Official Ninja Nerd Website: https://ninjanerd.org Ninja Nerds! During this lecture Professor Zach Murphy will be showing you the structures that make up the male reproductive system as we use a SOMSO anatomical model. We hope you enjoy this lecture and be sure to support us below! Join this channel to get access to perks: https://www.youtube.com/channel/UC6QYFutt9cluQ3uSM963_KQ/join APPAREL | We are switching merchandise suppliers. DONATE PATREON | https://www.patreon.com/NinjaNerdScience PAYPAL | https://www.paypal.com/paypalme/ninjanerdscience SOCIAL MEDIA FACEBOOK | https://www.facebook.com/NinjaNerdlectures INSTAGRAM | https://www.instagram.com/ninjanerdlectures TWITTER | https://twitter.com/ninjanerdsci @NinjaNerdSci DISCORD | https://discord.gg/3srTG4dngW #ninjanerd #MaleAnatomy #MaleReproductiveSystem

Official Ninja Nerd Website: https://ninjanerd.org Ninja Nerds! During this lecture Professor Zach Murphy will be showing you the structures that make up the female reproductive system anatomy, through the use of a SOMSO model. We also correlate the anatomy with its corresponding function. We hope you enjoy this lecture and be sure to support us below! Join this channel to get access to perks: https://www.youtube.com/channel/UC6QYFutt9cluQ3uSM963_KQ/join APPAREL | We are switching merchandise suppliers. DONATE PATREON | https://www.patreon.com/NinjaNerdScience PAYPAL | https://www.paypal.com/paypalme/ninjanerdscience SOCIAL MEDIA FACEBOOK | https://www.facebook.com/NinjaNerdlectures INSTAGRAM | https://www.instagram.com/ninjanerdlectures TWITTER | https://twitter.com/ninjanerdsci @NinjaNerdSci DISCORD | https://discord.gg/3srTG4dngW #ninjanerd #FemaleAnatomy #FemaleReproductiveSystem

A concussion is a type of mild traumatic brain injury that occurs when rapid movement of the head or an impact to the head causes the brain to move within the skull, potentially stretching axons and damaging cell membranes of neurons. In this video, I discuss the biochemical and structural changes in the brain that are associated with the symptoms of a concussion. TRANSCRIPT: Welcome to 2-minute neuroscience, where I explain neuroscience topics in 2 minutes or less. In this installment I will discuss concussions. A concussion is a type of mild traumatic brain injury that occurs when rapid movement of the head or an impact to the head causes the brain to move within the skull, potentially stretching axons and damaging cell membranes of neurons. When neuronal membranes are disrupted, it can cause the dysregulated flow of ions into and out of the cell, as well as the increased release of excitatory neurotransmitters like glutamate, which leads to further disruptions in ionic balance and a general inhibition of neuronal activity. Sodium-Potassium pumps work frantically to restore balance, but this causes depletion of energy stores and an energy crisis that’s compounded by lower than normal levels of blood flow. Additionally, the increased glutamate activity prompts excess calcium to enter cells; the high calcium levels can disrupt the function of mitochondria, amplifying the energy crisis. The decreased energy availability may last for days to a week or more and impact cognition. The trauma and subsequent effects can also damage the structural integrity of neurons and glia, further disrupting brain function. These structural and biochemical changes are associated with the symptoms of a concussion, which include (but aren’t limited to) headaches, confusion, memory loss, and dizziness. After a concussion, patients may also experience an increased susceptibility to another injury, and repeated concussions have been linked to longer-lasting effects on brain function. In some cases, patients who have experienced repeated concussions may begin, often years after the repetitive trauma, to display symptoms of early-onset dementia, mood disturbances, and Parkinsonian symptoms. The resultant condition, known as chronic traumatic encephalopathy, has also been linked to the appearance of neurofibrillary tangles and amyloid plaques, which are typically seen in neurodegenerative diseases like alzheimer’s disease. References: Barkhoudarian G, Hovda DA, Giza CC. The molecular pathophysiology of concussive brain injury. Clin Sports Med. 2011; 30(1):33-48. Giza CC, Hovda DA. The new neurometabolic cascade of concussion. Neurosurgery. 2014; 75 Suppl 4:S24-33.

Caffeine is the most widely-used mind-altering substance in the world. Although it's not completely clear how caffeine causes the stimulant effects it's well-known for, it's thought most of those effects are traceable back to its action as an antagonist at receptors for the neurotransmitter adenosine. In this video, I discuss how that antagonistic action may lead to arousal and wakefulness. TRANSCRIPT: Welcome to 2 minute neuroscience, where I simplistically explain neuroscience topics in 2 minutes or less. In this installment I will discuss caffeine. Caffeine is a stimulant drug and the most widely-consumed mind-altering substance in the world. It belongs to a class of compounds known as the methylxanthines, and is commonly found in a number of natural sources including the seeds of coffee plants and the leaves of tea plants. Most of the effects of caffeine are thought to be traceable back to its action as an antagonist at receptors for a neurotransmitter called adenosine. This means that caffeine binds to adenosine receptors and blocks adenosine from binding there and activating the receptor; thus, it reduces activity at the adenosine receptor. Although there are 4 subtypes of the adenosine receptor, most of caffeine’s effects are thought to be due to its antagonistic actions at the A1 and A2A subtypes. Its ability to promote wakefulness may be especially due to actions at the a2a receptor subtype. How exactly the antagonism of the adenosine receptor translates into the effects of caffeine is not completely clear. Research suggests, however, that adenosine receptors are involved in promoting and regulating sleep. One way this is thought to occur is that adenosine activity can prompt the release of the neurotransmitter GABA, which then inhibits neurons involved in arousal and wakefulness. This promotes sleep, but when caffeine antagonizes adenosine receptors it opposes this action and causes arousal. Adenosine receptors are also thought to be involved in reducing the activity of a number of neurotransmitters, including dopamine and norepinephrine, through methods ranging from inhibiting neurotransmitter release to affecting neurotransmitter binding. Thus, caffeine also blocks these effects, which may contribute to caffeine’s stimulating and reinforcing actions. REFERENCES: Fredholm BB, Bättig K, Holmén J, Nehlig A, Zvartau EE. Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacol Rev. 1999 Mar;51(1):83-133. Huang ZL, Urade Y, Hayaishi O. Prostaglandins and adenosine in the regulation of sleep and wakefulness. Curr Opin Pharmacol. 2007 Feb;7(1):33-8. Epub 2006 Nov 28. Huang ZL, Zhang Z, Qu WM. Roles of adenosine and its receptors in sleep-wake regulation. Int Rev Neurobiol. 2014;119:349-71. doi: 10.1016/B978-0-12-801022-8.00014-3.

Broca's area is a region in the frontal lobe that is thought to play an important role in language production, although its precise linguistic functions are still a bit unclear. In this video, I discuss Broca's area and some hypotheses regarding its function. For an article (on my website) that explains Broca's area, click this link: https://neuroscientificallychallenged.com/posts/know-your-brain-brocas-area TRANSCRIPT: Welcome to 2 minute neuroscience, where I explain neuroscience topics in 2 minutes or less. In this installment I will discuss Broca’s area. Although the anatomical definitions of Broca’s area are not completely consistent, it is generally considered to make up some part of a region called the inferior frontal gyrus, which is found in the frontal lobe. In the vast majority of individuals, Broca’s area resides in the left cerebral hemisphere. Broca’s area was named for the physician Paul Broca, who first identified the region as playing a potentially important role in speech production. Broca based this hypothesis on case studies of patients who had damage to the area and also displayed a deficit of speech. The particular condition Broca observed came to be known as Broca’s aphasia, and involves a deficit in the ability to produce language. In patients with Broca’s aphasia, reading and writing are also often impaired, but language comprehension is typically relatively preserved. The precise role of Broca’s area in language production, however, is still being debated. In other words, damage to Broca’s area can disrupt language production, but nobody is quite sure exactly what language-related function is lost to cause that disruption. Some have hypothesized Broca's area is involved with producing movements (like of the tongue and mouth) that allow speech to be produced. Others have argued it is involved with syntax, grammar, verbal working memory, or all of the above....Broca’s area is also thought to have a variety of other linguistic and non-linguistic functions. It has been recognized as playing an important role in language comprehension, movement, and even understanding the movement or actions of others. Thus, although Broca’s area does appear to play a role in language, the overall function seems to be more complex. REFERENCES: Grodzinsky Y, Santi A. The battle for Broca's region. Trends Cogn Sci. 2008 Dec;12(12):474-80. doi: 10.1016/j.tics.2008.09.001. Epub 2008 Oct 17. Nishitani N, Schürmann M, Amunts K, Hari R. Broca's region: from action to language. Physiology (Bethesda). 2005 Feb;20:60-9.

In this video I discuss acetylcholine, the first neurotransmitter ever discovered. The topics I cover include the locations of acetylcholine neurons in the brain, acetylcholine receptors, and some of the functions of acetylcholine. TRANSCRIPT: Welcome to 2 minute neuroscience, where I explain neuroscience topics in 2 minutes or less. In this installment I will discuss acetylcholine. Acetylcholine was the first neurotransmitter discovered, and is named for the two substances used to synthesize it: the nutrient choline and the enzyme acetyl coenzyme A. Neurons that contain acetylcholine are called cholinergic. There are several clusters of cholinergic neurons throughout the brain. Some are found in the basal forebrain; they include the medial septal nucleus, the nucleus of the diagonal band, and the nucleus basalis. Others are found in the brainstem, including the pedunculopontine nucleus and laterodorsal tegmental nucleus. Acetylcholine acts on two families of receptors, and each receptor family has several subtypes. One family is ionotropic; they are called nicotinic acetylcholine receptors because nicotine also binds to and activates the receptors. Their activation generally results in excitation of the neuron. Another family is metabotropic. These are called muscarinic acetylcholine receptors because a substance called muscarine binds to them; their effects depend on the subtype of the receptor. The action of acetylcholine in the synapse is terminated by an enzyme called acetylcholinesterase, which breaks acetylcholine down into acetate and choline. The choline is then transported back into neurons to synthesize more acetylcholine. Acetylcholine has a variety of functions in the nervous system. It is the main neurotransmitter used at neuromuscular junctions, and is responsible for muscle contraction. It is also widely used in the autonomic nervous system. Its functions in the brain are still not fully understood, but it does appear to play important roles in memory, arousal, and attention. REFERENCES: Kandel ER, Schwartz JH, Jessell TM 2000. Principles of Neural Science. 5th ed. New York. McGraw-Hill; 2013. Purves D, Augustine GJ, Fitzpatrick D, Hall WC, Lamantia AS, McNamara JO, White LE. Neuroscience. 4th ed. Sunderland, MA. Sinauer Associates; 2008.

Wernicke's area is a region in the cerebral cortex that historically has been considered important to language comprehension and the production of meaningful speech. In this video, I discuss the location of Wernicke's area, the deficit that occurs when it is damaged (Wernicke's aphasia), and hypotheses about its role in language. For an article (on my website) that explains Wernicke's area, click this link: https://neuroscientificallychallenged.com/posts/know-your-brain-wernickes-area TRANSCRIPT: Welcome to 2 minute neuroscience, where I explain neuroscience topics in 2 minutes or less. In this installment I will discuss Wernicke’s area. Although there is some debate over the exact location of Wernicke’s area, it is typically considered to reside in the cortex of the left cerebral hemisphere near the junction between the temporal and parietal lobes. Wernicke’s area was named for the German physician Carl Wernicke, who reported that damage to this region results in a deficit where patients are able to produce speech that resembles fluent language but actually is meaningless. The disorder came to be known as Wernicke’s aphasia, and patients who suffer from it do things like use made-up words or similar-sounding words substituted for one another to produce speech that makes little sense. Patients with Wernicke’s aphasia also suffer from a deficiency in their ability to understand language. Wernicke proposed a model for language that involved both the region he discovered and another language center: Broca’s area. Broca’s area is thought to play a role in speech production, and Wernicke’s model, which was later expanded on by neurologist Norman Geschwind and called the Wernicke-Geschwind model, suggested that Wernicke’s area creates plans for meaningful speech while Broca’s area is responsible for taking those plans and determining the movements (like of the tongue and mouth) required to turn those plans into vocalizations. It’s now thought, however, that this model is too simplistic. Studies indicate that language likely involves widespread networks and cannot be boiled down to a connection between two brain regions. Additionally, evidence now suggests that Wernicke’s area may be involved in speech production rather than just comprehension, and some have claimed it may not be as important to language comprehension as once thought. Thus, researchers are still trying to figure out the precise contribution of Wernicke’s area to language. REFERENCES: Binder, JR. The Wernicke area: Modern evidence and a reinterpretation. Neurology. 2015; 85(24): 2170-2175. Breedlove SM, Watson NV. Biological Psychology. 7th ed. Sunderland, MA: Sinauer Associates, Inc.; 2013.

Benzodiazepines are commonly used to treat anxiety disorders and sleep disorders. They are thought to exert their effects in the brain by acting at receptors for the neurotransmitter gamma-aminobutyric acid, or GABA. In this video, I cover the the mechanism of action for benzodiazepines. TRANSCRIPT: Welcome to 2 minute neuroscience, where I explain neuroscience topics in 2 minutes or less. In this installment I will discuss benzodiazepines. Benzodiazepines are a class of drugs named for their chemical structure that are commonly used to treat anxiety disorders and sleep-related disorders. They include well-known drugs like valium, xanax, and klonopin. There are dozens of drugs in the benzodiazepine class, but the mechanism by which they all exert their effects is thought to be similar. The sedating and anxiety-reducing effects of benzodiazepines are believed to be attributable to the drugs’ actions at receptors for the neurotransmitter gamma-aminobutyic acid, or GABA. In particular, benzodiazepines act at a subtype of GABA receptors called the GABAa receptor; GABAa receptors that also bind benzodiazepines are sometimes called benzodiazepine receptors. When benzodiazepines bind, or attach, to the GABA receptor, they bind at a location separate from where GABA itself binds, and exert an influence over GABA binding. This type of action is called an allosteric effect, and in the case of benzodiazepines it results in increased action at the GABA receptor. There is not complete consensus on exactly how benzodiazepine binding affects activity at the GABA receptor but there is evidence to suggest that it increases the likelihood that GABA binding will activate the receptor and/or increases the effect that GABA has when it binds to the receptor. That effect is to open an ion channel and allow the passage of negatively charged chloride ions into the neuron. This influx of negatively charged ions pushes the membrane potential further from zero, or hyperpolarizes it, and makes it less likely the neuron will fire an action potential. This type of neural inhibition is the basis for the effects of benzodiazepines, for by inhibiting the activity of neurons that make up networks involved with anxiety and arousal, the drugs are able to produce calming effects. REFERENCES: Gielen MC, Lumb MJ, Smart TG. Benzodiazepines modulate GABAA receptors by regulating the preactivation step after GABA binding. J Neurosci. 2012 Apr 25;32(17):5707-15. doi: 10.1523/JNEUROSCI.5663-11.2012. Möhler H, Fritschy JM, Rudolph U. A new benzodiazepine pharmacology. J Pharmacol Exp Ther. 2002 Jan;300(1):2-8.