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84 Cards in this Set
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Sensory receptors |
Receptors that detect sensory energy. Each type of receptor conveys different type of info 1)Modality: type of stimulus that activates sensory receptor 2)Intensity: strength of stimulus, sensory threshold (smallest intensity at which sensation is detected) 3)Duration: period of time sensory stimulation continues. Intensity decreases with duration 4) Location: ability to identify site of stimulation and distinguish btw stimuli applied at close distances |
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Examples of sensory receptors |
Rod and cones of retina hair cells located in inner ear nerve endings in skin taste buds hair cells on olfactory membrane |
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Sensory systems (3) |
1- Functional segregation 2- Hierarchical organization 3- Parallel Processing |
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Functional segregation |
Type of sensory system The 2 point threshold measures the minimum distance at which 2 stimuli are perceived as distinct. Different parts of the body have different threshold (2mm finger tip, 10 mm palm, 40mm arm). Greatest receptive capacity: finger tips, lips, tongue |
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Dermatomes |
area of skin intervated by a single spinal nerve. Cervical -->thorathic--> lumber--> sacral |
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Shingles (functional segregation) |
Viral infection caused by the chicken pox virus. Virus moves to dorsal root ganglion where it remains latent. Symptoms: pain, stripe of blisters that wraps around either the left or right side of your torso. Affects older adults and people with weakened immune system, stress Initial stage: burning pain and sensitive skin Sites: one side of upper abdomen, lower abdomen, shoulder, eye area |
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Hierarchical Organization |
type of sensory system Sensory Receptors --> Thalamic relay nuclei --> Primary sensory cortex --> Secondary sensory cortex --> Association cortex |
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Parallel Processing |
type of sensory system Ability of the brain to process different stimuli at once. We have this ability because the primary somatosensory cortex is subdivided into several different zones based on their cytoarchitecture. Each different zone receives input from one sent of somatosensory receptors. --> multiple representation of body in somatosensory cortex ex) visual system
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Types of Somatosensory receptors (4) |
1- Mechanoreceptors: responds to mechanical stimuli 2- Thermoreceptors 3- Chemoreceptors 4- Nocioreceptors |
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Types of Mechanoreceptors |
1. Meissner's corpuscles 2. Merkel's disk 3. Pacinian corpuscles 4. Ruffini's endings |
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Miessner's corpuscles |
40% of receptors on skin textured items move across skin, edge contours low frequency vibration Braile |
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Merkel's disks |
25% receptors in finger tips Form and roughness Sensitive to points and edges |
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Pacinian corpuscles |
10-15% of receptors in hand Detect vibrations transmitted through objects that contact hand or being grasped in hand |
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Ruffini's endings |
20% receptors in hand located deep in skin detect stretching force important in body position and posture |
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Transduction |
conversion of a sensory stimulus from one to another 1) Receptor potential : transduction begins when a stimulus changes the transmembrane potential of a sensory neuron (graded effect: stronger stimulus = larger receptor potential) 2) Generator potential: when the receptor potential exceeds the threshold and an AP is fired. Firing rate increases with stimulus strength (stronger stimulus, more APs) |
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Types of Somatosensory pathways |
1) Dorsal column medial lemniscus pathway 2) Spinothalamic pathway |
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Dorsal column medial lemniscus pathway |
Somatosensory pathway that: - conveys precisely localized information (fine touch) - myelinated afferents from narrowly tuned receptors - small, place and modality specific receptive fields - High synaptic security, "high fidelity" -Sensory neurons enter spinal cord via dorsal root ganglia and ascend ipsilaterally to the medulla, where they cross over and ascend in the medial lemnicus to the ventral posterior thalamus and then to primary somatosensory cortex
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Spinothalamic Pathway |
- subserves pain and temperature sensation - less precise, less well-localized - affective component of pain is due to divergent projection of system (limbic system) - small diameter, myelinated and unmyelinated afferents - receives input from free (bare) nerve endings that are the peripheral terminals of small-diameter myelinated (alpha delta) and unmyleinated (C) primary afferent fibers - stimulus transduction involves chemical step for nociceptors -insecure synapse, large receptive fields - Sensory neurons enter SC via dorsal root and immediately synapse and axons cross over to other side of SC. Then ascend to ventral posterior thalamus and then to primary somatosensory cortex. |
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Primary somatosensory cortex |
- First and largest cortical receiving area for information from somatosensory receptors - Neuron are topographically arranged, according to the part of the body from they receive info - receives info from ventral posterior thalamus - responsible for awareness of stimulus occurrence, quality, location, amplitude, duration 1: rapid skin receptors 2: deep pressure and joint 3a: muscle 3b: slow skin receptors Thalamus sends info to layer 5 in cortex |
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Somatosensory association area |
necessary for high order processing of somatosensory information ex: stereognosis: ability to recognize a small object by touch without vision - damage to this area can cause tactile agnosia |
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Pain |
unpleasant sensory or emotional experience associated with actual or potential tissue damage, described in terms of such damage |
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Nociception |
activation of sensory receptors by thermal, mechanical, or chemical energy impinging on the specialized nerve endings |
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Types of pain |
Acute: elicited by injury of body tissue and activation of nociceptors at the site of tissue damage. Lasts for a limited time and remits when the pathology resolves Chronic: elicted by injury but may be perpetuated by factors that are remote from originating cause. Extends for long periods, low levels of underlying pathology that doesn't explain pain. Environmental and affective factors interact. Physiochemical changes, remodelling may occur, more intense. Embedded, learn to have pain |
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Types of nociceptors |
Mechanical: Alpha-delta - sharp, pricking Thermal: Alpha-delta - slow burning, sharp Polymodal: C - hot, burning sensation, cold and mechanical |
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Pain measurement techniques |
tail flick apparatus hot plate apparatus cold pressor test (ice bucket, acute pain) |
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Nociceptor Fiber Groups |
- Alpha delta: myelinated fibers, transmit first or early pain, acute, well localized pain - C fibers: unmyelinated fibers, transmit second or late pain, dull, achy pain - Both: cell bodies in dorsal root ganglion and terminate in dorsal horn |
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First pain pathway |
Alpha delta fibers -- spinothalamic tract -- posterior ventral lateral nucleus of the thalamus -- primary and then secondary somatosensory cortex -- sensory discrimination in pain |
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Second pain pathway |
C fiber-- spinothalamic tract-- posterior ventral lateral nucleus of thalamus -- collaterals to limbic structures (pain affect) immediate emotional component: insular cortex and anterior cingulate cortex long term emotional component: prefrontal cortex |
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Phantom limb |
- sensation that an amputated limb is still attached to the body - most commonly occurring in arms or legs - physiological response of brain after amputation - self-image, visual feedback reward system brain has to rewire to visual change, new visual feedback system, brain learns to understand it - use of mirror and movement of present appendage relieves tension in the phantom limb
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Insular cortex |
region associated with immediate emotional responses that receives tactile information
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Insensitivity to pain |
mutation of the gene that codes for sodium channel. |
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Types of movement |
1) Reflex movement 2) Automatic repetitive movement 3) Voluntary movement
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Vernon Mountcastle |
first person to discover the five layers in the cortex |
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Steps in Motor Action |
1- Visual information required to locate target 2- Frontal lobe motor areas plan the reach and command the movement 3- Spinal cord carries information to hand 4- Motor neurons carry message to muscles of the hand and forearm 5- Sensory receptors on fingers send messages to cortex that action has been done 6- SC carries info to brain 7- Basal ganglia judges grasp forces and cerebellum corrects movement errors 8- Cortex receives message that action is complete
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Components of Motor System |
- cortex - cerebellum - basal ganglia - brain stem nuclei - spinal cord |
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Alpha motor neuron |
- a myelinated neuron whose axon forms synapses with extrafusal muscle fibers of a skeletal muscle; activation contracts the muscle fiber - Final common pathway: receives input from spinal interneurons, muscle spindles, upper motor neurons in the brain - Golgi tendon organs stimulates inhibitory interneurons, which inhibit the alpha motor neurons of those muscles (avoid damage) |
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Motor unit |
a somatic motor neuron and all the muscle fibers it stimulates. - When an AP travels down the axon it reaches all the fibers in the motor unit, and all will normally be activated. The neuron and all its fibers act as a unit. |
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Innervation ratio |
- Muscles differ in the number of motor units and muscles fibers that they contain. - Muscles that require specificity of movement have fewer fibers per unit
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Neuromuscular Junction |
the synapse between a the terminal buttons of an axon and a muscle fiber. AP travels down, opening of calcium channels, vesicles taken to membrane, acetylcholine released into junction it binds to nicotinic receptors of muscle fiber that propagates an AP in the muscle fiber and causes it to contract |
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Myasthenia gravis (NJ) |
Autoimmune disease where patients produce antibodies to nicotinitic receptors that block and destroy them preventing muscle contraction. (flaccid paralysis) Causes weakness which fluctuates with use of muscle. The degree of muscle weakness differs greatly among ppl. Hallmars: young adult women (40s), older men (60s), increases during periods of activity, impaired eyelid movement Symptoms/Signs: drooping eyelids,blurred vision, unstable gait, weakness in limbs, shortness of breath, impaired speech, difficult swallowing, change in facial expression
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Botulism Poisoning (NJ) |
Source: low-acid foods that were improperly canned, Gram positive anaerobic bacteria (Clostridium botulinum). Light chain of botulin toxin in axon inhibits the release of Ach preventing muscle contractions permanently (flaccid paralysis) Symptoms: double vision, droopy eyelids, trouble speaking/swallowing/breathing - 50% mortality rate, earlier diagnosis better prognosis (chronic fatigue, shortness of breath) - Nerve can regenerate a new axon without exposure to neurotoxin, takes long to recover
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Tetany (NMJ) |
Due to low calcium levels in the blood that leads to increased AP frequency of muscle cells or nerves that innervate them, painful muscle spasms, tremors, intermittent muscle contractions Low Ca increase the permeability of the neuronal membranes to sodium ions, causing depolarizations which increases chance of AP. Less excitation is required to open Na channels when there is low Ca concentration Low vitamin D (leads to poor Ca absorption), chronic diarrhea, repeated vomiting, hyperventilation Signs: carpopedal spasm, facial spasm by a tap on facial nerve, spasm of forearm when blood circulation is cut off Tmnt: oral/IV doses of calcium + hormone injecton to control parathyroid activity |
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Poliomyelitis / Polio (AMN) |
Virus that causes paralysis can be prevented with a vaccine. flaccid paralysis Virus gains entry by binding to immunoglobulin-like receptor, known as the polio virus receptor. Feco-oral/Inhalational infects pharynx and intestinal mucosa Inapparent (90%-95%) Apparent (5%-10%) 4 types - spinal paralytic poliomyelitis is the most common, results from lower moton neuron lesion of anterior horn cells of SC. Severe: quadiplegia, paralysis of abdominal thoracic muscles (iron lung)
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Post-Polio Syndrome |
Signs/symptoms: progressive muscle weakness and pain, general fatigue, exhaustion with min activity, muscle atrophy, breathing/swallowing problems, sleep apnea, low tolerance of cold temp Surviving motor nerve cells in the brain stem and SC extend new branches to reconnect the nerve cell to the muscle (sprouts). This allows for recovery, sprouts supply more muscle fibers than normal so they are overexerted and paralysis returns. |
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Amyotrophic Lateral Sclerosis |
Fatal disease of NS, characterized by progressive muscle weakness resulting paralysis. Motor neurons gradually degenerate and muscles shrink. Cause: unknown (might be genetic, too much glutamate accumulates in synaptic cleft because they dont have protein that removes the NT) Symptoms: muscle weakness in hands, arms, legs, muscles of speech, swallowing, breathing Twitching and cramping of muscles (hands+feet) Impairment of use of arms and legs Thick speech Severe: shortness of breath and swallowing |
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Motor Action |
1) Frontal lobe (pre-motor cortex and supplementary motor area): motion planning, evaluate signals from parietal and temporal lobes 2) Primary motor cortex ( lateral and ventromedial tracts): which muscles need to contract 3) Interneurons and motor neurons 4) Skeletal muscles Cerebellum: refining movement and balance Basal Ganglia: getting proper initiation of movement
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Cerebral cortex |
covering surface of the cerebrum consists of 6 layers (1 outermost, 6 innermost) 5th layer contains efferent cells that send info outside of cortex |
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Primary motor cortex |
the region of the posterior frontal lobes that contains neurons that control movements of skeletal muscles |
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Secondary motor cortex (2 parts) |
Supplementary motor area: organization and sequential timing of movements generated by internally guided stimuli, behavioral sequences. Not knowing what comes next Premotor area: learning and executing complex movements that are guided by sensory stimuli, movement when told to do so |
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Sensorimotor association cortex |
integrate information from senses for location of body in space |
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Motor pathways |
- Lateral: independent limb movements, right and left move independently. They terminate in contralateral half of spinal segment directly on neuron, fingers, toes (Lateral corticospinal, rubrospinal, corticobulbar) - Ventromedial: automatic trunk/limb movements, coordinated. Axons terminate more diffusely, innervate interneurons |
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Corticospinal tract |
primary motor cortex --> ventral midbrain --> middle pons --> middle medulla --> caudal medulla (cross over: lateral cortico/ no cross over: ventral cortico --> spinal cord (fingers, hands, feet, toes) Corticobulbar: same but terminates in pons (face and tongue) Corticorubro: crosses over in midbrain (lower arms, feet, lower legs, hands) |
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Apraxia |
- Inability to carry out learned skilled motor acts despite preserved motor and sensory functions, coordination and comprehension - Ideomotor: impaired ability to perform a skilled gesture with a limb upon verbal command or imitation. Knows what he wants but cannot execute acts (damage to motor cortex + association cortex) - Ideational: difficulty in executing a sequence of actions when performing a complex multistage task (making coffee, damage to posterior parietal lobe) |
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Basal ganglia |
Includes: caudate nucleus, putamen, global pallidus receive most their input from all regions of cerebral cortex and substantia nigra - Outputs: primary motor cortex, supplementary motor cortox and premotor cortex |
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Dopaminergic Paths |
The ventral tegmental area (VTA) cells project to: limbic area (mesolimbic projection) cortical area (mesocortical projection) Neurons in substantia nigra project to: striatum (nigrostriatal projection) Parkinsons |
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Parkinson's Disease |
Dopaminergic nerve cells in the substantia nigra develop nerve loss, and its degeneration and the resulting striatal dopamine depletion are responsible for the most motor abnormalities Tmnt: L-Dopa (decrease effect over time, does not prevent continuous loss, schizo), deep brain stimulation Hallmarks: insoluble polymers made of alpha synuclein make lewy bodies that are deposited in substantia nigra cell bodies. LBs cause neuronal degeneration. Features: - Resting tremor: most common first symptom, usually assymetric and most evident in one hand with the arm at rest - Bradykinesia: difficulty with daily activities such as writing, shaving. decreased blinking, masked face, slowed chewing and swallowing - Rigidity: muscle tone increased in both flexor and extensor muscle providing resistance to passive movement of joints, stooped posture, flexed knees and elbows - Postural instability: loss postural reflexes - Dsyfunction of ANS: impaired bladder, sweating - Depression - Cognitive: dementia, slowness Risk factors: old age, MZ twin with PD, postive family history, pesticides, well water - Possible protective effect: smoking |
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Huntington's disease |
autosomal dominant disease, 50% of inheritance, does not skip generations, appears around 30s - Degeneration of caudate and putamen (especially at GABA and Ach) -Genetic mutation of huntingtin gene on chromosome 4 lead to accumulation of gene's protein, huntingtin which impairs brain function Symptoms: - general restlessness, small unintentionally initiated movements, lack of coordination, abnormal postures and facial expressions, difficulty chewing, swallowing, speaking
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Cerebellum |
contains half of all neurons in brain feedback control of movement skilled movements cognitive behavior: making plans, sequencing language, remembering events Damage: under or overshooting targets, intentional tremor |
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Limbic System |
1- Cingulate gyrus: emotion regulation 2- Hippocampus: learning and memory 3- Amygdala: emotion processing 4- Mammillary bodies: memory plus their connections and relays (fornix connects hippo with mammillary bodies) |
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Amygdala |
located within temporal lobes - Lateral nucleus: receives sensory input - Basal nucleus: relay LN to CN - Central nucleus: input from LN and BN to
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Fear Response |
Fight or flight Cannon's theory of Autonomic Nervous System homeostasis: Sympathetic vs Parasympathetic Para: constricts pupils, inhibits heart, contracts bladders, relaxes rectum Symp:dilates pupil, inhibits salivation, accelerates heart, stimulates glucose release, secretion of epinephrine from kidney, contracts rectum |
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Fast Fear Response |
Sympathetic Nervous System --> Adrenal medulla --> adrenaline
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Slow Fear Response |
Hypothalamic-Pituitary-Adrenal (HPA) --> glucocorticoid response (steroids affect metabolism) - release of corticotropin and vassopressin into blood vessel at base of hypothalamus - release of adrenocorticotropic hormone from pituitary - release of corticol from adrenal cortex - cortisol = energy mobilization Cortisol has a negative feedback loop to turn off fear response HPA Axis: hypothalamus (CRH) --> Anterior pituitary (ACTH)--> Adrenal cortex (Cortisol <--) |
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Neural circuitry of fear |
Fearful stressor --> thalamus + somatosensory cortex 1) Subcortical pathway: fast path, fear response, T + SC --> direct to lateral and central nuclei of amygdala 2) Cortical pathway: slower, fear learning. T+SC--> cortical path thru neocortex +hippocampus--> LN of amygdala (dmPFC: fear accelerator, vmPFC: fear brakes, amygdala: fear response) |
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PTSD |
Disorder resulting from exposure to trauma or threatening situations. Memory disorder with failure to learn extinction Criteria: Stressor /Intrusive symptoms/Avoidance/ Negative alterations in cognition and mood/ Alterations in arousal and reactivity/ Duration (+1 month) - As stimulus becomes more like conditioned stimulus, increased activity in insula (anticipate anxiety) - As stimulus becomes less like conditioned stimulus, increased vhippo and vmPFC activation - decreased amygdala activation as extinction is learned PSTD neurocircuitry: Increased amygdala and dPFC (acceletor), decreased vmPFC (brake) Psychophisio response: heart rate, skin conductance and electromyography
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Sleep |
- decreased motor activity - decreased response to stimulation - stereotyped posture - relatively easy to reverse |
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Measures of sleep |
- respiration - heart rate - muscle activity - eye movement - brain activity
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EEG Activity during sleep |
Alpha: smooth electrical activity, relaxed state Beta: irregular electrical activity, state of arousal Theta: intermittent during early stages of slow-wave sleep and rem sleep Delta: regular synchronous, deepest stages of slow wave sleep |
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Stages of Sleep |
Non-REM sleep: stages 1-4, Slow wave sleep (stages 3 and 4) are deepest stages 1: light sleep, muscle activity slowed, muscle twitching, alternating period of alpha and theta activity 2: breathing pattern and heart rate slows, decrease body temp. No alpha activity, contains sleep spindles and K complexes 3: deep sleep,slow delta waves 4: very deep sleep, limited muscle activity, delta 5: REM, waves speed up and dreaming occurs, heart rate increases, rapid and shallow breathing, theta and beta |
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Functions of sleep |
Restorative Learning |
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Sleep Deprivation |
Acute - increased sleepiness, irritability, poor performance on tests of vigiliance, executive functioning, slurred speech, bloodshot eyes, pale skin, vacant stares, hallucinations, impaired immune system, heart rate variability - boost part of brain closely connected to depression, anxiety |
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REM deprivation |
- increased episodes of REM - irritability - anxiety - decreased concentration - decreased memory formation particularly of emotional memories - REM rebound |
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Sleep deprivation and obesity |
Sleep deprivation activates a part of the brain that is involved in appetite regulation. Produces 2 hormones (grhelin and leptin). Ghrelin stimulates appetite and leptin produced by fat cells tells the brain the current energy balance in the body. When leptin levels are high, this tells the body that we are full. Sleep deprivation = high ghrelin + low leptin |
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Glymphatic pathway |
Brain lacks a lymphatic system to get rid of waste. Sleep helps remove wastes products from interstitial spaces among brain cells. Metabolites are flushed way through IS by the flow of the CSF. Constriction of IS and restriction of CSF flow is observed in waking brain. Accumulation of metabolites (beta amyloid) constrict the IS, which drives sleep state. Adenosine (waste from glial cells) serves to induce sleep, its concentration decreases during sleep. |
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Sleep disorders |
- insomnia - narcolepsy - sleep apnea - sleep talking, walking, eating |
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Insomnia |
Prone to it: 60+, women, depressed Primary sleep insomnia: inability to sleep for general reasons not linked to health Secondary: due to incidental health conditions, asthma, cancer, depression Acute: last for one night to a few weeks (caused by life stress, emotional or physical discomfort, environment, meds, jetlag) Chronic: last for months (caused by depression, chronic stress, pain, medical conditions eg Alzheimers) |
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Fatal familial insomnia |
- attacks the thalamus, which is responsible for regulating our sleep, motor , sensory systems - disease cause automatic NS to become hyperactive and completely block REM and non REM, this increases amyloid plaques in brain and normal proteins begin to mutate. (prions naturally occurring proteins that lack nucleus, DNA, RNA, they are made up of misfolded prion protein coded for by PRNP gene) increasing insomnia, panic attacks, phobias Sympathetic arousal Hallucinations Weight loss Dementia / muteness |
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Sleep apnea |
caused by greatly enlarged tonsils leads to high BP, cardiac issues, stroke, accidents, increase insulin resistance choking during sleep, snoring, lethargy, memory loss, heartburn |
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Narcolepsy |
Slow wave sleeping disorder Symptoms: excessive day time sleeping, cataplexy, disrupted nocturnal sleep, hallucination, sleep paralysis Hypocretin - small group of neurons in hypothalamus die, these neurons produce orexin (chemical that caries wakefulness-promoting signal to other neurons in brain regions) |
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NT involved in arousal |
1) Acetlycholine: levels in striatum, frontal cortex and hippocampus closely related to animal's activity 2) Noepinephrine: locus coeruleus, important in arousal and vigilance, axons innervate every part of the brain, activated best by unexpected new stimuli 3) Serotonin: raphe nucleus, facilitates ongoing acctivities, suppress processing of sensory information Calm, wakefulness (creativity, problem solving) from hypothalamus 4) Histamine: tuberomamillary nucleus, increase cortical activation. Activated by glutamate and inhibited by GABA 5) hypocretin (orexin): lateral hypothalamus, facilitate motor activity, promote weight gain
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Acetylcholine |
stimulation of Ach neuron in pons and basal forebrain produce activation and cortical desynchrony Ach agonists increase EEG signs and cortical arousal, while antagonists decrease EEG signs of arousal Levels of Ach in neocortex are high during waking and REM, but low during slow wave sleep |
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Adenosine |
promotes sleepiness by targeting arousal networks caffeine attaches to adenosine receptors on the nerve endings and blocks them, the nerves cannot get adenosine which causes neurons in the brain to fire and sleepiness is reduced |
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Ventro Lateral Preoptic Nucleus |
found in hypothalamus sleep promoter, contains GABA neurons, that inhibit TMN and promote sleep |
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Flip-flop |
The major sleep promoting region (vlPN) and the major wakefulness promoting regions (basal forebrain and pontine regions - Act, locus coeruleus- noradrengenic, raphe nuclei- serotinin, tuberomammillary - histamine)are reciprocally connected to the inhibitory GABAergic neurons. When flip-flop is in the wake state, the arousal systems are active and the vlPN is inhibited. When the flip-flop is in the sleep state, the vlPN is active and the arousal systems are inhibited. Advantage: quick switch from one to another Disadvantage: can be unstable (narcolepsy) Orexin-ergic neurons help stabilize the sleep/waking flip-flop, holds it in waking state |
