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.

Cocaine afflicts many individuals and is potently addictive. Originally hailed as a wonder-drug in the late 19th century, cocaine is now considered an illegal substance. Cocaine’s addictive properties can be attributed to changes in the dopamine reward pathway of the Ventral Tegmental Area and Substantia Nigra, Prefrontal Cortex, Dorsal Striatum, Nucleus Accumbens, Amygdala, Globus Pallidus, and Hippocampus. This drug affects the brain in two processes: binge and crave. The binge process highlights cocaine’s ability to block dopamine reuptake from the synapse resulting in hyperstimulation of the postsynaptic neuron in the dopamine reward pathway. The crave process promotes drug-seeking behavior through conditional and contextual cues. Understanding the effects of cocaine in the brain may grant insight in creating future medication and therapies to treat individuals addicted to this drug.

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:

"New research reveals a previously unrecognized circuit for regulating blood glucose levels. This circuit supports a recently proposed mechanism for why patients undergoing gastric bypass surgery show reduced symptoms of diabetes, well before weight loss. Our bodies turn the carbohydrates, fats and proteins found in food into useful sugars, fatty acids and amino acids. After a meal, the pancreas works to keep our blood sugar level, or glycemia, high enough to keep our brain fed, yet low enough not to damage delicate tissues. It does that by secreting the regulatory hormone insulin. Insulin stimulates the storage of glucose as starch in the liver and muscle. While some amino acids can enhance insulin production, one of them actually does the opposite. Researchers demonstrated that nutritional tyrosine is converted to the neurotransmitter dopamine in the gut and stomach after eating..."

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

This is a learning module on the effects of social media on mental health, intended for secondary education students. This module has been created for students who have grown up in the digital age by a college student who has grown up in a similar technological environment. Students will come out of this module knowing more about the present state of mental health, how social media exacerbates mental health concerns, and the small, realistic changes they can make to improve their social media habits. 

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:

"Autism spectrum disorder is a developmental disorder for which effective pharmacological treatments are currently limited. One promising candidate for treatment, however, is the gene EphB6. which, among other things, helps regulate the gut microbiome. To explore EphB6’s link to both the gut microbiome and autism, researchers deleted the gene from the genome of mice. That deletion induced autism-like behavior relative to mice retaining the EphB6 gene, including spending more time on self-grooming and showing a lower preference for mouse “strangers.” Deleting EphB6 also altered the composition of the mice’s gut microbiome, decreasing the abundance of certain bacteria. Interestingly, transplanting the fecal microbiota of EphB6-deficient mice into certain wild-type mice induced autism-like behavior. Meanwhile, transplanting the fecal microbiota from wild-type mice to EphB6-deficient mice seemed to reduce autism-like behavior. Further experiments linked EphB6 deletion to vitamin B6 and dopamine defects..."

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