This course considers the process of neurotransmission, especially chemicals used in the brain and elsewhere to carry signals from nerve terminals to the structures they innervate. We focus on monoamine transmitters (acetylcholine; serotonin; dopamine and norepinephrine); we also examine amino acid and peptide transmitters and neuromodulators like adenosine. Macromolecules that mediate neurotransmitter synthesis, release, inactivation and receptor-mediated actions are discussed, as well as factors that regulate their activity and the second-messenger systems and ion fluxes that they control. The involvement of particular neurotransmitters in human diseases is considered.

Biology is designed for multi-semester biology courses for science majors. It is grounded on an evolutionary basis and includes exciting features that highlight careers in the biological sciences and everyday applications of the concepts at hand. To meet the needs of today’s instructors and students, some content has been strategically condensed while maintaining the overall scope and coverage of traditional texts for this course. Instructors can customize the book, adapting it to the approach that works best in their classroom. Biology also includes an innovative art program that incorporates critical thinking and clicker questions to help students understand—and apply—key concepts.

By the end of this section, you will be able to:Describe the symptoms, potential causes, and treatment of several examples of nervous system disorders

This course explores the cognitive and neural processes that support attention, vision, language, motor control, navigation, and memory. It introduces basic neuroanatomy, functional imaging techniques, and behavioral measures of cognition, and discusses methods by which inferences about the brain bases of cognition are made. We consider evidence from patients with neurological diseases (Alzheimer's disease, Parkinson's disease, Huntington's disease, Balint's syndrome, amnesia, and focal lesions from stroke) and from normal human participants.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Researchers from the United Kingdom recently discovered several genes that protect neurons in Parkinson’s disease, creating possibilities for new treatment options. Two of the genes affect how mitochondria break down amino acids to generate nucleotides -- the metabolism of these molecules produces the energy that cells need to live. Dysfunctional mitochondrial metabolism has been linked to Parkinson’s, and these researchers previously showed that boosting this generation of nucleotides can protect neurons. Based on these findings, they set out to identify the genes that control this process. Some forms of Parkinson’s are caused by mutations in the genes _PINK1_ and _PARKIN_, which are instrumental in mitochondrial quality control. Fruit flies with mutations in these genes accumulate defective mitochondria and exhibit Parkinson’s-like changes, including loss of neurons. The researchers used _PINK1_ and _PARKIN_ mutant flies to search for other critical Parkinson’s genes..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Parkinson's disease is a neurodegenerative disease that affects more than 10 million people across the globe. Despite improvements in treating the disease, doctors still have many unanswered questions, including when to start treatment. Now, researchers at the University of Rochester have taken another look at a past clinical trial to begin to answer that key question. Parkinson's occurs when neurons in a part of the brain called the substantia nigra die off. These neurons produce the neurotransmitter dopamine, and with the loss of those neurons, patients develop tremors, have difficulty moving, and show slow movement, among other symptoms. Restoring the dopamine with L-dopa or boosting levels with a dopamine agonist can help. Some studies have suggested that early dopaminergic treatment could protect neurons and slow disease progression. But that evidence isn't yet convincing, and the drugs might also cause uncontrolled, involuntary movements, leaving this an open question in the field..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"FAF1 is a protein involved in various biochemical processes including cell death, inflammation, and cell proliferation and is implicated in certain diseases, including cancer and Parkinson’s disease. To date, FAF1 has been assumed to be locked within the cytosol—with no secretion mechanism reported for the protein. Now, researchers have discovered two mechanisms by which FAF1 can be secreted and transmitted between cells. Experiments on human neuroblastoma cells showed that FAF1 was secreted as cargo within exosomes, as well as in a free, non-exosomal form. Experiments also showed that FAF1 promoted the formation of exosomes, suggesting a regulatory role for the protein in exosome biogenesis. Additionally, extracellular FAF1 was transmitted to neighboring neuronal cells via endocytosis, triggering cell death through apoptotic and necrotic pathways. As the first to reveal these FAF1 secretion pathways this study could lead to ways of interfering with cell death by inhibiting FAF1 secretion..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Parkinson’s Disease (PD) is one of the most common neurodegenerative diseases. While most of the attention focuses on motor symptoms. PD can also cause gastrointestinal symptoms such as constipation, nausea, and vomiting. Growing evidence suggests that the gut microbiota influences PD pathogenesis via the microbiota-gut-brain axis and that using fecal microbiota transplantation (FMT) to normalize the gut bacterial community has beneficial effects on PD. To explore the underlying mechanisms, researchers established a chronic rotenone-induced PD mouse model. Rotenone treatment led to gut microbiome changes, gastrointestinal impairment, and poor motor performance, which was then alleviated by FMT. FMT also reduced intestinal inflammation and barrier destruction. Subsequently, FMT attenuated blood-brain barrier impairment and neuroinflammation in the substantia nigra (SN), thus decreasing the damage to dopaminergic neurons..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Parkinson’s disease (PD) is the second-most common neurodegenerative disorder worldwide, and a cure remains elusive. Although its hallmarks are motor symptoms resulting from neuronal loss, increasing attention has been paid to the effect of gut microbiota on PD. A recent study examined this connection by focusing on the effect of a unique protein. Osteocalcin (OCN), a protein secreted by osteoblasts during bone formation, can pass through the blood-brain barrier. OCN can modulate brain function, and patients with PD are highly susceptible to osteoporosis, suggesting a link between bone health and PD. Using a mouse model of PD, researchers found that injecting OCN had a protective effect, ameliorating motor deficits and neuronal loss. Antibiotic exposure prior to OCN treatment revealed that this effect was dependent on gut microbiota..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Although the brain has always been viewed as a sterile organ, recent studies have suggested the existence of a ‘brain microbiome,’ perturbations of which could cause neuroinflammatory conditions. Unfortunately, experiments aimed at detecting a brain microbiome are limited by a low bacterial biomass. Bacteria must be detected through an overwhelming amount of host DNA, and the low biomass additionally raises the risk of amplifying exogenous contaminants. A recent study tested the hypothesis that there is a bacterial brain microbiome. Using 16S rRNA sequencing, researchers evaluated brain samples from healthy individuals and individuals suffering from Parkinson’s disease (PD), along with murine brains. They found that while amplicon sequencing detected bacterial signals in both human and murine brains, the estimated bacterial biomass was extremely low. Careful reanalysis suggested that bacterial signals were explained by exogenous DNA contamination and false-positive amplification of host DNA..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Lectures and discussions in this course cover the clinical, behavioral, and molecular aspects of the brain aging processes in humans. Topics include the loss of memory and other cognitive abilities in normal aging, as well as neurodegenerative conditions such as Parkinson's and Alzheimer's diseases. Discussions based on readings taken from primary literature explore the current research in this field.

Gene insertion of opsin, light-activated cell-membrane channels, into neurons of interest allows researchers to manipulate light to either excite or inhibit neuronal activity to gain a better understanding of brain function and dysfunction, and explore therapeutic applications.

This course covers amino acid sequence control of protein folding, misfolding, amyloid polymerization and aggregation. Readings and discussions address topics such as chaperone structure and function, folding and assembly of fibrous proteins, and pathologies associated with protein misfolding and aggregation in Alzheimer's, Parkinson's, Huntington's and other protein deposition diseases. Students are required to write and present a research paper.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The human protein Tid-1 sits at the nexus of many key cellular processes and signaling pathways. These processes include cellular proliferation, growth, survival, aging, apoptosis, and even movement. Tid-1 is a member of the heat shock protein 40 family and helps other proteins fold correctly after translation or refold after a damaging stress event. Dysregulated Tid-1 behavior is involved in numerous human diseases including cancers, cardiomyopathies, and neurodegenerative disorders. Given its wide influence within the cell, Tid-1 could be a key biomarker or even therapeutic target for these diseases, but to leverage Tid-1 effectively, researchers need to understand its functionality in detail. To this end, a team of scientists consolidated the current research on human Tid-1. They found that Tid-1’s protein-protein interactions corresponded to its roles in various diseases and provide insight into how Tid-1 affects pathogenic developments..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Spinal cord stimulation offers long-term relief to patients managing chronic pain, without the need for opioids. This winning combination has spurred incredible growth in the industry, with approximately 50,000 spinal cord stimulators being implanted each year and an estimated market of 7 billion U.S. dollars by 2020. But despite this progress, exactly how the technology works remains unclear. Especially with regard to potential changes in brain activity. A new review article in the journal Anesthesiology takes a closer look at these potential supraspinal pathways and actions. Covering both preclinical and clinical articles, the review starts with the 1960s, when an idea known as Gate Control Theory was proposed to explain how conventional tonic stimulation works. The theory suggests that a combination of presynaptic inhibition and inhibitory interneuronal communication occurs in the spinal cord following the electrical activation of large-diameter afferent fibers..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.