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Bruce Mc Kay

Bonus: biopsych rap video- full GPA bonus point The neuron doctrine: neurons are the fundamental structural and functional unit of the nervous system (Cajal)(He was very self-absorbed/narcissistic)first brain tissue transplants Reticular theory: neurons are continuous with each other and form a diffuse nervous network (Golgi) -it makes sense that the nervous system is billions of independent but connected units, and not just one big net Neurons unstained all look basically the same, greyish-whitish -when stained we can identify them, tell if they are diseased, what they do or should do Cells in the nervous system: Neurons: specialized cells for reception, conduction, and transmission of electrochemical signals, many sizes and shapes, can transmit messages long distances Soma: contains genetic information, basically the same for most cells Dendrites: thin branch like extensions (dendritic spines), allows for synaptic transmission Axon: conducts the action potential to the end point (muscle, gland etc) Myelin Sheath: insulates the axon Used to have unipolar or bipolar neuron where signal could go more than one way, now we have multipolar neuron where it only goes in one direction 1. Purkinje cell many (thousands) of inputs, many many dendrites 2. Retinal bipolar cell, simple, two inputs Glial cells: outnumber neurons, all communication is done in close proximity, they can not generate action potentials (the smarter the organism it has in relation more glial cells) Oligodendrocytes: extensions rich in myelin to create myelin sheaths in CNS (inhibit reconnection of nerves in CNS unlike Schwann cells) Astrocytes: largest glia, star-shaped, sense and synchronize brain activity to regulate blood vessel tone Radial Glia/; scaffold for migrating neurons early in development Schwann cell: sends out myelin wrappings and covers axon, not in brain but in periphery nerves, can guide axonal regeneration (they can reconnect nerves that get cut in small injuries) Microglia: involved in response to injury or disease, remove waste material, get rid of things that invade the brain Multiple sclerosis: demyelination of neurons due to death of Schwann cells (PNS) or oligodendrocytes (CNS), cutting off insulation can cause a cross of signal, interference Glioblastoma: A highly invasive brain tumor in adults, glial cells reproduce themselves in an adult brain (they’re not supposed to) The nerve impulse 1. Action potential- within the neuron electrical signals that transmit information 2. Synaptic transmission- between neurons, chemical signals transmitted Membrane potential: a neuron can vary its membrane potential to transmit information Concentration gradients: of charged molecules (ions)-maintained by selective membrane permeability. Molecules are distributed unevenly across the membrane. Under rest conditions the neuron does not allow flow through the membrane. Electrical gradients: of charged molecules (ions) distributed unevenly across the membrane. At rest there is a net positive charge outside the cell relative to a net negative charge inside the cell and thus there is a potential difference- voltage (inside a cell -70mv) Sodium ions are on the outside of the cell and potassium ions on the inside of the cell (outside defined as 0mv) When a channel opens an ion can cross the membrane, a large influx of sodium entering the cell, and the potassium leaves the cell causing it to become more negative Sodium potassium pump returns the balance sending K back to inside and Na to the outside Sodium potassium pump: leaves more positive on the outside and more negative on the inside K+ potassium leak channels, causes it to become more negative shortly before sodium potassium pump restores balance A combination of the concentration gradient and the electrical gradient determine the distribution of charged molecules at equilibrium. Ions contributing to resting voltage Potassium (K+) Sodium (Na+) Chloride (Cl-) Negatively charged proteins (A-) synthesized within the neuron -particles tend to move down their concentration gradient -like repels like and opposites attract (sodium and potassium abundant in sea water, evolution, which is why we still use it) Microelectrode made of glass (because it can be extremely thin) pressed into the membrane, is used to measure the action potential of neurons -action potential causes depolarization and cell becomes less negative, then the sodium channels open across the membrane,(there is a bit of positive amino acid residue on the protein channel and as the K+ moves it repels causing the channel to open) voltage gets more and more positive, at a certain point the potassium channels open, as K+ leaves it becomes more negative inside the cell (Repolarization). Sodium potassium pumps begin pumping K+ back in and Na+ out. The voltage change must reach a threshold before the action potential can fire. Depolarization has to be big enough for the channels to open. Hyperpolarization is inhibitory. When threshold is reached, voltage activated ion channels are opened (all or none, when threshold is reached the neuron fires and the action potential occurs) (technically not an “all”, many signals are sent but not all of them are sent down the cell, there are short action potentials that get completed but don’t conduct down the axon, medium ones sometimes do and larger ones do, this is why computer analogy is innacurate) Action potentials: can exist anywhere in the cell, mostly in the axon -axon potential starts at axon hillock and propagate forwards down the axon and into the synaptic terminals, in some cells it is in dendrites, part way down the axon -sometimes action potential also goes backward into dendrite as well as down the axon (back- propagation) -back propagation signals back to previous cell to show that action potential has occurred Myelin sheath: made with glial cells, the action potential moves faster down the axon as it keeps the potential from leaking through the membrane so it moves down the axon instead. (charge isn’t wasted). Saltatory conduction: action potential “jumping” from node to node in the axon, more of an electrical conduction (not a jumping motion), used to be thought of as a literal jump but due to old tools that were used to measure that couldn’t measure the charge in the axon because it was insulated. The reflex arc for leg flexion: 1. The circuit is too slow if action potentials were solely responsible 2. Multiple small inputs result in a bigger response than a single input (temporal summation) 3. When one muscle is excited a different one relaxes 4. The speed of conduction along an axon is 40m/s, speed of conduction through a reflex arc is slower and more variable 15m/s or less. Presumably the delay occurs at the synapse Checking knee jerk reflex (patellar stretch reflex) shows whether the spinal cord is working properly EPSP: excitatory post-synaptic potentials: excite a post-synaptic neuron, due to an influx of Na+ ions (increase in positive charge inside the cell) depolarization IPSP: inhibitory post-synaptic potentials inhibit a post-synaptic neuron, due to efflux of K+ ions or influx of Cl- ions (increase in negative charge inside the cell) hyperpolarization Synaptic integration: adding or combining a number of individual signals into one overall signal Temporal summation: integration of events happening at different times, small events happening almost at the same time can add up to a larger event Spatial summation: integration of events happening at different places, all at once attached to the same set of dendrites -allows for a big enough EPSP to cause action potential -when it involves sending immediate messages we don’t use summation (ex pain), different wiring for different uses, infinite combination of wiring possibilities, only a handful are commonly used Lifecycle of neurotransmitter molecules:  Neuron sysnthesizes the neurotransmitter  The arrival of an Action Potential at the terminal opens voltage activated Ca+ channels  The entry of the Ca+ causes vesicles (membrane bound containers) to fuse with the terminal membrane and release their contents (neurotransmitters)  Exocytosis: the process of neuron transmitter release  Neurotransmitters bind to post synaptic receptors  Neurotransmitters unbind (it is possible to re-bind again)  Neurotransmitters are reuptaken into pre-synaptic cell or degraded (by enzymes)  The post synaptic cell may send a message back to the presynaptic cell  Glial cells contain the cleft and neurotransmitters don’t leak out Released neurotransmitter molecules produce signals in postsynaptic neurons by binding to receptors Receptors are specific for a given neurotransmitter Ligand- a molecule that binds to another A neurotransmitter is a ligand of its receptor *2 different kinds of sodium channels, one opens chemically and another kind opens due to ions Cell receptors: Ligon-gated receptors: on dendrites to allow neurotransmitters to transmit message to create action potential, opens sodium gate, sodium floods in from surrounding fluid to change voltage Voltage-gated receptors: between soma and axon Receptors: there are multiple receptor types for a given Neurotransmitter Lonotropic receptor: associated with ligon-activated ion channels. Ionotropic receptors: Neurotransmitter binds and the associated ion channel opens or closes causing IPSP or EPSP. Metabotropic receptors: does not cause any change in ions, effects are slower, longer lasting, more diffuse, more varied, may cause bigger response for another NT, change cell structure in some way, these changes underlie learning and memory Inactivation and reuptake of neurotransmitters: Neurotransmitters released in the synapse are subjected to reuptake or inactivation Reuptake: presynaptic cell takes up most of the neurotransmitter molecules intact and reuse them, transporters are special membrane proteins that facilitate reuptake Major neurotransmitters: Glutamate: major EXCITATORY neurotransmitter EPSPs very important for neuroplasiticty involving learning, memory, second most common in the brain, sodium in Gamma aminobutyric acid (GABA): major INHIBITORY neurotransmitter IPSPs, anti-anxiety medications, notable drugs: benzodiazepines, barbiturates, alcohol, has the most synapses almost everywhere in the brain, more than half of the synapses in the brain, chloride in or potassium out, most of the time our brain does a lot of inhibition so that we can focus on what we are trying to do at the time Communications between neurons depends on a match between neurotransmitter and receptor (like a lock and key) To be psychoactive, drugs must mimic endogenous neurotransmitters Ethanol activates GABA receptors: alcohol is a CNS depressant, but in low doses is effectively a stimulant because it depresses the inhibitory control exerted by prefrontal cortex inhibiting the inhibitor- disinhibition With higher BAC levels more areas of the brain are affected until the brain stem respiratory nuclei are depressed. Why don’t we experience all alcohol effects at once? Many different types of GABA receptors so some require more alcohol to be affected for example the breathing controls require most amount of alcohol. Dopamine: all rewarding drugs increase dopamine levels, involved in reward pathway, motor control, limbic system dopamine regulates mood, ventral tegmental area/ nucleus accumbens related to drug addiction Norepinephrine: synthesized from dopamine, sympathetic nervous system, limbic system (regulation of mood) adrenaline Serotonin: brain stem (sleep regulation), limbic system (mood regulation), visual and auditory system Acetylcholine: parasympathetic, Endorphins: natural pain control, peptide molecules CNS- Central nervous system -brain- what is contained in the skull -spinal cord- top vertebra Peropheral nervous system PNS -every other nerve outside of skull and spine, bring info in and out of CNS Sections of the brain: used to describe orientation, based on slices of the brain Horizontal: a slice parallel to the ground Sagittal: down the middle- ex a midsagittal section separates the left and right halves Coronal (frontal): like slicing bread, standard to reveal pathology in MRI Brain: Top- dorsal Bottom- ventral Front- anterior Back- posterior Spinal cord: Up: anterior Down: posterior Dorsal: back Ventral: toward stomach Inward: medial Outward: lateral “cephalic flexure” we are bipedal causing directions between brain and spinal cord to change, due to 90 degree angle between brain and spinal cord Tract: set of axons within CNS Nerve: set of axons within PNS Nucleus: cluster of neuron cell bodies in the CNS, same vicinity with similar function ex. Hypothalamus Ganglion: cluster of neuron cell bodies within the PNS Spinal cord: located within the vertebrae, millions of axons and cell bodies and yet only about as thick as the pinky finger gray matter- inner component, primarily cell bodies. White matter- outer area mainly myelinated axons Dorsal- afferent, sensory Ventral- efferent, motor Bell-Magendie Law: ventral is where motor output comes out and dorsal is where sensory input comes in 31 pairs of spinal nerves : segmented layers coming out for motor and in for sensory Cervical C1-C8 Thoracic: T1-T12 Lumbar: L1-L5 Sacral: S1-S5 Coccygeal: Coc1 Dermatome: area of the body innervated by the left and right dorsal (sensory routes), segregated Somatic nervous system: interacts with external environment Afferent nerves: skin, eyes, etc coming back to Efferent: motor to muscles, going away from Autonomic Nervous System: regulates body’s internal environment, homeostasis, sympathetic (gas, fight or flight) activates bronchi to take in more oxygen, widens pupils, heart beats faster, inhibits the rest such as digestion and parasympathetic nerves (brake pedal, rest and relaxation) returns heart, breathing, pupils to normal, increases the speed of digestion. Both tend to have opposite effects, most organs have input from both kinds of nerves Two-stage neural paths, neuron exiting CNS synapses on a second stage neuron before the target organ. All of these fibers leave the spinal cord. Hirschprung’s disease: lack of parasympathetic input to a portion of the lower bowel resulting in chronic constipation (megacolon) Raynaud’s disorder: extreme vasoconstriction of tips of fingers, toes, nose, ears, (in cold environments) resulting in numbness Paralysis and sensory loss: occurs following a complete transection of the spinal cord, symptoms depend on level of lesion Cranial nerve functions 1.olfactory- for smell, to test: give them something so smell, olfactory input bypasses the thalamus so it becomes more powerful in comparison to other senses 2. optic nerve- seeing, detects photons via retina, when lesioned complete blindness occurs 3. Oculomotor- eye muscles all but the other two- direct and consensual pupillary responses, shine light in one eye and check the other, checks midbrain 4. Trochlear-eye muscles superior oblique 5. trigeminal-eye muscles lateral rectus. Trigeminal- face- sensory (touch, temp, etc) face motor- mastication (chewing) 6. Abducens- facial taste 7. facial nerve- muscles for showing emotion 8. vestibular nerve- hearing and balance 9. glossopharyngeal nerve- taste, swallowing 10. vagus nerve-swallowing, parasympathetic nervous system 11. accessory nerve-shoulders raise and lower 12. hypoglossal nerve-stick tongue straight out Dorsal structures: sensory functions Ventral structures: motor functions Cervical spinal cord Medulla (caudal) Medulla (rostral) Typical disorders associated with damage to the medulla: stroke, cerebellar herniation, trauma, drug overdose Outcomes: loss of motor control, loss of sensory input, loss of gag reflex and ability to speak, blood pressure dysregulation, loss of breathing, death Pons locus coeruleus Typical disorders associated with pons: stroke, trauma Outcomes: loss of sensory input, loss of motor output, impaired eye movements, locked in syndrome (patient fully conscious but only able to move eyes up and down) Midbrain Typical disorders associated with midbrain: stroke, trauma Outcomes: loss of sensory input, loss of motor output, impaired eye movements including abnormal pupil movements Forebrain: subcortical structures Major structures of limbic system Cingulate gyrus Thalamus Hypothalamus Mamillary body Hippocampus Amygdala Olfactory bulb Telencephalon- subcortical structures Limbic system- regulation of Motivated behaviors and emotion Mammillary bodies, hippocampus, amygdala, fornix, cingulate gyrus, septum (limbic ring or papez circuit) Thalamus- major relay between sensory nuclei and cerebral cortex: “lower” information is passed through the thalamus on its way to the cortex Medial geniculate nucleus- audition Lateral geniculate nucleus- vision Medial dorsal thalamus- limbic lobe, memory, emotion Ventral posteromedial thalamus- sensory input from face Reticular thalamus- adjusts (gates) activity level of rest of thalamus Typical disorder associated with damage to the mediodorsal thalamus: Korsakoff’s syndrome -most commonly seen in alcoholics (or others with a thiamine deficiency) -amnesia comparable to medial temporal lobe amnesia in early stages, anterograde amnesia for episodic memories -severe retrograde amnesia develops in later stages -progressive Hypothalamus- endocrine regulation of behaviors essential for survival and continuity of the species Nuclei within the hypothalamus control (in part) eating and drinking -experiments suggest two hypothalamic centers: VMH ventromedial a satiety centre, LH lateral a hunger center -lesions of VMH produce hyperphagia -lesions of LH produce aphagia and adipsia Nuclei within the hypothalamus are sexually dimorphic: larger in males, size of male SDN correlated with testosterone levels. Nuclei in preoptic, suprachiasmatic and anterior regions of the hypothalamus are larger in men than in women Suprachiasmatc nucleus (SCN) in the medial hypothalamus is the brain’s circadian clock -lesions don’t reduce sleep time but ruin the circadian periodicity -exhibits electrical metabolic and biochemical activity that can be entrained by the light-dark cycle -transplant SCN transplants the sleep-wake cycle -mechanisms of entrainment of SCN cells to light-dark cycles. Rare retinal ganglion cells with no rods or cones, retinohypothalamic tracts Basal ganglia: -collection of nuclei -part of neural loops that receive cortical input and send output back via the thalamus -enables “behavior switching” ex selecting which behavior to produce and then initiating or terminating that behavior Basal ganglia- lesion to substantia nigra (dopamine neurons)= parkinsonism. Symptoms: bradykinesia, shuffling gait, cogwheel rigidity, pill-rolling tremor, mask-like face, about 1 in 250 people Cerebellum: controls movement through actions on the descending motor pathways Characteristics of cerebellar lesions: Ataxia: incoordination between movements of body parts Dysmetria: inability to make a movement of appropriate distance Dysdiadochokinesia: inability to make rapid alternating movements of a limb Asynergia: inability to combine movements of individual limb segments into a coordinated and multi-segmental movement Intention (actin) tremor: involuntary oscillations present during activity but absent at rest All signs are ipsilateral to the lesion site consolidation Hippocampus is the gateway to the declarative memory Typical disorder of hippocampal pathology: dense anterograde amnesia, stroke of anterior choroidal artery Amygdala is important for emotion and fear: Typical disorder- kluver-bucy syndrome -first seen in monkeys following bilateral surgical removal of anterior temporal lobes (including amygdala) -major symptoms- absence of a fear response; placidity -rare cerebral neurological disorder in humans Flow of cerebrospinal fluid CSF synthesized in choroid plexus  lateral ventricles –(foramen of Monroe)-> 3 ventricle – th (aqueduct of Sylvius)-> 4 ventricle  various cisterns and sinuses  absorbed by arachnlid villi and into cerebral veins Interrupting the flow of cerebrospinal fluid: Hydrocephalus Non-communicating hydrocephalus: obstruction in the ventricles Communicating hydrocephalus: blockage in the subarachnoid space Hydrocephalus ex vacuo: secondary to neuronal loss (Huntington’s) Symptoms: headache, nausea, vomiting, seizures, coma, sudden in adults, gradual in infants, treatment- shunt Blood supply to the brain: Telencephalon- cerebral cortex Frontal lobe- organization of behavior; expressive speech; societal rules; voluntary motor control Parietal lobe: representation of external body surface; hemi Blood reaches the brain through :  Internal carotid arteries (semi exposed by vertebrae)  Vertebral arteries, run along vertebrae -the brain can only survive without blood for approx. 5 seconds -20-30% of energy you use whenever you are doing nothing is going to brain function -bracuocephalic branch off aeorta The sudden twisting of the neck can kill people via cutting off the arteries The circle of Willis distributes blood into the brain: -middle cerebral arteries -anterior cerebral arteries -anterior communicating artery -posterior cerebral artery -posterior communicating artery Through all these sets of arteries there are communicating arteries that make a complete circle to have blood flow in all directions at the base of the brain stem -if there was a blockage somewhere you could potentially reroute blood somewhere else -animals without circle of willis are very vulnerable to strokes Vasilar artery runs through structure of the brain Cortical areas supplied by ACA, MCA and PCA (anterior cerebral artery, middle cerebral artery, posterior cerebral artery) come off interior cortoid artery, blockages would result in loss of functioning downward of these arteries. Stroke: any interruption of blood flow to the brain; sudden in onset; behavioural deficits correlate with site of event, most common cause of adult disability, very general term. Behavioral deficits reflect the specific part of the brain and thus arterial system that has been compromised, the symptoms reflect exactly where the blood flow is lost General symptoms: sudden confusion or trouble speaking, sudden weakness on one side of the body, blurred vision, dizziness/ loss of coordination -if recognized in first 20-30 minutes it can be treatable, if not there may be permanent damage Symptoms of disruption to blood supply: behavioral deficits reflect the specific part f the brain and thus the arterial system that has been compromised MCA: eg left side -right side arm would have weakness -speech disruption, difficulty in expression -hearing problems ACA: eg left side -left side leg weakness -confusion Variability in ACA architecture: One on each side usually one in the middle, but every one is different it is possible to have two on one side, one on the other, variable PCA: -loss of vision -memory problems, amygdala and hippocampus are in temporal lobe -sometimes the periphery of vision disappears (tunnel vision) because PCA supplies peripheral vision -experience of near-death, tunnel, life replaying, light at the end Stroke: ischemia Cerebral ischemia- disruption of blood supply Arteriosclerosis- hardening (loss of elasticity) of blood vessels, general term Atherosclerosis- wall of blood vessels thicken, usually due to fat deposits, restricts the flow through the vessel Thrombosis- a plug forms in the brain Embolism- a plug forms elsewhere and moves to the brain, air bubbles can be embolisms When air causes an embolism, it compresses and so it can’t be forced though Stroke: hemorrhage, blood kills neurons they require the glial cells to pass the oxygen and nutrients, when blood gets into the brain death of neurons is immediate Aneurysm- a weakened point in the blood vessel that makes a stroke more likely, may be congenital (present at birth) or due to trauma or infection. Little ball like structures that grow out the side of a blood vessels due to pressure the wall pushes outward, this ball gets larger and is very vulnerable, once it reaches a critical size it tears and blood leaks out of it. Symptoms: none, most grow on circle of willis and go unnoticed until they rupture, need to check if there’s a family history. Hemorrage-blood vessel ruptures and bleeds out into the brain PS263 Wednesday Closed-head injuries often cause bleeding- when the brain is pushed rapidly against the skull, can cause tearing or shearing. Brain injuries due to blows that do not penetrate the skull- the brain collides with the skull. The brain will squish. Damages not only part of the brain that is hit (coup injury near the hit) but on the otherside when it bounces back (counter coup injuries). If the damage is violent enough vessels will rupture and blood spreads across the brain. Contusions- closed head injuries that involve damage to the cerebral circulatory system (contusion another word for bruise) Hematoma- the bruise that forms Symptoms vary with the site of brain damage Damage due to cerebral ischemia Does not develop immediately Most damage due to excess neurotransmitter release (trying to reach out and connect with each other so more are put out ex. Glutamate) the glutamate binds to the receptors over activates its receptors especially NMDA leading to an influx of Na and Ca which causes cells to die. Once some cells die the cells around it die and so on. Structures like hippocampus are particularly vulnerable; this process doesn’t take place for first 20-30 mins and once it begins masses of cells begin dying. Stroke third most leading cause of disability, after heart disease and cancer U of T has research of stroke patients and one project is on NMDA receptors in stroke, we can’t block these receptors as they are crucial for survival, they have second messenger pathways that get affected by influx of calcium so they are trying to find a way to block these secondary pathways that cause death. Other problems with blood flow: Migraines Symptoms: Flashing lights, headache, pulsating sensations, nausea, photophobia, phonophobia Many theories, one: -stress increases then decreases serotonin levels, causes blood vessels to constrict then dialate, inflammatory molecules are released, dilation of cerebral vessels + inflammation is painful Cause: triggers? Food, weather, emotion? Treatments: analgesics, anti-emetics, serotonin agonist-like drugs, caffeine Protecting the brain: Physical protection -skull, many milimetres thick, keeps brain safe from external trauma, has several plates that allow it to squish during birth then in development they fuse together, brain can move around inside skull, inside of top of the skull is very smooth, no abrasive surface against the brain, but bottom of skull not as smooth, lots of sharp spots near cerebellum, small sharp bony processes in between frontal lobe size (ethmoid bones), formen magnum where the spinal cord comes out -meninges: CNS is encased in bone and covered in three layers of meninges Dura matter: tough outer membrane, thick like shoe layer, keeps brain from being abrased against the inside of the skull Arachnoid matter: web-like, all of the blood vessels surrounding the brain, resorb blood coming from spinal cord, not very protective Pia matter: thin membrane that wraps around, it is not very useful, very fine, adheres to surface of the brain The meninges act as baffles between the hemispheres and the cerebellum, they go into the fissures of the brain and divide it up, reduces the movement of the brain keeps it relatively stationary upon impact -cerebrospinal fluid (CSF) the fluid serves as a cushion Clinical correlate: meningitis Inflammation of the meninges -severe headache -nuchal rigidity, unable to move neck due to cranial accessory nerve inflammation which causes you to be unable to move the neck as the nerve goes down to neck -sudden high fever -often altered mental status -caused by bacteria or viruses -can be fatal -not crippling pressure but takes place everywhere so causes vague symptoms initially such as confusion, poor coordination Clinical correlate: epidural anesthesia Needle depth set: pass needle through dense ligamentum flavum (impossible to inject in this space) when a popping occurs the needle is into the epidural space and injection can proceed. These nerves are bare so by using anesthesia the pain can be blocked. Mechanism of action: combine local anesthetics with opioids, blocks sensory input at therapeutic doses, muscle output at higher doses. Medical imaging of blood flow (or accumulation) is based on adaptations of x ray -angiography -computer tomography (CT scan) X-rays are not adequate for brain injuries, only useful for imaging radio-opaque (electron dense) materials Cerebral angiography- inject something that causes the blood to be radio-opaque, must absorb xrays less or more than surrounding tissue. We can see a blockage or blood flow that isn’t shown. Contrast x- rays. Some newer x-rays allow you to see blood flow in real time. X-ray computed tomography: (CT) 2-Dimages combined to create a 3D image, many images taken in a rotating x-ray machine. Apply x-rays f known strength at all angles, measure the difference on the other side of the head. Software fills in what the density of the tissue must be. They then use a computer to plot the calculations into an image. Light grey, white- high density, dark grey, black-low density. Can see midline, ventricles, blood. Penetrating injuries can tell us a lot about brain structure and function: -most of what we know is due to damaged brains and study of what deficits resulted -once bullets were created there was more specificity to the injury, we could see more precisely what happens where -cerebellum mapped due to WWI injuries Golgi staining helped to find what kinds of cells were where and did what Every part if the brain has different types of cells, cells of the same type tend to have same or similar functions Artificially activating neurons with a stimulating electrode evokes the behavior normally sub served by those neurons Lesioning not always relevant, if it was an inhibitory cell the results affect cells in another location Stereotaxic frame for human neurosurgery- hold the head, has rulers, allows for use of an atlas of the brain to find certain structures in surgery. Is now MRId with the rulers on it so shows own coordinates in your brain. Stereotaxic atlas: tells us how to get to what part of the brain (mm) Bregma: a point on the top of the skull often used as a reference point A lot of stereotaxic surgery is to put electrodes in to find out what neurons do what. Willard Penfield pioneered this, he was in Canada. Electrical stimulation: lesioning experimental or pathological can remove a damaged or inactive structure, electrical stimulation can be used to activate a structure, stimulation may have opposite effect to what would be seen if it was lesioned. Stimulator has positive and negative on each pole and the can shuffle which one is turned on. Stimulator is in there for a long time, there is damage with putting it in. at some point the glial cells wage battle against it and eventually become immune to the stimulation at which point it would need to be changed. Transcranial Magnetic stimulation: sometimes also activates local muscles as they also depend on ions to fire, stimulate area near surface of skull. Could be risky to people who have seizures as this occurs under low stimulation. EEG electroencephalography ME magnetoencephalography -can see what parts are activated during certain processes. Only shows what is going on under the surface of the brain. MRI magnetic response imaging: produces 2D and 3D images with high spatial resolution, superior resolution compared to CT, uses very strong magnets to align protons, Radiofrequency waves topple the protons as their spins return to normal they emit energy which is measured. These images are as detailed as a fresh tissue sample. Limited by the size of the hole. Functional MRI: wherever the blood is neurons around there must be active and using this blood BOLD Blood oxygen level dependent signal used to see where the blood is oxygenated and non- oxygenated. Positron emission tomography: pet, given glucose with positive substance that causes glucose to spread the positrons which emit photons when it is used, shows where in the brain it is being used, unlike MRI you only see function, not location, but is less costly. -brain is activated all the time, thus for experiments for pET or MRI need to have proper baseline condition to subtract. Brain development P= phenotype (brain function or behavioral output) G= genes E= environment 2 cells becme 1 trillion cells, 1 quadrillion synapses P1+G1+E1= P2 Genetics plays a key role, determines baseline and physiology of the body and its potential P2+ G2+ E2= P3 Experience plays a key role, dire consequences when something goes wrong Pn+ Gn+ En= Pn+1 Important steps in neuronal development: -induction of neural plate: a patch of tissue on the dorsal surface of the embryo becomes neural plate, visible three weeks after conception, three layers of embryonic cells: ectoderm (outside), mesoderm (middle), endoderm (inner). Neural plate cells are embryonic stem cells, have “unlimited capacity” for self renewal, can become any kind of mature neural cell Totipotent-earliest cell can become any type of body cell Multipotent- with development, neural plate cells are limited to becoming one of the range of mature nervous system cells Neural plate- folds into “neural groove”- fully fuses to be “neural tube”, inside is cerebal ventricles and neural tube -failure of neural tube closure leads to spina bifida, ancephaly -neural proliferation: neural tube cells proliferate, three swellings at anterior end become, midbrain, forebrain and hindbrain in humans, stem cells have the ability to become any type of cell -migration: once cells have been created through cell division in the neural tube, they migrate, migrating cells are immature, lacking axons and dendrites. Radial migration: moving out, along radial glial cells. Tangential migration: moving sideways. 1. somal migration: an extension that leads migration, cell body follows 2. glial-mediated migration: cell moves along a radial glial network -differentiation ( axon and growth) -myelination -axon growth and synapse formation: once migration is complete and structures have formed (aggregation), axons and dendrites begin to grow. Growth cone: at the growing tip of each extension, expans and retracts filopodia as if finding its way, guidance molecules, Sperry Chemoaffinity hypothesis: postsynaptic targets release a chemical that guides axonal growth -neuron death and synapse rearrangement, Gradient hypothesis: Seeks to explain topographic maps. Combination of molecules on the cells moving around have to match the combination of cells on the destination, if combination on growth cone matches the combination on target site then they are received, if they don’t match the cone retracts and continues. Lie address on a letter but as combination of molecules not numbers and letters Why is it better to start off with a huge number of connections and then pare them down? -soma migrates first (which is easier than as full neuron with dendrites and axon due to less friction), it migrates while the brain is still small then everything stretches, once the neurons get to where they go, because you don’t create new connections they overwire because you can always cut them back but you can’t grow new ones as an adult -we are overwired at birth so basically ready to learn anything possible to be learnt -synaptogenesis: formation of new synapses, depends on presence of glial cells especially astrocytes , chemical signal exchange is needed between pre-and post- synaptic neurons, is needed, true for adults as well -about 50% more neurons are produced than the number needed, death is normal -neurons die due to failure to compete for chemicals provided by targets, destroying some cells increases survival rate of remaining cells Getting rid of cells and neurons: -if you dn’t use it there’s no point maintaining it so it is lost, if synapse is lost, so is neuron Necrosis: active cell death, very messy, cell splits open, releases all its toxic contents (digestive enzymes etc) to neighbors which erodes neighbors, happens in trauma or hemorrhage Apoptosis: safer and cleaner, cell selected to be removed and it splits off into several small membrane bound pieces that get picked up by cells that remove waste, happens everywhere in the body Experience and developmental; programs interact to wire-up the cortex: Early visual deprivation: blindfolding a newborn, they become blind as adult, death of unused neurons, deficits in depth and pattern vision, fewer synapses and dendritic spines in primary visual cortex Enriched environment: less reduction of cortices, greater dendritic environment, more synapses per neuron, musical training reorganizes sensory and motor cortices, less neuron death -cross model rewiring experiments demonstrate the plasticity of sensory cortices, with visual input the auditory cortex can “see”, visual cortex could hear well, auditory cortex could see, not quite as well but plasticity makes it possible -early music training influences the organization of human auditory cortex- fMRI studies and somatosensory/motor cortex Neurogenesis in an adult: -mature brain changes and adapts -hippocampus and olfactory stream create new neurons for your entire life -adult neural stem cells created in the ventricles and adjacent tissues -hippocampus cells die rapidly and need to be replaced and incorporate into brand new circuits that form -exercise to increase production of neurons and blood flow to those areas Postnatal growth of brain: -myelination of axons , myelination of prefrontal cortex continues into adolescence, baby born without myelin and it grows and expands the brain, takes about 25 years -synaptogenesis -increased dendritic branches -overproduction of synapses may underlie the greater plasticity of the young brain -in autistic brains there is trouble with tethering of pre and post-synaptic neurons Bain tumors: -a tumor (neoplasm) is a mass of cells that grows independently of the rest of the body- a cancer -benign ( very localized, easily operable) vs. metastatic -incidence about 5-6 per 100 000/ year quite low -most brain tumors are infiltrating -metstatic, start somewhere else and move in the brain, highly aggressive, difficult to remove, usually needs radiation or chemotherapy about 105 are metastatic, start in lungs, malignant -medulla area tumors, more likely in young people, tend to be in neurons -tumors in adults are more often glial Symptoms: -depends on where the tumor is and how big it is, elevated intracranial pressure in general results in headaches and vomiting, the headache is constant, can get worse but always there *Important* Grades and stages: Grade- structure of the cells 1. Well differentiated, similar to normal cells 2. Moderately differentiated 3. Poorly differentiated 4. Anaplastic (similar to mitotic embryonic cells) Stage- where it is physically, how much it moves 0. Carcinoma in situ, highly localized pre-cancerous lesion 1. Cancer localized to one part of the body 2. Localized but advanced 3. Localized but advanced (2 or 3 depends on type of cancer) 4. Cancer has metastasized to other parts of body What can be done? Radiation and chemotherapy- stop cells from dividing, good to slow down the cancer growth but also stops the division of other cells such as hair, skin, stomach Neurosurgery: map out parts of the cortex, open skull, cut out dura, excise tumor -small holes are drilled -separate dura matter from skull with a small wedge -a cord is used to saw upwards from the skull without damaging the brain -cut semi-diagonally so that the plate removed doesn’t just drop down when reattached -small metal hooks used to hold it back on Traumatic brain Injury- concussions (aka mild traumatic brain injury- MTBI) -no loss of consciousness, if there is any it is very brief, no evidence of problem in MRI or CT -no apparent brain damage with a single concussion, multiple concussions may result in bain damage and a dementia referred to as “punch-drunk” syndrome- dementia puglistica, similar to what happens in Alzheimer’s and Parkinson’s, hardened deposits in neurons, loss of neuron and glial cells, shrinking of the brain, tangled neurons, Chronic traumatic encephalography (CTE) boxers, football players Traumatic brain injuries- discernable with brain imaging or obvious macroscopic damage during autopsy -coup, countre cup injuries, hematoma, contusions Brain infections and Toxins: typically cause swelling in the brain, which is at the expense of brain tissue and diminished function of brain or loss of neurons Bacterial infections: -often lead to abscesses, pockets of pus -meningitis from inflammation of meninges -treat with penicillin or other antibiotics Viral infections: -some preferentially attack neural tissues (rabies) -treat with anti-virals or perhaps vaccines Encephalitis: resulting inflammation Some causes: Bacterial Neurosyphilis- may produce a syndrome of insanity and dementia, when bacterium invades into brain, if syphilis goes untreated for a very long time Tuskagee syphilis trials: Alabama 1970’s didn’t treat black people with syphilis to see what happens Guatemalan prisons- American government in 2008, didn’t treat them to see what happens Rabies: high affinity for the nervous system Transported retrogradely through peripheral nerves to CNS, symptoms: hydrophobia, personality changes, Herpes encephalitis: retrograde transport of virus into brain via trigeminal ganglion, transports itself bck through nerve to transgeminal ganglia and stays dormant until something happens and it reactivates out via same axon, which is why it happens in same spot, may lie dormant for years in neuronal somata -sometimes goes back into synapse and into the brain Symptoms: dizziness, loss of confusion, paralysis, hallucinations personality changes, ultimately coma and then death Protozoa: -toxoplasmosis, flu-like symptoms, then brain inflammation, extremely dangerous to infants, most problematic to pregnant women and baby will have severe mental problems, transported by cats Creutzfeld-Jakob Disease (CJD) -human manifestation of prions (cause normal proteins to misfold into mutant proteins, occurs exponentially, brain fills with uselessly folded proteins) very aggressive, rapid in onset -bovine spongiform encephalopathy (mad cow), chronic wasting disease (elk, deer), scrapie (sheep) kuru (humans) -less common from eating mad cow, more common from spontaneous growth -only way to kill bacteria is with fire Neurotoxins -may enter general circulation from the GI tract or lungs or through skin -toxic psychosis- chronic insanity -the Mad Hatter: hat makers often had toxic psychosis due to mercury -red tide: saxitoxin, fishermen or people that eat fish from a toxin in algae, blocks sodium channels, heart muscles don’t work, brain dies -tytrototoxin: puffer fish toxin, intermediate dose is like half functioning brain, a tiny bit makes tongue numb -Bisphenol A (an estrogen analogue from plastic) possible neurotoxin? BPAs, fish born as female or turn female, in water supply -can the flu vaccine be neurotoxic? -1976 wine flu vaccine, incidence of guillain-barre syndrome (movement disorder) about 1 per 100,000 -incidence in general population 1 in 100 000 -1976 vaccine was contaminated with a bacterium that may have caused the problems -apparently no causal link -toronto star (2009) reports government of Canada will protect GlaxoSmithKline against vaccine- related lawsuits but not to doctors who may inject it the wrong way -most vaccines have a bit of mercury as preservative but not dangerous amount at all Genetic factors: PKU phenylketonuria- can’t metabolize certain food, treatable, untreated leads to progressive brain damage, mental retardation, seizures Down Syndrome: probability increases with advancing maternal age, extra chromosome 21, characteristic facial and body appearance, mental retardation, other health problems (thyroid, heart), can have down syndrome or non down syndrome child Advancing paternal age- Schizophrenia, autism, bipolar disorder? Epilepsy: -primary symptom is seizures, but not all who have seizures have epilepsy (ex febrile convulsion does not make you epileptic) -uncontrolled rhythmic discharge of neurons, synchronously -convulsions: motor seizures, some are merely subtle changes of thought, mood, behavior Causes: brain damage, genes (over
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