GST and increase the exposure of brain to toxic electrophiles. Reactive electrophiles not inactivated by GST may contribute in adverse effects caused by these drugs.

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Stashina, Elena V., Nikolay A. Gavrilov, and Petr D. Shabanov. "Neurobehavioral effects of choninergic drugs in prenatal period." Reviews on Clinical Pharmacology and Drug Therapy 15, no. 3 (September 15, 2017): 5–21. http://dx.doi.org/10.17816/rcf1535-21.

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Environmental toxicants, chemicals exhibiting with cholinotropics properties, and drugs – agonists and antagonists of M- and N-cholinergic receptors by acting on the developing brain of the fetus in the embryonic period of ontogenesis, cause a change the activity of the cholinergic mechanisms of the brain during critical periods of prenatal development with the subsequent disruption of the formation of different brain systems, primarily the ontogeny of nerve cells and brain neurotransmitter systems. These changes in the long term is correlated with neurobehavioral deficits from adult individuals, dysfunction of the reproductive system of adult offspring. The relevance of the study of prenatal effects of cholinergic factors on the central mechanisms of reproductive function, memory processes and learning during ontogenetic development of the organism due to the need of prevention and treatment of subsequent mental, behavioral, and sexual dysfunctions, and abnormal sexual behavior, infertility.

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Journal articles on the topic 'Brain – Effect of drugs on'

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