DOCSLIB.ORG

Effects of Antidepressant Treatment on Inhibitory Avoidance Behavior and Amygdaloid ␤-Adrenoceptors in Rats Lynette C

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Effects of Antidepressant Treatment on Inhibitory Avoidance Behavior and Amygdaloid ␤-Adrenoceptors in Rats Lynette C Effects of Antidepressant Treatment on Inhibitory Avoidance Behavior and Amygdaloid b-Adrenoceptors in Rats Lynette C. Daws, Ph.D., Ray Lopez, Ph.D., and Alan Frazer, Ph.D. Chronic treatment of rats with a variety of antidepressants showed a marked deficit in retention. This effect was also b results in the down-regulation of 1-adrenoceptors in the observed after acute administration of these drugs, although b amygdaloid nuclei. The present study sought to determine if they did not down-regulate amygdaloid 1-adrenoceptors at this specific neurochemical effect caused an alteration in this time. It seems that the ability of these antidepressants to inhibitory avoidance conditioning, a behavior considered to potentiate the amnesic effect of scopolamine is unrelated to b b be mediated by -adrenoceptors in the amygdala. Rats their effect on 1-adrenoceptor number in the amygdala and b treated chronically with either desipramine (DMI) or that the extent of antidepressant-induced amygdaloid 1- b phenelzine (PHEN), which down-regulate 1-adrenoceptors adrenoceptor down-regulation is not sufficient, by itself, to in the amygdala, or fluoxetine (FLUOX), which does not do cause a deficit in an inhibitory avoidance task. this, did not exhibit a deficit in the retention of the [Neuropsychopharmacology 19:300–313, 1998] inhibitory avoidance task. However, when scopolamine was © 1998 American College of Neuropsychopharmacology. given prior to acquisition of the task in a dose that, by itself, Published by Elsevier Science Inc. did not affect retention, DMI- and PHEN-treated rats KEY WORDS: Inhibitory avoidance; Desipramine; ous reports emphasizing the putative role of the b Phenelzine; Fluoxetine; 1-Adrenoceptors; Amygdala amygdala in mediating the behavioral actions of antide- pressants (Horovitz 1966; Gorka et al. 1979; Broekkamp Chronic treatment of rats with a wide range of antide- and Lloyd 1981; Sarter and Markowitsch 1985; Duncan pressants produces a significant reduction in the num- et al. 1986; Beck and Fibiger 1995). It should be noted, ber of b-adrenoceptors in brain (Banerjee et al. 1977; see however, that the behavioral effects observed in these Heninger and Charney 1987). In particular, quantitative studies followed acute administration of antidepres- autoradiographic studies have shown that different sants; whereas, the down-regulation of b -adrenocep- types of antidepressants most consistently down-regu- 1 tors takes time (ca. 1 week) to occur (Ordway et al. 1991). late b -adrenoceptors in the amygdala (Ordway et al. 1 Thus, both acute and chronic effects of antidepressants 1988, 1991). This finding is of interest in light of previ- implicate the amygdala as a primary target of the phar- macological actions of this class of drugs. The purpose From the Department of Pharmacology (LCD, RL, AF), The Univer- of this study was to attempt to identify a behavioral sity of Texas Health Science Center at San Antonio, San Antonio, Texas; alteration that results from the down-regulation of and South Texas Veterans Health Care System (AF), Audie L. Murphy b Memorial Veterans Hospital Division, San Antonio, Texas, USA. amygdaloid -adrenoceptors. Address correspondence to: Lynette C. Daws, Department of b-adrenoceptors in the amygdala have been impli- Pharmacology, University of Texas Health Science Center at San cated in mediating inhibitory (passive) avoidance be- Antonio, 7703 Floyd Curl Drive, San Antonio, TX, 78284-7764, USA. Received October 23, 1997; revised January 16, 1998; accepted havior (e.g., Gallagher et al. 1977; Liang et al. 1986, 1990; January 20, 1998. Campeau and Davis 1995; Introini-Collison et al. 1996). NEUROPSYCHOPHARMACOLOGY 1998–VOL. 19, NO. 4 © 1998 American College of Neuropsychopharmacology Published by Elsevier Science Inc. 0893-133X/98/$–see front matter 655 Avenue of the Americas, New York, NY 10010 PII S0893-133X(98)00016-5 NEUROPSYCHOPHARMACOLOGY 1998–VOL. 19, NO. 4 Antidepressant Treatment and Behavior 301 Gallagher et al. (1977) observed that injection of into the illuminated compartment facing away from the b-adrenoceptor antagonists in the amygdala of rats pro- closed door. The rat was allowed a 10-second habitua- duced retrograde amnesia on an inhibitory avoidance tion period before the door was opened, allowing free task that was both time- and dose-dependent and ste- passage of the rat into the dark compartment. Once the reospecific. This work has been confirmed and ex- rat had entered the dark compartment (i.e., all four tended by McGaugh and his colleagues (Liang et al. paws being within the dark compartment), the door 1986; McGaugh 1989). Although there is a learning was closed behind the rat and a 0.5 mA shock delivered component to inhibitory avoidance behavior, there is for a 3-second duration. Approximately 5 seconds later, also an emotional component attributable to its pairing the rat was removed from the chamber and placed into of a nonaversive stimulus with an aversive one. The a holding container until all cage mates has been pro- retention of memory caused by this pairing is manifest cessed. All rats were then returned to their home cage. as an increased latency for rats to enter the dark com- The latency for the rat to enter the dark compartment, partment of a two-compartment chamber after being i.e. acquisition latency, was recorded. Twenty-four hours shocked there in a training trial. It is possible to view later, retention was tested. This was done by placing the increased latency as a type of “freezing” behavior, a each rat into the illuminated compartment, as described behavior considered indicative of a state of fear or anxi- above, with the exception that the guillotine door was ety (Leaton and Borszcz 1985). This behavior may, already open. The latency to enter the dark compart- therefore, be particularly relevant to study, because ment was recorded as a measure of retention of the task. some antidepressants are efficacious in panic disorder Rats that did not enter the dark compartment within 10 (Sheehan et al. 1980; Murphy et al. 1985; Kahn et al. minutes were given a ceiling score of 600 seconds. To 1986), and some view anxiety as a central component of verify the involvement of amygdaloid b-adrenoceptors the depressive syndrome (Katz et al. 1984). The present in mediating inhibitory avoidance behavior, a separate study aims to characterize the effect of acute and group of rats received intra-amygdala administration of chronic treatment with antidepressant drugs on inhibi- propranolol or vehicle. tory avoidance behavior in rats and to correlate this with changes in b -adrenoceptor number in the amygdala. Surgery. Rats were anesthetized with sodium pento- 1 barbital (65 mg/kg intraperitoneally [IP]), placed into a stereotaxic frame, and bilaterally implanted with 22- MATERIALS AND METHODS gauge stainless steel guide cannulae into the amygdala. The tips were directed at the dorsal surface of the Animals amygdala complex (A.P. 22.3 mm, M.L. 14.6 mm, D.V. 2 Male Sprague–Dawley rats (270–350 g, Harlan, India- 7.5 mm; Paxinos and Watson 1986). Two skull screws napolis, IN) were housed either in groups of three, or served as anchors for the cranioplastic cement used to individually (postsurgery). The colony was maintained hold the cannulae in place. The patency of the cannulae on a 14:10 light/dark cycle with the lights on at 7:00 was maintained by inserting a 28-gauge stylet. a.m. All training was conducted between 0800 and 1300 Intra-Amygdala Drug Administration. Propranolol (34 6 8 hours. Room temperature was maintained at 23 2 C, or 68 nmol) or phosphate buffered saline (PBS, pH 7.4) and rats were provided with food and water ad libitum. was administered through a 28-gauge injector con- All animal procedures were in strict accordance with nected to a 10 ml Hamilton microsyringe by polyethyl- the NIH Guide for the Care and Use of Laboratory Ani- ene tubing (PE-20). The injector was designed so that, mals. All efforts were made to minimize both the num- when inserted into the cannula, the top protruded 1 mm ber of rats used and discomfort to the rats during exper- in the brain tissue. Both microsyringe and tubing were imental procedures. filled with fluid. Twenty minutes prior to acquisition training, one microliter of the drug solution was deliv- Inhibitory Avoidance Task ered sequentially into each amygdala. Each injection was given over a 60 s period. The injector was left in the Rats were trained on a one trial step-through inhibitory cannula for an additional 15 s to allow diffusion of the avoidance task. The inhibitory avoidance chamber was drug away from the injector tip. Stylets were replaced made from Plexiglas and was comprised of two com- immediately after termination of the injection. Reten- partments separated by a guillotine door. The smaller tion was tested 24 hours later. compartment (20 3 16 3 24 cm) was illuminated by a 60-watt light, mounted 50 cm above the Plexiglas base. Histology. At the conclusion of the experiment, one The base of the larger, dark compartment (30 3 20 3 20 microliter of Chicago blue dye was injected into the cm), consisted of a series of metal rods separated by 1 amygdala over a 60 s period to mark the site of the injec- cm, through which an electric shock could be delivered. tor tip. Rats were then decapitated, and the brain was On the day of acquisition training, each rat was placed rapidly removed and stored in 10% formalin for 24 302 L.C. Daws et al. NEUROPSYCHOPHARMACOLOGY 1998–VOL. 19, NO. 4 hours. The brain was frozen (2158C) prior to sectioning tested 24 hours later, after which the rats were sacri- (40 mm thick slices) through the cannula tracts. Sections ficed and brains stored as described above.
Load more

Recommended publications
  • Arecoline Promotes Migration of A549 Lung Cancer Cells Through Activating the EGFR/Src/FAK Pathway
    toxins Article Arecoline Promotes Migration of A549 Lung Cancer Cells through Activating the EGFR/Src/FAK Pathway Chih-Hsiang Chang 1,†, Mei-Chih Chen 2,3,†, Te-Huan Chiu 1 , Yu-Hsuan Li 1, Wan-Chen Yu 1, Wan-Ling Liao 1, Muhammet Oner 1, Chang-Tze Ricky Yu 4, Chun-Chi Wu 5, Tsung-Ying Yang 6, Chieh-Lin Jerry Teng 7, Kun-Yuan Chiu 8, Kun-Chien Chen 6, Hsin-Yi Wang 9, Chia-Herng Yue 10, Chih-Ho Lai 11 , Jer-Tsong Hsieh 12 and Ho Lin 1,13,14,* 1 Department of Life Sciences, National Chung Hsing University, Taichung 40227, Taiwan; [email protected] (C.-H.C.); [email protected] (T.-H.C.); [email protected] (Y.-H.L.); [email protected] (W.-C.Y.); [email protected] (W.-L.L.); [email protected] (M.O.) 2 Medical Center for Exosomes and Mitochondria Related Diseases, China Medical University Hospital, Taichung 40447, Taiwan; [email protected] 3 Department of Nursing, Asia University, Taichung 41345, Taiwan 4 Department of Applied Chemistry, National Chi Nan University, Nantou 54561, Taiwan; [email protected] 5 Institute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan; [email protected] 6 Division of Chest Medicine, Taichung Veterans General Hospital, Taichung 40705, Taiwan; [email protected] (T.-Y.Y.); [email protected] (K.-C.C.) 7 Division of Hematology/Medical Oncology, Taichung Veterans General Hospital, Taichung 40705, Taiwan; [email protected] 8 Division of Urology, Taichung Veterans General Hospital, Taichung 40705, Taiwan; [email protected] 9 Department of Nuclear Medicine, Taichung
    [Show full text]
  • Comparing the Effect of Venlafaxine and the Combination of Nortriptyline and Propranolol in the Prevention of Migraine
    Comparing the Effect of Venlafaxine and the Combination of Nortriptyline and Propranolol in the Prevention of Migraine Arash Mosarrezaii1, Mohammad Reza Amiri Nikpour1, Ata Jabarzadeh2 1Department of Neurology, Imam Khomeini Hospital, Urmia University of Medical Sciences, Urmia, Iran, 2Medical Student, Urmia University of Medical Sciences, Urmia, Iran Abstract Background: Migraine is a debilitating neurological condition, which can be categorized into episodic and chronic groups based on its clinical pattern. Avoiding the risk factors exacerbating migraine is not enough to reduce the frequency and severity of migraine headaches, and in the case of non-receiving proper drug treatment, episodic migraines have the potential to become chronic, which increases the risk of cardiovascular complications RESEARCH ARTICLE and leaves great impact on the quality of life of patients and increasing the health-care costs. The objective of this research was to compare the effects of venlafaxine (VFL) and nortriptyline and propranolol in preventing migraines. Methods: This research is an interventional study performed on 60 patients with migraine admitted to the neurological clinic. Patients were visited at 3 time intervals. In each stage, the variables of headache frequency, headache severity, nausea, vomiting, and drowsiness were recorded. Data were analyzed using SPSS 23 software. Results: VFL drug with a daily dose of 37.5 mg is not only more tolerable in the long term but also leaves better effect in reducing the frequency and severity of headaches compared to the combination of nortriptyline and propranolol. Conclusion: VFL is an appropriate, effective, and tolerable alternative to migraine treatment. Key words: Migraine, nortriptyline, propranolol, venlafaxine INTRODUCTION Patients with CM are less likely to have full-time job than patients with episodic type, and they are at risk of job igraine is known as a common incapacity, anxiety, chronic pain, and depression 2 times neurological disorder and causes more than patients with episodic migraine.
    [Show full text]
  • Upregulation of Peroxisome Proliferator-Activated Receptor-Α And
    Upregulation of peroxisome proliferator-activated receptor-α and the lipid metabolism pathway promotes carcinogenesis of ampullary cancer Chih-Yang Wang, Ying-Jui Chao, Yi-Ling Chen, Tzu-Wen Wang, Nam Nhut Phan, Hui-Ping Hsu, Yan-Shen Shan, Ming-Derg Lai 1 Supplementary Table 1. Demographics and clinical outcomes of five patients with ampullary cancer Time of Tumor Time to Age Differentia survival/ Sex Staging size Morphology Recurrence recurrence Condition (years) tion expired (cm) (months) (months) T2N0, 51 F 211 Polypoid Unknown No -- Survived 193 stage Ib T2N0, 2.41.5 58 F Mixed Good Yes 14 Expired 17 stage Ib 0.6 T3N0, 4.53.5 68 M Polypoid Good No -- Survived 162 stage IIA 1.2 T3N0, 66 M 110.8 Ulcerative Good Yes 64 Expired 227 stage IIA T3N0, 60 M 21.81 Mixed Moderate Yes 5.6 Expired 16.7 stage IIA 2 Supplementary Table 2. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of an ampullary cancer microarray using the Database for Annotation, Visualization and Integrated Discovery (DAVID). This table contains only pathways with p values that ranged 0.0001~0.05. KEGG Pathway p value Genes Pentose and 1.50E-04 UGT1A6, CRYL1, UGT1A8, AKR1B1, UGT2B11, UGT2A3, glucuronate UGT2B10, UGT2B7, XYLB interconversions Drug metabolism 1.63E-04 CYP3A4, XDH, UGT1A6, CYP3A5, CES2, CYP3A7, UGT1A8, NAT2, UGT2B11, DPYD, UGT2A3, UGT2B10, UGT2B7 Maturity-onset 2.43E-04 HNF1A, HNF4A, SLC2A2, PKLR, NEUROD1, HNF4G, diabetes of the PDX1, NR5A2, NKX2-2 young Starch and sucrose 6.03E-04 GBA3, UGT1A6, G6PC, UGT1A8, ENPP3, MGAM, SI, metabolism
    [Show full text]
  • Schizophrenia Care Guide
    August 2015 CCHCS/DHCS Care Guide: Schizophrenia SUMMARY DECISION SUPPORT PATIENT EDUCATION/SELF MANAGEMENT GOALS ALERTS Minimize frequency and severity of psychotic episodes Suicidal ideation or gestures Encourage medication adherence Abnormal movements Manage medication side effects Delusions Monitor as clinically appropriate Neuroleptic Malignant Syndrome Danger to self or others DIAGNOSTIC CRITERIA/EVALUATION (PER DSM V) 1. Rule out delirium or other medical illnesses mimicking schizophrenia (see page 5), medications or drugs of abuse causing psychosis (see page 6), other mental illness causes of psychosis, e.g., Bipolar Mania or Depression, Major Depression, PTSD, borderline personality disorder (see page 4). Ideas in patients (even odd ideas) that we disagree with can be learned and are therefore not necessarily signs of schizophrenia. Schizophrenia is a world-wide phenomenon that can occur in cultures with widely differing ideas. 2. Diagnosis is made based on the following: (Criteria A and B must be met) A. Two of the following symptoms/signs must be present over much of at least one month (unless treated), with a significant impact on social or occupational functioning, over at least a 6-month period of time: Delusions, Hallucinations, Disorganized Speech, Negative symptoms (social withdrawal, poverty of thought, etc.), severely disorganized or catatonic behavior. B. At least one of the symptoms/signs should be Delusions, Hallucinations, or Disorganized Speech. TREATMENT OPTIONS MEDICATIONS Informed consent for psychotropic
    [Show full text]
  • NIH Public Access Author Manuscript Neuroscience
    NIH Public Access Author Manuscript Neuroscience. Author manuscript; available in PMC 2016 January 22. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: Neuroscience. 2015 January 22; 0: 775–797. doi:10.1016/j.neuroscience.2014.10.044. Early-life Exposure to the SSRI Paroxetine Exacerbates Depression-like Behavior in Anxiety/Depression-prone rats Matthew E. Glover1, Phyllis C. Pugh1, Nateka L. Jackson1, Joshua L. Cohen1, Andrew D. Fant2, Huda Akil3, and Sarah M. Clinton1,§ 1Department of Psychiatry and Behavioral Neurobiology, University of Alabama-Birmingham, USA 2Division of Chemical Biology and Medicinal Chemistry, Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, USA 3Molecular and Behavioral Neuroscience Institute, University of Michigan, USA Abstract Selective serotonin reuptake inhibitor (SSRI) antidepressants are the mainstay treatment for the 10–20% of pregnant and postpartum women who suffer major depression, but the effects of SSRIs on their children’s developing brain and later emotional health are poorly understood. SSRI use during pregnancy can elicit antidepressant withdrawal in newborns and increase toddlers’ anxiety and social avoidance. In rodents, perinatal SSRI exposure increases adult depression- and anxiety- like behavior, although certain individuals are more vulnerable to these effects than others. Our study establishes a rodent model of individual differences in susceptibility to perinatal SSRI exposure, utilizing selectively-bred Low Responder (bLR) and High Responder (bHR) rats that were previously bred for high versus low behavioral response to novelty. Pregnant bHR/bLR females were chronically treated with the SSRI paroxetine (10 mg/kg/day p.o.) to examine its effects on offspring’s emotional behavior and gene expression in the developing brain.
    [Show full text]
  • Selective Labeling of Serotonin Receptors Byd-[3H]Lysergic Acid
    Proc. Nati. Acad. Sci. USA Vol. 75, No. 12, pp. 5783-5787, December 1978 Biochemistry Selective labeling of serotonin receptors by d-[3H]lysergic acid diethylamide in calf caudate (ergots/hallucinogens/tryptamines/norepinephrine/dopamine) PATRICIA M. WHITAKER AND PHILIP SEEMAN* Department of Pharmacology, University of Toronto, Toronto, Canada M5S 1A8 Communicated by Philip Siekevltz, August 18,1978 ABSTRACT Since it was known that d-lysergic acid di- The objective in this present study was to improve the se- ethylamide (LSD) affected catecholaminergic as well as sero- lectivity of [3H]LSD for serotonin receptors, concomitantly toninergic neurons, the objective in this study was to enhance using other drugs to block a-adrenergic and dopamine receptors the selectivity of [3HJISD binding to serotonin receptors in vitro by using crude homogenates of calf caudate. In the presence of (cf. refs. 36-38). We then compared the potencies of various a combination of 50 nM each of phentolamine (adde to pre- drugs on this selective [3H]LSD binding and compared these clude the binding of [3HJLSD to a-adrenoceptors), apmo ie, data to those for the high-affinity binding of [3H]serotonin and spiperone (added to preclude the binding of [3H[LSD to (39). dopamine receptors), it was found by Scatchard analysis that the total number of 3H sites went down to 300 fmol/mg, compared to 1100 fmol/mg in the absence of the catechol- METHODS amine-blocking drugs. The IC50 values (concentrations to inhibit Preparation of Membranes. Calf brains were obtained fresh binding by 50%) for various drugs were tested on the binding of [3HLSD in the presence of 50 nM each of apomorphine (A), from the Canada Packers Hunisett plant (Toronto).
    [Show full text]
  • EUROPEAN COMMISSION Brussels, 11.7.2011 SEC(2011)
    EUROPEAN COMMISSION Brussels, 11.7.2011 SEC(2011) 912 final COMMISSION STAFF WORKING PAPER on the assessment of the functioning of Council Decision 2005/387/JHA on the information exchange, risk assessment and control of new psychoactive substances Accompanying the document REPORT FROM THE COMMISSION on the assessment of the functioning of Council Decision 2005/387/JHA on the information exchange, risk assessment and control of new psychoactive substances {COM(2011) 430 final} EN EN TABLE OF CONTENTS 1. Introduction...................................................................................................................3 2. Methodology.................................................................................................................4 3. Key findings from the 2002 evaluation of the Joint Action on synthetic drugs ...........5 4. Overview of notifications, types of substances and trends at EU level 2005-2010......7 5. Other EU legislation relevant for the regulation of new psychoactive substances.....12 6. Functioning of the Council Decision on new psychoactive substances .....................16 7. Findings of the survey among Member States............................................................17 7.1. Assessment of the Council Decision ..........................................................................17 7.2. Stages in the functioning of the Council Decision .....................................................18 7.3. National responses to new psychoactive substances ..................................................20
    [Show full text]
  • Drug Name Plate Number Well Location % Inhibition, Screen Axitinib 1 1 20 Gefitinib (ZD1839) 1 2 70 Sorafenib Tosylate 1 3 21 Cr
    Drug Name Plate Number Well Location % Inhibition, Screen Axitinib 1 1 20 Gefitinib (ZD1839) 1 2 70 Sorafenib Tosylate 1 3 21 Crizotinib (PF-02341066) 1 4 55 Docetaxel 1 5 98 Anastrozole 1 6 25 Cladribine 1 7 23 Methotrexate 1 8 -187 Letrozole 1 9 65 Entecavir Hydrate 1 10 48 Roxadustat (FG-4592) 1 11 19 Imatinib Mesylate (STI571) 1 12 0 Sunitinib Malate 1 13 34 Vismodegib (GDC-0449) 1 14 64 Paclitaxel 1 15 89 Aprepitant 1 16 94 Decitabine 1 17 -79 Bendamustine HCl 1 18 19 Temozolomide 1 19 -111 Nepafenac 1 20 24 Nintedanib (BIBF 1120) 1 21 -43 Lapatinib (GW-572016) Ditosylate 1 22 88 Temsirolimus (CCI-779, NSC 683864) 1 23 96 Belinostat (PXD101) 1 24 46 Capecitabine 1 25 19 Bicalutamide 1 26 83 Dutasteride 1 27 68 Epirubicin HCl 1 28 -59 Tamoxifen 1 29 30 Rufinamide 1 30 96 Afatinib (BIBW2992) 1 31 -54 Lenalidomide (CC-5013) 1 32 19 Vorinostat (SAHA, MK0683) 1 33 38 Rucaparib (AG-014699,PF-01367338) phosphate1 34 14 Lenvatinib (E7080) 1 35 80 Fulvestrant 1 36 76 Melatonin 1 37 15 Etoposide 1 38 -69 Vincristine sulfate 1 39 61 Posaconazole 1 40 97 Bortezomib (PS-341) 1 41 71 Panobinostat (LBH589) 1 42 41 Entinostat (MS-275) 1 43 26 Cabozantinib (XL184, BMS-907351) 1 44 79 Valproic acid sodium salt (Sodium valproate) 1 45 7 Raltitrexed 1 46 39 Bisoprolol fumarate 1 47 -23 Raloxifene HCl 1 48 97 Agomelatine 1 49 35 Prasugrel 1 50 -24 Bosutinib (SKI-606) 1 51 85 Nilotinib (AMN-107) 1 52 99 Enzastaurin (LY317615) 1 53 -12 Everolimus (RAD001) 1 54 94 Regorafenib (BAY 73-4506) 1 55 24 Thalidomide 1 56 40 Tivozanib (AV-951) 1 57 86 Fludarabine
    [Show full text]
  • Vaginal Administration of Contraceptives
    Scientia Pharmaceutica Review Vaginal Administration of Contraceptives Esmat Jalalvandi 1,*, Hafez Jafari 2 , Christiani A. Amorim 3 , Denise Freitas Siqueira Petri 4 , Lei Nie 5,* and Amin Shavandi 2,* 1 School of Engineering and Physical Sciences, Heriot-Watt University, Edinburgh EH14 4AS, UK 2 BioMatter Unit, École Polytechnique de Bruxelles, Université Libre de Bruxelles, Avenue F.D. Roosevelt, 50-CP 165/61, 1050 Brussels, Belgium; [email protected] 3 Pôle de Recherche en Gynécologie, Institut de Recherche Expérimentale et Clinique, Université Catholique de Louvain, 1200 Brussels, Belgium; [email protected] 4 Fundamental Chemistry Department, Institute of Chemistry, University of São Paulo, Av. Prof. Lineu Prestes 748, São Paulo 05508-000, Brazil; [email protected] 5 College of Life Sciences, Xinyang Normal University, Xinyang 464000, China * Correspondence: [email protected] (E.J.); [email protected] (L.N.); [email protected] (A.S.); Tel.: +32-2-650-3681 (A.S.) Abstract: While contraceptive drugs have enabled many people to decide when they want to have a baby, more than 100 million unintended pregnancies each year in the world may indicate the contraceptive requirement of many people has not been well addressed yet. The vagina is a well- established and practical route for the delivery of various pharmacological molecules, including contraceptives. This review aims to present an overview of different contraceptive methods focusing on the vaginal route of delivery for contraceptives, including current developments, discussing the potentials and limitations of the modern methods, designs, and how well each method performs for delivering the contraceptives and preventing pregnancy.
    [Show full text]
  • Phencyclidine: an Update
    Phencyclidine: An Update U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES • Public Health Service • Alcohol, Drug Abuse and Mental Health Administration Phencyclidine: An Update Editor: Doris H. Clouet, Ph.D. Division of Preclinical Research National Institute on Drug Abuse and New York State Division of Substance Abuse Services NIDA Research Monograph 64 1986 DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service Alcohol, Drug Abuse, and Mental Health Administratlon National Institute on Drug Abuse 5600 Fishers Lane Rockville, Maryland 20657 For sale by the Superintendent of Documents, U.S. Government Printing Office Washington, DC 20402 NIDA Research Monographs are prepared by the research divisions of the National lnstitute on Drug Abuse and published by its Office of Science The primary objective of the series is to provide critical reviews of research problem areas and techniques, the content of state-of-the-art conferences, and integrative research reviews. its dual publication emphasis is rapid and targeted dissemination to the scientific and professional community. Editorial Advisors MARTIN W. ADLER, Ph.D. SIDNEY COHEN, M.D. Temple University School of Medicine Los Angeles, California Philadelphia, Pennsylvania SYDNEY ARCHER, Ph.D. MARY L. JACOBSON Rensselaer Polytechnic lnstitute National Federation of Parents for Troy, New York Drug Free Youth RICHARD E. BELLEVILLE, Ph.D. Omaha, Nebraska NB Associates, Health Sciences Rockville, Maryland REESE T. JONES, M.D. KARST J. BESTEMAN Langley Porter Neuropsychiatric lnstitute Alcohol and Drug Problems Association San Francisco, California of North America Washington, D.C. DENISE KANDEL, Ph.D GILBERT J. BOTV N, Ph.D. College of Physicians and Surgeons of Cornell University Medical College Columbia University New York, New York New York, New York JOSEPH V.
    [Show full text]
  • Psychedelics in Psychiatry: Neuroplastic, Immunomodulatory, and Neurotransmitter Mechanismss
    Supplemental Material can be found at: /content/suppl/2020/12/18/73.1.202.DC1.html 1521-0081/73/1/202–277$35.00 https://doi.org/10.1124/pharmrev.120.000056 PHARMACOLOGICAL REVIEWS Pharmacol Rev 73:202–277, January 2021 Copyright © 2020 by The Author(s) This is an open access article distributed under the CC BY-NC Attribution 4.0 International license. ASSOCIATE EDITOR: MICHAEL NADER Psychedelics in Psychiatry: Neuroplastic, Immunomodulatory, and Neurotransmitter Mechanismss Antonio Inserra, Danilo De Gregorio, and Gabriella Gobbi Neurobiological Psychiatry Unit, Department of Psychiatry, McGill University, Montreal, Quebec, Canada Abstract ...................................................................................205 Significance Statement. ..................................................................205 I. Introduction . ..............................................................................205 A. Review Outline ........................................................................205 B. Psychiatric Disorders and the Need for Novel Pharmacotherapies .......................206 C. Psychedelic Compounds as Novel Therapeutics in Psychiatry: Overview and Comparison with Current Available Treatments . .....................................206 D. Classical or Serotonergic Psychedelics versus Nonclassical Psychedelics: Definition ......208 Downloaded from E. Dissociative Anesthetics................................................................209 F. Empathogens-Entactogens . ............................................................209
    [Show full text]
  • Guideline- Management of Migraine and Cluster Headache
    Hull & East Riding Prescribing Committee Guideline- Management of Migraine and Cluster Headache 1. BACKGROUND Headache is a common neurological condition which accounts for 4.4% of primary care consultations and 30% of neurology appointments. Primary headache disorders include migraine, tension-type and cluster headache. Twice as many women as men are affected by headache disorder. This is thought to be due to changes in hormone levels during the menstrual cycle, which can be more pronounced at puberty and menopause. Recommendations within this guideline are based on best evidence and national/international guidelines. They are followed by consultants and specialist nurses working within the neurology department. Some recommendations may be for medicines prescribed outside their product license i.e. off label. It is noted in the guideline when the medicine is off label and relevant guidelines should be followed when prescribing medicines off label. A number of British Association for the Study of Headache (BASH) leaflets have been linked in this guidance; these can be given to patients and cover the off license use of medicines and information about duration of prophylactic treatments. The colours on the drug names in this guidance refer to the classification in the joint formulary i.e. Red – specialist prescriber only Amber – prescribed in accordance with approved shared care framework Blue - Guideline Led prescribed on advice of specialist or in line with national / local guideline Green – other items listed on formulary suitable for initiation and prescribing by any prescriber If printed in black and white please refer to joint formulary for classification of medicines. Migraine Migraine is often underdiagnosed, misdiagnosed and undertreated.
    [Show full text]