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Suicide attempts in pa- admitted schizophrenic patients generic coreg 6.25mg free shipping. Psychopharmacology 1982;76: tients with panic disorder buy coreg 12.5mg. Gender differences in psychiatry: epidemiology and men generic coreg 25 mg overnight delivery. No gender effect on age therapy in the aftercare of acute schizophrenics. Am J Psychiatry 1992;149: chiatry 1978;35:1169–1177. Sex differences in dexes in first-episode schizophrenic patients. Am J Psychiatry the functional organization of the brain for language. Gender and the onset of schizophrenia: neurohu- 147. Neural sexual mosaicism: sexual differentiation of 126. Sex differences in brain morphology, and schizophrenia. Schizophr Bull 1990;16: patterns of hemispheric cerebral metabolism—a multiple 195–203. Two sexually dimorphic cell J Psychiatry 1996;153:799–805. Gender differences in 1176 Neuropsychopharmacology: The Fifth Generation of Progress regional cerebral blood flow during transient self-induced sad- relationship to the premenstrual syndrome. Relationship between receptor in the living human brain. Neurosci Lett 1996;204: symptom severity and steroid variation in women with premen- 25–28. Differences between sulfate, 5 -pregnane-3,20-dione and 3 -hydroxy-5 -pregnan- males and females in rates of serotonin synthesis in human brain. Sex differences in levels over the menstrual cycle and their relation to premenstrual regional cerebral blood flow. Sex and handedness differ- crine changes in luteal function in patients with premenstrual ences in cerebral blood flow during rest and during cognitive syndrome. Age and regional cerebral during the luteal phase in women with premenstrual tension blood flow at rest and during cognitive activity. Effects of normal aging, are higher in women with premenstrual irritability and dys- sex, and risk factors for stroke on regional cerebral blood flow phoria than in controls. Psychoneuroendocrinology 1992;17: (rCBF) in normal volunteers. Gender differ- with premenstrual syndrome and controls. Biol Psychiatry 1998; ences in cerebral blood flow as a function of cognitive state with 43:897–903. Gender differences 4 subunit suppression prevents withdrawal properties of an en- in the normal lateralization of the supratemporal cortex: MRI dogenous steroid. Cerebral glucose kinetics of hippocampal GABAA-gated current and increases metabolic rates in normal human females versus normal males. Concentrations of 3¨ - differences in regional cerebral glucose metabolism in normal reduced neuroactive steroids and their precursors in plasma of volunteers. Marked decrease cognition-specific cortical activity by gonadal steroids: a posi- of plasma neuroactive steroids during alcohol withdrawal. Effect of estrogen treatment on neuroactive steroids in major depression. Am J on brain activation patterns in postmenopausal women during Psychiatry 1998;155:910–913. In vivo measurement spinal fluid content of neurosteroids in patients with unipolar of dopamine receptors in human brain by positron emission major depression who are receiving fluoxetine or fluvoxamine. Ann NY Acad Sci 1988; Proc Natl Acad Sci USA 1998;95:3239–3244. Ar- one is associated with increases in cortical allopregnanolone and chives of Neurology and Psychiatry 1931;26:1053–1057. Premenstrual syndromes: over- hydroxy-5 [ ]-pregnan-20-one: endogenous metabolites of view from a methodologic perspective. Am J Psychiatry 1984; progesterone that are active at the GABA receptor. Anxiolytic activity assessment of menstrually related mood disorders. Am J Psychia- of the progesterone metabolite 5 -pregnan-3 -ol-one. Stress-induced ual of mental disorders, third edition, revised. Washington, DC: elevations of gamma-aminobutyric acid type A receptor-active American Psychiatric Association, 1987.
A comparison of sodium and yohimbine-stimulated plasma neuropeptide Y (NPY) levels bicarbonate and sodium lactate infusion in the induction of in combat related PTSD purchase coreg 25mg amex. Panic symptoms after inhalation free triodothyronine buy cheap coreg 25mg, total triiodothronine buy coreg 12.5 mg low cost, Thyroxine-binding of carbon dioxide. Sodium d-lactate infu- anxiety sensitivity in the pathogenesis of panic: replication and sion in panic disorder patients. False suffocation alarms, spontaneous panics, and sensitivity in childhood anxiety disorders and nonill comparison related conditions. The CeA and BNST Although the amygdala complex is generally defined by sev- have been grouped together because fibers from the Bla that eral distinct groups of cells, including the lateral, basal, ac- project to the BNST pass through the CeA and cells in the cessory basal central, medial, and cortical nuclei, new data lateral division of the CeA project to the BNST. Thus, many indicate that it is more useful to think of the amygdala as effects previously attributed to the CeA may really depend the basolateral amygdala (Bla) and to think of its several on the BNST. The Bla receives sensory Autonomic and Hormonal Measures information from the thalamus, cortex (169), and ventral Anatomically, the CeA and the BNST are well situated to hippocampus (54) and then activates or modulates synaptic mediate the various components of the fear response. Both transmission in target areas appropriate for the reinforce- structures send prominent projections to areas such as the ment signal with which the sensory information has been lateral hypothalamus, which is involved in activation of the associated. This involves both positive and negative associa- sympathetic autonomic nervous system seen during fear and tions. However, because most of the literature on the amyg- anxiety (155). Direct projections to the dorsal motor nu- dala has analyzed the role of the Bla and its adjacent target, cleus of the vagus, nucleus of the solitary tract, and ventro- the central nucleus of the amygdala (CeA), in aversive condi- lateral medulla may be involved in lateral extended amyg- tioning, this work serves as the main focus of this chapter. Because the periaqueductal gray Projections to the parabrachial nucleus may be involved in (PAG) has received considerable attention in the study of respiratory (as well as cardiovascular changes) during fear, defensive behavior and the hippocampus in the study of because electrical stimulation and lesions of this nucleus contextual fear conditioning, these data are reviewed next. Indirect Finally, brain systems and neurotransmitters involved in the projections of the CeA to the paraventricular nucleus inhibition of fear are reviewed, given the clinical significance through the BNST and preoptic area may mediate the of this information. Basolateral Nucleus of the Amygdala to CeA or BNST Pathway as It Relates to Conditioned and Attention and Vigilance Unconditioned Fear Projections from the lateral extended amygdala to the ven- tral tegmental area may mediate stress-induced increases in Figure 64. Direct projections to the dendritic field of the locus ceruleus or indirect projections through the paragigantocellularis nu- Michael Davis: Department of Psychiatry, Emory University School of cleus may mediate the increase in firing rates of cells in the Medicine, Atlanta, Georgia. Direct 932 Neuropsychopharmacology: The Fifth Generation of Progress FIGURE 64. Schematic diagram of the outputs of the basolateral amygdala to various target areas and how these connections may be involved in fear and anxiety. Direct sion in thalamic sensory relay neurons during states of fear. The lateral extended amygdala also detection in a state of fear or anxiety. The rapid development of conditioned bradycardia during pavlovian aversive conditioning, criti- Elicitation of Fear Responses by Electrical or cally dependent on the amygdala, may reflect a general in- Chemical Stimulation of the Extended crease in attention. Amygdala Electrical stimulation or abnormal electrical activation of Motor Behavior the amygdala (i. Direct projections to the nu- by temporal lobe epileptic discharge is fear. Schematic diagram of the outputs of the central nucleus of the amygdala and the lateral division of the bed nucleus of the stria terminalis to various tar- get areas and how these connections may be related to specific aspects of fear and anxiety. BNST, bed nu- cleus of the stria terminalis; CER, conditioned emotional response; EEG, electroencephlographic; N, nucleus. Chapter 64: Neural Circuitry of Anxiety and Stress Disorders 933 of the blue. It is frequently, but not invariably, associated servations led Kapp et al. In humans, attention or arousal manifested in a variety of CRs which electrical stimulation of the amygdala elicits feelings of fear function to enhance sensory processing. This mechanism is or anxiety as well as autonomic reactions indicative of fear rapidly acquired, perhaps via an inherent plasticity within (57,99). Although other emotional reactions occasionally the nucleus and associated structures in situations of uncer- are produced, the major reaction is one of fear or apprehen- tainty but of potential import; for example, when a neutral sion. Electrical stimulation by the cholinergic agonist carbachol or the neurotransmitter of the amygdala can also activate cholinergic cells that are glutamate produces prominent cardiovascular effects that involved in arousal-like effects depending on the state of depend on the species, site of stimulation, and state of the sleep and perhaps the species. CeA stimulation can also produce gastric ulceration and can increase gastric acid, and these features can be asso- Motor Behavior ciated with chronic fear or anxiety. It can also alter respira- Electrical or chemical stimulation of the CeA produces a tion, a prominent symptom of fear, especially in panic dis- reduction of prepotent, ongoing behavior, a critical compo- order. Electrical stimulation of the amygdala heart rate when the -aminobutyric acidA (GABAA) antago- also elicits jaw movements and activation of facial motoneu- nist bicuculline was infused into the Bla but not the CeA rons, which may mimic components of the facial expressions (215). Local infusion of N-methyl-D-aspartate (NMDA) or seen during the fear reaction. These motor effects may be AMPA into the basolateral nucleus also increased blood indicative of a more general effect of amygdala stimulation, pressure and heart rate (230). Repeated infusion of initially namely, that of modulating brainstem reflexes such as the subthreshold doses of bicuculline into the anterior basolat- massenteric, baroreceptor nictitating membrane, eyeblink, eral nucleus led to a 'priming' effect in which increases in and the startle reflex. This change in threshold lasted at least Summary of the Effects of Stimulation of the 6 weeks and could not be ascribed to mechanical damage Amygdala or generalized seizure activity based on EEG measurements. Viewed in this way, the pattern of behaviors seen during Similar changes in excitability were produced by repetitive fear may result from activation of a single area of the brain infusion of very low doses of corticotropin-releasing hor- (the extended amygdala), which then projects to various mone (CRH) or the related peptide, urocortin (210).
Further generic 12.5 mg coreg with mastercard, NMDA receptors may be important in Given the lackof findings associated with the dopamine processes that lead to synaptic pruning seen in adolescence buy coreg 6.25mg amex, system in the brain in schizophrenia cheap 25 mg coreg mastercard, the elucidation of which has been hypothesized to be abnormal in schizophre- other potential neurotransmitter substrates of this illness has nia (10). Cognitive functioning depends on the plasticity been an area of recent investigation. Glutamatergic dysfunc- mediated in part by NMDA receptors, and schizophrenics tion has been hypothesized to occur in schizophrenia, and often have cognitive deficits (11). Finally, the reduction of this has been one of the most active areas of neurotransmit- gray matter in several brain regions seen in schizophrenia has been suggested to be the result of neurotoxicity mediated ter research in this illness during the past few years. A constellation of symptoms, chapter, the glutamate hypothesis of schizophrenia is re- findings, and hypotheses of schizophrenia can be parsimon- viewed, the complexity of the molecules associated with the iously explained by NMDA-receptor dysfunction. Thus, although NMDA-re- ceptor abnormalities have been hypothesized in schizophre- nia, apparent NMDA-receptor dysregulation could be asso- GLUTAMATE AND SCHIZOPHRENIA ciated with abnormalities of another receptor subtype that interacts with the NMDA receptor, which in turn results Several lines of evidence have implicated glutamatergic dys- in a breakdown of normal glutamatergic transmission in function in schizophrenia. Meador-Woodruff: Department of Psychiatry, University of Michigan, Ann Arbor, Michigan. Kleinman: Clinical Brain Disorders Branch, National Institutes The four classes of glutamate receptors are functionally and of Mental Health Neuroscience Center, Washington, DC. The iono- 718 Neuropsychopharmacology: The Fifth Generation of Progress FIGURE 52. Recent data suggest that glutamatergic transmission requires three cells: a presynaptic glu- tamate-releasing cell, a presynaptic glial cell that releases the endogenous agonist for the glycine co- agonist site (recently reported to be D-serine), and a postsynaptic neuron. The various glutamate re- ceptors and transporters are differentially ex- pressed by these three distinct cell populations. The glutamate uptake transporter EAAT3 (excitatory amino acid transporter 3), which is not shown on this figure, appears to be expressed primarily on the cell body and dendrites. Three families of ionotropic glutamate receptors (N-methyl-D-aspartate, AMPA, and kainate) are known, each of which is composed of distinct subunits and has identifiable binding sites. The metabotropic receptors cluster into three groups, members of which share pharmacologic and structural features. Chapter 52: Neurochemistry of Schizophrenia: Glutamatergic Abnormalities 719 tropic glutamate receptors, AMPA ( -amino-3-hydroxy-5- dynorphin, and zinc have also been identified. Additionally, methyl-4-isoxazole propionic acid), kainate, and NMDA magnesium ions blockthe ion channel of the NMDA recep- are each composed of four or five subunits that form ligand- tor complex at physiologic concentrations. The metabotropic glutamate receptors is voltage-dependent; partial depolarization of the cell mem- (mGluRs) are all seven transmembrane-domain, G protein- brane extrudes the magnesium ion. Finally, a site of four genes that have been named GluR1 through GluR4. In addition, the final subunit protein dependent (i. Thus, a potential exists for considerable petitive antagonists. The assembled AMPA receptors contain several bind- tion. NR1 homomers have been shown to form glycine ing sites: one for glutamate, another at which competitive binding sites, but an NR2 subunit appears to be required antagonists such as CNQX (6-cyano-7-nitro-quinoxalindi- to form both glutamate and MK-801 binding sites (29–32). Subunit composition appears to confer affinity for compounds that bind to the glutamate agonist site, whereas receptors with NR2A or NR2B subunits have unique pharmacologic properties to the final receptors higher affinities for MK-801 binding than do receptors with (15–19). For example, decreased calcium influx in AMPA NR2C or NR2D subunits (31). In addition, NMDA recep- receptors that contain the GluR2 subunit drastically dimin- tors containing particular NR1 splice variants have a higher ishes the electrophysiologic activity of these receptors. Receptors with NR2B sub- posed of subunits derived from genes for the low-affinity units are associated with a higher affinity for polyamine GluR5 through GluR7 and high-affinity KA1 through KA2 modulators (31,34). Therefore, differential subunit combi- subunits (13,14). The transcripts associated with these five nations confer unique binding properties to the NMDA subunits also undergo alternative splicing and editing. Final receptors and probably are associated with subtle electro- assembled kainate receptors may be composed of five identi- physiologic differences within a population of NMDA re- cal subunits, or they may be heteromers composed of low- ceptors. These mGluRs belong to a unique subset of G termed NR1 and NR2A through NR2D (13,14). An NR3 protein-coupled receptors with seven transmembrane do- gene has also been identified, although this subunit appears mains and large, extracellular amine termini. When ex- to be expressed primarily during early development pressed in heterologous systems, group I mGluRs have been (20–22). NR1 is expressed as one of eight isoforms because shown to stimulate phospholipase C, phosphoinositide hy- of alternative splicing of exons 5, 21, and 22 (13,14,23, drolysis, and the formation of cyclic adenosine monophos- 24). As in the case of the AMPA and kainate receptors, phate (cAMP) (41–44). In heterologous systems, groups II transcription of the NR1 subunit presents an important level and III mGluRs inhibit forskolin-stimulated cAMP forma- for the regulation of the expression of functional NMDA tion and adenylyl cyclase, possibly via a G protein (39,40, i receptors. This regulation can influence certain properties 45,46). The metabotropic receptors have been the target of of the final functional NMDA receptors, including the considerable recent interest because a functional relation- pharmacology of their binding sites. A primary agonist site exists for the binding of gluta- unique role in glutamatergic neurotransmission. A separate glycine co-agonist site must also be occu- receptors interact at multiple levels, as AMPA, kainate, and pied before glutamate can activate the ion channel; recent metabotropic receptors all affect NMDA-receptor activity.
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