PSYC 402: Biological Psychology Report a Broken Link

Psychology 402 examines the relationship between brain and behaviour. The task of biological psychology, often referred to as behavioral neuroscience, is to explain behaviour in terms of brain functioning. This course explores the biological basis of behaviour, learning, memory, language, and thinking, as well as disorders that arise from nervous system malfunctioning.

Essay Topic B- 1: Sleep and Dreams


Required Readings

As the homepage for Kalat's text, this site provides additional learning resources, relevant Internet links, chapter outlines, glossaries, and more.

Supplementary Readings

Sleep and Dreams
Great strides have been made in recent years in identifying the neural mechanisms that account for brain wave patterns that characterize the various stages and qualities of sleep and dreams. We have also identified the brain circuits that initiate sleep and that account for the transition from one stage of sleep to the next. Using the pre-selected articles as a base, your essay should construct an account of the neural mechanisms involved in sleep. Begin your essay by identifying the basic phenomena associated with sleep so that you can then connect the neural accounts with the aspects of sleep you have described.
Bjorvatn, B., & Ursin, R. (1998). Changes in sleep and wakefulness following 5-HT1A ligands given systematically and locally in different brain regions. Reviews in the Neurosciences, 9(4), 265-273.
Reviews how the administration of 5-HT1A agonists to various areas of the brain influence sleep and wakefulness.

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Kayama, Y., & Koyama, Y. (1998). Brainstem neural mechanisms of sleep and wakefulness. European Urology, 33(Suppl. 3), 12-15.
Discusses how three diffuse projection systems originating in the brainstem may control sleep and wakefulness. The areas of the brainstem from which the diffuse projection systems arise are the locus coeruleus, the dorsal raphe nucleus, and the laterodorsal and pedunculopontine tegmental nuclei.

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Describes the neural mechanisms involved in the regulation of REM sleep, and discusses how the administration of 8-OHDPAT, a selective 5-HT1A receptor agonist, influences sleep.
Nitz, D., & Siegel, J. (1997). GABA release in the dorsal raphe nucleus: Role in the control of REM sleep. American Journal of Physiology – Regulatory, Integrative, and Comparative Physiology, 273(1, Pt. 2), R451-R455.
Evidence implicates GABA release in the production of REM sleep and in the cessation of serotonergic dorsal raphe neuronal firing. The serotonergic dorsal raphe neurons play an important role in the control of the sleep/wake cycle.

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Nitz, D., & Siegel, J. M. (1997). GABA release in the locus coeruleus as a function of sleep/wake state. Neuroscience, 78(3), 795-801.
Data suggests that GABAergic inhibition causes the locus coeruleus neurons to stop discharging during REM sleep and that GABAergic neurons located in the locus coeruleus may be selectively active during REM sleep.

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Nitz, D., & Siegel, J. M. (1996). GABA release in posterior hypothalamus across sleep-wake cycle. American Journal of Physiology – Regulatory, Integrative, and Comparative Physiology, 271(6, Pt. 2), R1707- R1712.
Research indicates that GABA release in the posterior hypothalamus can facilitate slow wave sleep by mediating the inhibition of the posterior hypothalamic neurons. The inactivation of the posterior hypothalamic neurons have previously been implicated with the induction of sleep.

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Discusses the role of serotonin in the sleep/wake cycle and the use of microdialysis to monitor serotonin levels in the brain during various stages of the cycle.

Essay Topic B- 2: Stress and Its Effect on the Brain and Body


Supplementary Readings
Excessive human stress is widely regarded as a major social problem, and as a contributing factor to, or a cause of, numerous physical and mental diseases. Stress is thought to cost businesses and governments billions of dollars annually in decreased productivity, absenteeism, staff turnover, alcohol abuse, and poor labour-management relationships. Unfortunately, although stress is a popular topic (and a real social concern) it is frequently misunderstood by the general public and by some professionals. Stress fits squarely in the domain of biological psychology, and Kalat addresses this topic in Chapter 12 of the textbook. Writing a term paper on stress may add worthwhile information to your knowledge of biological psychology.

This topic requires you to address the question of what stress is, and how the brain and body respond during stress. In particular, you will need to identify why the human stress response produces serious health problems, as well as how the main stress hormone, cortisol, poses its own threat to the well-being of the brain.
Lupien, S. J., Nair, N. P., Briere, S., Maheu, F., Tu, M. T., Lemay, M., McEwen, B. S., & Meaney, M. J. (1999). Increased cortisol levels and impaired cognition in human aging: Implication for depression and dementia later in life. Reviews in the Neurosciences, 10(2), 117-139.
Summarizes research from human and animal studies that have found that exposure to high levels of glucocorticoids may damage the hippocampus, a brain structure implicated with learning and memory. Article also discusses how increased glucocorticoid secretion may be related to dementia and depression in the elderly, and suggests some of the factors that may be responsible for increased glucocorticoid secretion.

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McIntosh, L. J., & Sapolsky, R. M. (1996). Glucocorticoids may enhance oxygen radical-mediated neurotoxicity. Neurotoxicology, 17(3-4), 873-882.
Study examines how glucocorticoids may disrupt cellular oxidative homeostasis and exacerbate the toxicity of reactive oxygen species (ROS) generating compounds in the brain.

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Discusses whether glucocorticoid secretion permits, stimulates, and/or suppresses a stress response by analysing the role of glucocorticoids in cardiovascular function, fluid volume and hemorrhage, immunity and inflammation, metabolism, neurobiology, and reproductive physiology.

Essay Topic B- 3: The Biological Basis of Schizophrenia


Supplementary Readings
In addition to being one of the most perplexing disorders we know about, schizophrenia is a devastating affliction that disrupts our highest cognitive abilities. A variety of research supports the conclusion that schizophrenia is a developmental disorder that disrupts brain development. The brain condition it produces has been compared to a switchboard with faulty connections. This topic requires you to cover the various theories concerning the biological basis of schizophrenia. For each theory addressed, provide evidence for the claims made and describe how the research was conducted.
Discusses the implications of indoleamines and phenethylamines, which are psychedelic hallucinogens mediated by 5-HT(2A) receptors that alter glutamatergic transmission, for the pathophysiology and treatment of schizophrenia.
Bennett, M. R. (1998). Monoaminergic synapses and schizophrenia: 45 years of neuroleptics. Journal of Psychopharmacology, 12(3), 289-304.
Reviews historical developments in the search for the etiology of schizophrenia. Addresses the role of neuroleptics and dopamine (DA) receptors, especially the D4 DA receptors, in this search.

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Hietala, J., & Syvalahti, E. (1996). Dopamine in schizophrenia. Annals of Medicine, 28(6), 557-561.
Dopamine is a neurotransmitter that has been implicated as a biological causal factor of schizophrenia. Article proposes that research that monitors and relates changes in dopaminergic pathways to the psychopathology characteristic of schizophrenia should be conducted.

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Hirsch, S. R., Das, I., Gary, L. J., & de Belleroche, J. (1997). A pivotal role for glutamate in the pathogenesis of schizophrenia, and its cognitive dysfunction. Pharmacology Biochemistry and Behavior, 56(4), 797-802.
Discusses the evidence which suggests that glutamate dysfunction and deficiency may play a role in the development of schizophrenia.

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Presents a critical literature review which highlights evidence that supports a neurodevelopmental component to schizophrenia. Reviews data from clinical studies by focusing on the following life phases: conception and birth, infancy, childhood prior to the onset of the illness, life after the illness, and postmortem.

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Examines the strength, weaknesses, and therapeutic implications of the NMDA receptor hypofunction hypothesis of schizophrenia. This hypothesis is based on the neurotoxic and psychotomimetic effects of PCP and related NMDA antagonist drugs.
Tamminga, C. A. (1998). Schizophrenia and glutamatergic transmission. Critical Reviews in Clinical Neurobiology, 12(1-2), 21-36.
Reviews evidence from studies that used diverse methods, such as postmortem neurochemistry, in vivo human brain imaging, clinical pharmacology, and animal models to discover that diminished glutamatergic transmission may play a role in schizophrenia. Tamminga also proposes a "working" glutamatergic hypothesis of schizophrenia that addresses the effects of diminished glutamatergic transmission on the hippocampus.

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Examines evidence from family, twin, and adoption studies which indicates a genetic component to schizophrenia. Also discusses the use of molecular genetic technologies, and neurophysiological and neuroimaging methodologies to discover genetic information about schizophrenia.
Tsuang, M. T., & Faraone, S. V. (1995). The case for heterogeneity in the etiology of schizophrenia. Schizophrenia Research, 17(2), 161-175.
Is there a single, necessary, and sufficient cause of schizophrenia? Article discusses the heterogeneity/homogeneity etiological debate surrounding schizophrenia by examining three possible causes of schizophrenia: genes, obstetric complications, and viral infections.

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Reviews research which used family, twin, and adoption paradigms to study the familial transmission of schizophrenia. Article also discusses how genetic linkage studies have allowed researchers to begin to identify chromosomal sites that may contain genes responsible for schizophrenia. In addition, the clinical and ethical implications of genetic research are addressed.

Essay Topic B- 4: How the Brain Mediates and Controls the Sensation of Pain


Supplementary Readings
Few topics are so directly relevant to our everyday experience as pain. One of the fascinating aspects of pain research is that it deals with a topic that is as subjective as it is objective. Everyone experiences pain, but to different degrees and for different reasons. Nevertheless, ample evidence indicates that the brain systems that mediate pain are remarkably similar across species. This topic requires you to identify the various mechanisms in the sensory pathway for pain, and then show how central mechanisms mediate the pain gate that controls activity in the pathway. You will also need to address the question of how cognitive centres in the brain can influence the intensity of pain.
Apfel, S. C. (2000). Neurotrophic factors and pain. Clinical Journal of Pain, 16(Suppl.2), S7-S11.
Discusses how various neurotrophic factors, such as nerve growth factor, brain-derived neurotrophic factor, and glial-cell derived neurotrophic factor may be involved in physiologic and pathologic pain pathways. The implications of these factors for the treatment of pain are also addressed.

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Baron, R. (2000). Peripheral neuropathic pain: From mechanisms to symptoms. Clinical Journal of Pain, 16(Suppl. 2), S12-S20.
Describes a number of independent pathophysiological mechanisms found in the peripheral and central nervous systems that lead to sensory symptoms, spontaneous pain, and evoked pain.

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Pawl, R. P. (1999). A review of functional imaging of the brain and pain. Current Review of Pain, 3(4), 249-255.
Reviews the use of functional imaging techniques, such as positron emission tomography and functional magnetic imaging, to analyse the experience of pain. Article discusses the areas of the brain that appear to be activated during the pain experience, and compares findings from various studies.

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Highlights the various spinal pathways and areas of the brain that contribute to the affective component of pain. The interaction between pain sensation intensity, pain unpleasantness, and secondary affect is also addressed.
Sorkin, L. S., & Wallace, M. S. (1999). Acute pain mechanisms. Surgical Clinics of North America, 79(2), 213-229.
Describes the neurological and pharmacological mechanisms that interact to either produce or reduce a pain response that occurs after tissue injury.

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Reviews six experimental studies that assessed the validity of placebo analgesia and the mechanism by which it occurs. Studies indicate that endogenous opiates may mediate placebo analgesia.

Urban, M. O., & Gebhart, G. F. (1999). Central mechanisms in pain. Medical Clinics of North America, 83(3), 585-596.
Discusses the various mechanisms that modulate nociceptive input into the central nervous system. Also addresses the effects of modulation on the development and maintenance of chronic pain and hyperalgesia.

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Weinbroum, A. A., Rudick, V., Paret, G., & Ben-Abraham, R. (2000). The role of dextromethorphan in pain control. Canadian Journal of Anesthesia, 47(6), 585-596.
Summarizes the neuropharmacological properties of dextromethorphan (DM), and reviews its use in pain management.

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Yaksh, T. L. (1999). Regulation of spinal nociceptive processing: Where we went when we wandered onto the path marked by the gate. Pain, Suppl. 6, S149-S152.
Discusses how the Gate Control Hypothesis inspired a number of contributions to the field of pain control. The Gate Control Hypothesis led to a greater understanding of how transmitter systems function to produce gating systems, and fostered the development of better therapeutic techniques to control pain resulting from tissue and nerve injury.

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Essay Topic B- 5: The Biological Basis of Memory


Supplementary Readings
How the human brain stores our experiences is an attractive research topic in the neurosciences today. Solid support exists for the claim that memories we are aware of, called “explicit memories,” are mediated by a brain system that involves the temporal lobe and the prefrontal cortex. In contrast, memories we remain unconscious of, are probably mediated by the cerebellum and basal ganglia.

For this topic, you might choose to examine the brain basis of a single type of memory, or you might prefer to survey the overall memory systems in the brain. Alternatively, you could focus on long-term potentiation, a prime candidate for the mechanism by which memories are stored in the brain in the first place. Review Chapter 13 of the textbook before deciding on this topic.

The hippocampus is thought to play a key role in learning and memory, and this article attempts to characterize that role by reviewing comparative studies involving birds that scatter-hoard their food in caches. Evidence suggests that learning and memory are facilitated by increased synaptic number and efficacy, and that avian hippocampal size is influenced by the number of food-storing experiences a bird has.

Long-term potentiation (LTP) has long been thought to play a role in learning and memory. Article discusses study results that provide empirical support for this theory with its discovery that the disruption of LTP in the amygdala can prevent animals from learning fear conditioning.

The majority of evidence that currently exists to support the role of long-term potentiation (LTP) in learning and memory is derived from studies that disrupt the occurrence of LTP during learning. This article reviews research that has saturated hippocampal LTP prior to training, rather than disrupting LTP during training.

Describes the genetic, behavioral, and electrophysiological approaches that researchers use to determine the mechanisms of memory. A discussion about the implications of cAMP-mediated gene expression for the establishment of long-term memory is also included.

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Reviews the role of the hippocampus in spatial learning and contextual conditioning; discusses the molecular and cellular substrates of place learning in mice; and summarizes the role of long-term potentiation, short-term plasticity, and changes in spiking in hippocampal-dependent place learning. Article focuses mostly on genetic studies of learning and memory.

Outlines the different areas of the brain that are associated with the formation of explicit and implicit memory, and discusses how the different regions of the brain facilitate learning. Article also reviews the role of the cerebellum in trace conditioning.

Essay Topic B- 6: The Biological Basis of Addiction


Supplementary Readings
Drug addiction is a serious and enduring problem of economic, social, medical, and psychological consequences. Addictive drugs seem to bypass motivational states and directly stimulate the extensive pleasure systems in the brain, primarily through activation of the nucleus accumbens and the extended amygdala.

For this topic, you might present a broad overview of addiction mechanisms in the brain, including an examination of how drugs act at synapses. Alternatively, you could examine a single addictive drug (e.g., alcohol, cocaine, amphetamine, heroin) and describe how the addictive process emerges.
Presents an overview of existing evidence which indicates that dopamine (DA) may be involved in a common biochemical mechanism underlying drug addiction.
Ciccocioppo, R. (1999). The role of serotonin in craving: From basic research to human studies. Alcohol and Alcoholism, 34(2), 244-253.
Discusses the evidence which suggests that serotonin (5-HT) may be involved in the mechanisms of craving and relapse. Serotonergic systems are thought to regulate impulse-control mechanisms, and Ciccocioppo proposes that a 5-HT deficiency may cause a person to lose control over his or her drug-taking behaviour.

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Everitt, B. J., Parkinson, J. A., Olmstead, M. C., Arroyo, M., Robledo, P., & Robbins, T. W. Everitt, B. J., Parkinson, J. A., Olmstead, M. C., Arroyo, M., Robledo, P., & Robbins, T. W. (1999). Associative processes in addiction and reward. The role of amygdala-ventral striatal subsystems. Annals of the New York Academy of Sciences, 29(877), 412-38.
Describes a study where the processes of primary reinforcement, psychomotor activation, pavlovian conditioning, and the role of drug cues in drug-seeking behaviours of rats interact to allow researchers to study complex motivated behaviours. Article also maps these processes onto the different areas of the brain they activate, such as the amygdaloid and other limbic cortical-ventral striatal subsystems.

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Gamberino, W. C., & Gold, M. S. (1999). Neurobiology of tobacco smoking and other addictive disorders. Psychiatric Clinics of North America, 22(2), 301-312.
Reviews how the neurobiology of tobacco smoking may reinforce tobacco use. Also discusses the evidence which suggests that dopaminegic projections and glutamate and serotonin neurotransmitters may be common neurobiologic substrates involved in all addictions.

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Leshner, A. I., & Koob, G. F. (1999). Drugs of abuse and the brain. Proceedings of the Association of American Physicians, 111(2), 99-108.
Describes the areas of the brain that are affected by the following types of drugs: cocaine, amphetamine, opiates, sedative hypnotics, nicotine, and tetrahydrocannabinol. Discusses the biochemical changes that occur in the brain after repeated and prolonged drug abuse.

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Suggests that laboratory research involving the assessment of cue-reactivity can integrate the knowledge that currently exists about the biomedical and psychosocial mechanisms that contribute to alcohol craving and relapse.
Uses the incentive-sensitization theory of addiction to evaluate current biopsychological views of addiction. Article argues that negative reinforcement, positive reinforcement, and hedonic theories of addiction do not adequately explain compulsive drug-seeking and drug-taking behaviours.
Volkow, N. D., Fowler, J. S., & Wang, G. J. (1999). Imaging studies on the role of dopamine in cocaine reinforcement and addiction in humans. Journal of Psychopharmacology, 13(4), 337-345.
Uses positron emission tomography to determine the role of dopamine (DA) in cocaine reinforcement and addiction. Study demonstrates that the rate and level of dopamine transporter (DAT) blockade can influence the intensity and perception of a high, and that DA disruption can lead to the compulsive administration of cocaine.

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Wise, R. A. (1996). Neurobiology of addiction. Current Opinion in Neurobiology, 6(2), 243-251.
Discusses how drugs such as heroin, cocaine, nicotine, alcohol, phencyclidine, and cannabis activate common reward circuits in the brain and may operate on common habit-forming mechanisms.

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Wise, R. A. (1996). Addictive drugs and brain stimulation reward. Annual Review of Neuroscience, 19, 319-340.
Suggests that drugs of abuse may activate brain stimulation reward mechanisms and may be rewarding because they act on brain circuits that are common to natural and biological rewards.

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Essay Topic B- 7: The Biological Basis of Affective Disorders


Supplementary Readings
Known as the “common cold of psychiatric disorders,” depression, and the less common condition of mania, are major challenges for neuroscientists today. The problem is compounded by the multiple etiologies involved in depression and the fact that many cases of depression may involve little or no underlying brain disorder. Nevertheless, biologically based types of depression are prominent, and current research is beginning to unravel the nature of the brain and the chemistry dysfunction associated with it.

For this topic, you could present an overview of the many biological factors hypothesized to cause affective disorders. Alternatively, you might choose to examine a single factor in greater depth. You might wish to review the reading package before making your decision.
Anand, A., & Charney, D. S. (2000). Norepinephrine dysfunction in depression. Journal of Clinical Psychiatry, 61(Suppl. 10), 16-24.
Reviews current knowledge about the role of norepinephrine and the noradrenergic system in depression. Also discusses the use of selective norepinephrine reuptake inhibitors (selective NRIs) to treat depression.

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Delgado, P. L., & Moreno, F. A. (2000). Role of norepinephrine in depression. Journal of Clinical Psychiatry, 61(Suppl. 1), 5-12.
Although the exact roles of norepinephrine (NE) and serotonin (5-HT) in depression are unknown, neurotransmitter depletion studies have demonstrated that both noradrenergic and serotonergic systems are involved in antidepressant action, but are not necessarily causal factors of depression. Article discusses some of the evidence about the role of NE and 5-HT in depression, and suggests areas for future research into the neurobiology of depression.

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Desai, H. D., & Jann, M. W. (2000). Major depression in women: A review of the literature. Journal of the American Pharmaceutical Association, 40(4), 525-537.
Reviews gender differences in the prevalence of depression, and its etiology, risk factors, clinical features, course, and management. Also discusses the biological and psychosocial factors that contribute to the higher prevalence rates of major depression in women.

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Frazer, A. (2000). Norepinephrine involvement in antidepressant action. Journal of Clinical Psychiatry, 61(Suppl. 10), 25-30.
Summarizes the acute pharmacologic effects of currently prescribed antidepressants to treat depression, including reboxetine, a new selective norepinephrine reuptake inhibitor. Article also discusses how the long-term effects of selective norepinephrine reuptake inhibitors can be predicted from their short-term effects, and proposes that the effects of drugs on central noradrenergic transmission may alleviate some symptoms of depression.

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Article describes how bipolar disorder clinically presents itself, discusses other psychological disorders that are frequently comorbid with bipolar disorder, and reviews the drugs that can act as effective mood stabilizers for the disorder. Article also outlines a comprehensive management plan that can be used to treat patients with bipolar disorder.

Jamison, K. R. (2000). Suicide and bipolar disorder. Journal of Clinical Psychiatry, 61(Suppl. 9), 47-51.
Suicide can be an unfortunate manifestation of severe psychiatric distress. This article discusses suicide in the context of bipolar disorder.

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Kaye, J., Morton, J., Bowcutt, M., & Maupin, D. (2000). Stress, depression, and psychoneuroimmunology. Journal of Neuroscience Nursing, 32(2), 93-100.
Reviews psychoneuroimmunology studies to outline what is known about the relationships between stress, depression, and the neurological, endocrine, and immunological systems.

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Leonard, B. E. (2000). Evidence for a biochemical lesion in depression. Journal of Clinical Psychiatry, 61(Suppl. 6), 12-17.
Discusses the evidence which indicates that lesions in the serotonergic, noradrenergic, and/or monoaminergic systems may be responsible for depression.

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Considers the roles that N-methyl-D-aspartate (NMDA) receptor-mediated synaptic plasticity and the NMDA receptor play in the development and treatment of depression.
Trimble, M. R., & Krishnamoorthy, E. S. (2000). The role of toxins in disorders of mood and affect. Neurologic Clinics, 18(3), 649-664.
Examines the neurobiology of mood, as well as the interaction between mood and cognitive function. Also describes how environmental toxins can cause mood disorders.

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Summarizes the neurochemical pathway abnormalities that occur during the onset of depressive disorders in rats, and discusses the implications of these abnormalities for the onset of action and the efficacy of pharmacological treatments.