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Psych230 Exam 2
| Question | Answer |
|---|---|
| Emotion | Subjective mental state that is usually accompanied by distinctive behaviors, feelings, and involuntary physiological changes |
| physical sensations | result of activation of the autonomic nervous system |
| Sympathetic nervous system | fight or flight response |
| parasympathetic nervous system | prepares the body to relax and recuperate |
| what are the eight basics emotions | joy/sadness, affection/disgust, anger/fear, expectation/surprise |
| what did Darwin argue? | emotional expression may have originated from a common ancestor and that nonhuman animals show comparable emotional expressions (facial muscles and innervation patterns are the same) |
| what are the 8 distinctive emotional expressions and can they be detected across cultures? | anger, sadness, happiness, fear, disgust, surprise, contempt, and embarrassment; yes |
| why may we have evolved to have universally recognized facial expressions? | for protection, overcoming language, avoiding predators (for survival), social interactions |
| facial feedback hypothesis | sensory feedback from our facial expressions can affect our mood - ex: people performing a task who take on a happy or sad face report stronger feelings of the emotions they were stimulating |
| Is there a one-to-one relation between a specific emotion and changed activity in a particular brain region? | No, each emotion involves different patterns of activation across a network of brain regions with emotion |
| emotions are associated with bilateral changes in what brain regions? | insula, amygdala, caudate, putamen, cingulate cortex, and prefrontal cortex |
| Fear conditioning | type of classical conditioning where a previously neutral stimulus is repeatedly paired with an unpleasant experience causing the subject to act fearful in response to the previously neutral stimulus |
| what does fear conditioning allow researchers to do? | to identify important brain mechs involved in learning, memory, and threat detection which can help researchers develop therapies for treating anxiety and PTSD |
| what brain region is involved with fear? | amygdala along with the hippocampus and cortex |
| what happens if there is bilateral damage to the amygdala? | person shows little to no fear |
| what is the activity of brain regions when it comes to love vs. friendship | - results in increased activity in the insula, anterior cingulate cortex, and caudate putamen - reduced activity in the posterior cingulate, amygdala, and right prefrontal cortex |
| stressor | anything that disrupts the physiological balance in an organism |
| stress response | brain's adaptations designed to aid in survival in response to a threat or perception of a threat |
| what type of stress response can be activated? | neuroendocrine, immunological, behavioral |
| allostasis | adjusting physiological parameters to accommodate current or anticipated stressors |
| Allostatic load | continually adapting to stressors incurs costs (energy expenditure, tissue damage, vulnerability to disease) |
| What are the two main pathways in response to stress? | - fight or flight reaction (super-fast response) - hypothalamic pituitary adrenal (HPA) axis (slower and more prolonged) |
| fight or flight pathway | hypothalamus activates the sympathetic nervous system to cause the adrenal medulla to release epinephrine and norepinephrine |
| what does the release of epinephrine and norepinephrine act to do? | boost heart rate, breathing etc. in preparation for action |
| Hormonal pathway (HPA axis) | - hypothalamus releases CRH which acts on the anterior pituitary - pituitary then releases ACTH which causes the adrenal cortex to release adrenal steroid hormones such as cortisol to ready body for action |
| how does stress related diseases emerge | often when the stress response is activated for too long or too frequently and when it is not activated for a physiological reason (e.g. psychological or social stresses) |
| how does social support and stress level affect immune responsitivity | - happy social life and lower stress --> less likely to develop cold when exposed to virus and produce more antibodies in response to vaccination |
| how does the illusion of control affect stress and coping | as long as there is even an illusion of control over the occurrence of a stressful event, stress (glucocorticoid levels) remains low |
| are unpredicted or predicted stressors more stressful | unpredicted/unexpected |
| how does an outlet of frustration factor into stress and coping | an outlet of frustration results in a lower level of glucocorticoid and decrease likelihood of ulceration |
| how does having social support affect stress levels | isolated animals show stronger stress responses to a stress than group housed animals |
| how does personality factor into stress and coping | what is stressful depends on the goals of the organism (e.g., dominance, affiliation) and on genetically determined differences in overall fearfulness |
| What is early life stress (ELS) | chronic activation of the stress response early in life which is known to "scar' the brain and reshape mental health trajectories |
| early life experiences can be both ___ and ____ | postnatal and prenatal |
| postnatal ELS | - profound physical, cognitive, and social development delays - youth who experienced differential brain development showed increased psychopathology correlates |
| how can we mitigate risk of postnatal ELS for orphans | placement into high quality foster care |
| what was found in eastern European orphanages on ELS for orphans | the longer the child spent in the orphanage, the higher their resting glucocorticoid level even after getting adopted |
| Prenatal stress | if certain types of stressors are experienced during fetal life you may experience lifelong increases in risk of certain stress related disorders |
| what happened to fetuses during the Dutch Hunger Winter? | burned having severely altered metabolism and increased risked of metabolic disorders (diabetes, heart disease, obesity, etc.) when they "learned" about food availability during this famine |
| what changes did offsprings have that remained throughout life during the famine | epigenetic changes |
| what transgenerational effect occurred due to the famine | offspring of fathers who were exposed to the famine prenatally were heavier and had a higher BMI than offsprings of unexposed fathers |
| Maternal Immune activation (MIA) | - byproducts of immune system activation can make their way into the embryo and negatively alter neurodevelopment - chronic stress can activate immune system in bad ways |
| is all stress bad? | no, it's adaptive and can promote resilient phenotype and allow children faced with adversity to develop adaptive coping strategies |
| how does environmental pollutants and stress play a role in the development of autism in fetuses | - higher instances in those living in lower SES which is correlated with higher exposure to stress - there's an association between exposure to air pollution along with high levels of prenatal stress and the development of ASD |
| evolutionary neuroendocrinology | study of how neuroendocrine systems arose and changed over time |
| comparative neuroendocrinology | study of how neuroendocrine systems are similar/different throughout the animal kingdom |
| glucocorticoids | - "classic" stress response - bind to glucocorticoid receptor (GR) - e.g. cortisol/corticosterone |
| Mineralcorticoids | - blood pressure/osmolarity - bind to mineralocorticoid receptor (MR) - e.g., aldosterone |
| what are similarities between glucocorticoids and mineralcorticoids | - derived from cholesterol - secreted from adrenal cortex - exert effects via transcriptional regulation |
| what types of samples are used to measured glucocorticoids | blood, saliva, fur/hair, urine, feces |
| what types of assays are used to measure glucocorticoids | protein based (ELISA, radioimmunoassay) and molecular structure/size based (liquid chromatography/Tandem mass, spectrometry) |
| what are some outward markers of stress | repetitive behavior (ex; pacing), lethargy, weight loss or gain, aggression |
| circadian regulation of glucocorticoid levels | cortisol peaks around time of awakening and is lowest in the middle of the inactive (sleeping) phase - inverted in nocturnal organisms |
| glucocorticoid level's seasonal rhythm is determined by what? | the amount of light per day |
| circannual regulation | - day length modulates daily glucocorticoid rhythms - shooter days --> sharper peak at beginning of waking phase |
| what can the seasonal rhythm of glucocorticoid levels affect | immune function, adaptive color change, metabolism, reproduction, etc. |
| what is the correlation between body size and basal glucocorticoid levels | - smaller animals need a higher baseline metabolic rate (need to metabolize carbs due to loss of heat) - strength of relationship varies by taxa |
| monogamous animals' adaptation to stress | - have higher circulating levels of glucocorticoids than promiscuous counterparts - they're more exploratory and seem to be more resilient to stress |
| what mutations caused monogamous animals to be more resilient to stress? | mutations caused glucocorticoid receptors to have lower affinity for corticosterone as well as high levels of corticosteroid binding globulin (CBG) which binds to free CORT and prevents it from binding to receptors |
| what is a theory to why average baseline glucocorticoid levels are rising each year | somehow related to temperatures |
| maternal match hypothesis | - early life cues trigger epigenetic changes that prepares an organism for the condition it's born into - if predicted environment matches the actual future environment this improves fitness ("match"); can be detrimental if not |
| environmental stress and telomere length in North American red squirrels | offspring telomere length correlate with environmental stressors experienced by pregnant red squirrels; effects of experiencing environmental stress in utero may affect longevity and growth rate |
| food scarcity and bottlenose dolphins | - dolphins shift their attentiveness and maternal style in response to environmental conditions (ex: food scarcity) resulting in offsprings born in these conditions becoming independent earlier but may suffer less guidance and support from parents |
| what factors can cause animals in captivity to experience stress | diet, enrichment, socialization factors |
| what is a serious problem for managed populations of endangered species when they experience stress in captivity? | stress can affect fertility |
| what was the solution for cheetahs in captivity that were experiencing adrenal fatigue that caused them to not be able to breed | social support with puppies |
| what are sensory receptor organs | organs specialized to detect a certain stimulus |
| what do receptor cells within sensory receptor organs do | convert stimulus into electrical signals |
| what is an adequate stimulus | type of stimulus to which a sensory organ is particularly adapted |
| what is the end point of all sensory organs | converting info to neural signals |
| sensory transduction | conversion of energy from stimulus into a change in membrane potential in a receptor cell |
| what does the doctrine of specific nerve energies state? | receptors and neural channels for different senses are independent of each other |
| what does the concept of labeled lines say? | = Brain recognizes distinct senses because potentials travel along separate nerve tracts - Neural activity in different lines signal different things (smell, touch, sound, etc.) - we have different receptors and lines for each type of touch |
| Pacinian corpuscles | skin receptor that detects vibrations and pressure |
| what happens when the Pacinian corpuscles detect a vibration/pressure | stimulus to the corpuscle opens stretch-sensitive channels made and produces a graded receptor potential/generator potential When the potential is big enough, the receptor reaches threshold and generates an action potential |
| what is protein that make up stretch sensitive channels called? | Piezo |
| Touch is detected only when what? | A AP is generated |
| how is stimulus location determined? | from the positio of the activated receptors |
| how are the intensity of sensory events encoded? | by the number and frequency of action potentials |
| action potentials produced by sensory neurons always have the same what? | same size and duration |
| range fractionation | as strength of a stimulus increases, more neurons sensitive to higher intensities are recruited |
| adapation | progressive loss of response to a maintained stimulus |
| what receptors display adaption and decrease frequency of action potentials with constant stimulation | phasic receptors |
| what receptors show slow or no decline in AP frequency | tonic receptors |
| why do some receptors reduce responding with constant stimulation | sensory systems emphasize change in stimuli which is more important for survival thus preventing the nervous system from being overwhelmed by too much info coming in |
| what are other ways to control incoming info? | accessory structures or top down processing |
| what is top down processing? | higher brain centers (ex: cortex) suppresses some sensory inputs and amplify others |
| what does the dorsal column system deliver | touch info to the brain |
| what is the touch pathway (dorsal column system) | touch receptor (cell body in spinal cord) --> medulla (in brain stem) --> thalamus --> primary somatosensory cortex |
| where does information corss over in the dorsal column system | in the medulla where it then goes to the thalamus for initial processing |
| what side of the body does the brain process touch information? | from the contralateral side |
| receptive field | - region in which a stimulus will alter a sensory neuron's firing rate - differs in size, shape, and response to types of stimulation |
| how do we determine what touch a cortical neuron responds to | can record from the cell and touch different parts of the body; the cell will fire when you touch the area it responds |
| where is the receptor field the smallest? | fingers compared to back |
| if there is a smaller receptive field are there more neurons or less | more |
| if there are more neurons in the cortex dedicated to that area, what does it mean for the size of the receptive field and the sensitivity of that body area | there is a smaller receptive field, and the body part is better at detecting touch |
| what makes the somatosensory cortex plastic? | - intentional stimulation of a specific body region can expand its cortical representation; loss of use will cause it to shrink - neuron number dedicated to a region can be changed by experience |
| pain | - unpleasant experience associated with tissue damage - help sus to withdraw from its source, engage in recuperative actions, and to signal to others |
| congenital insensitivity to apin | inherited syndrome where the person does not experience pain |
| what are the three aspects of pain | - sensory discriminative quality (throbbing, gnawing, shooting) - motivation affective (emotional) quality (tiring, sickening, fearful) - cognitive evaluative quality (no pain, mild, excruciating) ---> level of pain |
| why is pain hard to measure | subjective, hard to describe, sex differences, hormones can interfere, not processed in the same way as vision |
| nociceptors | peripheral receptors (or free nerve endings) that respond to painful stimuli |
| where are nociceptors located? | - in the dermis and have specialized receptor proteins on the cell membrane that respond to various signals |
| what allows free nerve endings to be able to respond to different stimuli like temperature changes, chemicals and pain | they have different receptor proteins |
| what is the spinothalamic system pathway for pain | nociceptor --> spinal cord (crosses midline here) --> thalamus --> somatosensory cortex and other cortical areas |
| what happens after damaged cells release substances that excite free nerve endings functioning as nociceptors | - APs generated in the periphery can excite blood vessels and mast cells to produce inflammation - the stimulated mast cells release histamines and a chloroquine like signal |
| what happens after information enters the dorsal root | - it synapses on neurons in the dorsal horn - pain fibers release glutamate and substance P in the spinal cord - dorsal horn cells then send info across the midline and up to the thalamus |
| where do receptors synapse onto spinal neurons | dorsal horn |
| phantom limb pain/neuropathic pain | - may be due to inappropriate signaling of pain by neurons - microglial cells release chemicals that make the dorsal horn neurons hyperexcitable and cause chronic pain |
| what may be one way to treat phantom limb pain | - use of visual stimulation (a mirror gives the illusion of having both limbs intact and individual is asked to command both hands to move in symmetry. the illusion of controlling missing hand relieves phantom sensation) |
| how does social rejection correlate with activity of anterior cingulate cortex | the more distress or feelings of rejection someone feels, the greater the activity in the anterior cingulate cortex |
| what medication can be taken to reduce activity of anterior cingulate when subjected to social distress pain | Tylenol |
| analgesia | absence or reduction in pain sensation |
| opioids | endogenous opiate like peptides in the brain |
| opiates | drugs that reduce |
| periaqueductal gray (PAG) | - area in midbrain involved in pain perception - electrical stimulation and produce potent analgesia |
| how can we block pain information | by gating action in the spinal cord so info can't reach the brain |
| pure tone is described by what two measures | amplitude/intensity and frequency |
| amplitude/intensity | perceived as loudness; measured in decibels |
| frequency | number of cycles per second of vibration, measured in Hz and perceived as pitch |
| what does the external ear and pinna do | captures and funnels sound waves into the ear canal |
| what do the ridges and valleys of the external ear modify? | - the character of sound frequencies that reach the middle ear - also important for vertical location |
| what does the middle ear do? | concentrate sound energies |
| once the sound waves enter the middle ear what does it strike? | the tympanic membrane (eardrum) and cause it to vibrate which moves the ossicles |
| ossicles | Malleus, incus, and stapes |
| what does the ossicles do? | concentrate and amplify the vibrations on the oval window |
| what two muscles in the middle ear improve auditory perception and protect the inner ear from loud potentially damaging sounds and minimizes self made sounds | tensor tympani and stapedius |
| Tensor tympani | attached to the malleus and tympanic membrane |
| stapedius | attached to stapes |
| what do the inner ear structures convert sound into | neural activity |
| what is the fluid filled cochlea comprised of? | - scala vestibuli (vestibular canal) - scala media (middle canal) - scala tympani (tympanic canal) |
| what does the scala media contain | the organ of Corti which is the receptor system within the inner ear that converts vibrations from sound into neural activity |
| auditory sensory cells (hair cells) are embedded where? | in the basilar membrane and vibrate in response to sound and transduce the movements into electrical activity |
| what part of the basilar membrane respond to high frequency? | base of the basilar membrane |
| what part of the basilar membrane responds to low frequency? | the apex of the basilar membrane |
| auditory pathway | cochlea --> vestibulocochlear nerve --> cochlear nuclei --> superior olivary nuclei (brainstem --> inferior colliculus (midbrain) --> medial geniculate nuclei (in thalamus) --> auditory cortex |
| what does the vestibulocochlear nerve (cranial nerve VIII) contain? | auditory fibers from the cochlea |
| how many branches do the auditory nerve fibers divide into and where to they go? | two branches; go to the cells in the cochlear nuclei |
| superior olivary nuclei (brainstem) | receive bilateral input and is helpful for identifying location of sound |
| inferior colliculi (in the midbrain) | auditory integration center of the midbrain and helps initiate reflexes like turning towards a sound and contributes to startle reflex |
| intensity differences | differences in loudness at the two ears; louder where sound hits first; bigger difference with higher frequency sounds |
| latency differences | differences between the two ears in the time of arrival of sounds |
| what is used to tell where a sound comes from? | binaural cues (intensity and latency differences) |
| what is used to identify sound in a vertical plane? | spectral filtering |
| spectral filtering | pinna selectivity reinforces some frequencies and reduces others; provides critical info about elevation (vertical location) |
| hearing loss | decreased sensitivity to sound, ranging from moderate to severe |
| deafness | loss of hearing so profound that speech cannot be perceived even with the use of hearing aids |
| conduction deafness | disorders of the outer or middle ear that prevents sounds from reaching the cochlea |
| sensorineural deafness | problem in the cochlea that interferes with the transduction of sound vibrations into neural activity |
| central deafness | damage to auditory brain areas such as by stroke, tumors, or traumatic brain injury |
| what can cause ototoxic effects? | may be due to drugs such as antibiotic streptomycin |
| what can noise pollution and loud sounds cause? | can damage hair cells resulting in tinnitus |
| cochlear implants | - used to treat deafness due to hair cell loss - electrical currents stimulate the auditory nerve |
| hearing aids | can help with conduction deafness where individuals need the volume to be louder |
| how do hearing aids work? | the microphone captures sound waves, amplifies and strengthens the signals, and sends them into the ear canal |
| what does the vestibular system detect | position and movement of the head |
| semicircular canals | three fluid filled tubes in different planes |
| what does movement of the head in any one axis cause? | sets up a flow of fluid in the semicircular canal deflecting the stereocilia int he ampulla and signaling the brain that the head has moved |
| what are the 3 principle axes? | pitch axis, yaw axis, and the roll axis |
| olfaction (smell) | detects airborne chemicals |
| gustation (taste) | responds to chemicals in the mouth |
| what is the main adaptive role of the chemical senses? | evaluation of potential foods |
| what are the three kinds of taste papillae are distributed on the tongue? | circumvallate, foliate, fungiform |
| what does each papilla hold have? | multiple taste buds each of which consists of 50-100 taste receptor cells |
| what doe taste cells extend cilia into? | taste pore, the opening at the surface of the taste bud, to expose them to tastants |
| what sense doesn't send info through the thalamus? | smell |
| olfactory system pathway | olfactory receptor cells --> mitral cells --> olfactory bulb --> primary olfactory cortex |
| what does mammalian odor detection rely on ? | olfactory sensory neurons in the epithelium within the nasal cavity |
| what happens at the receptor cell? | odorants interact with receptors on the cilia and dendritic knob |
| what is olfactory bulb organized into? | many glomeruli that pass info from similar types of OSNs to mitral cells in the olfactory bulb |
| where does the sense of smell start with? | receptor neurons in the nose within the olfactory epithelium |
| what neurons can be replaced in adulthood? | olfactory receptor neurons |
| what are the five basic tastes | salty, sour, sweet, bitter, umami |
| how is the taste of saltiness transduced | sodium ions are transported across taste cell membranes causing depolarization that sends info to the brain |
| how is the taste of sour transduced | all acids release hydrogen ions (H+); the more acidic the food, the ore sour it tastes; this same receptor detects carbonation in drinks |
| what do receptors for sweet, bitter, and umami stimualte? | G protein coupled receptors that cause a cascade of intracellular events |
| what do each taste cell transduce? | only one of the five tastes |
| what are the five steps in taste transduction? | - tastants bind to corresponding receptors on taste cells - multiple intracellular pathways are activated - neurotransmitter is released and the primary sensory neurons fires - APs are sent to the brain - Ca2+ tirggers transmitter release |
| supertasters | exhibit heightened sensitivity to some bitter and sweet tastes, suggesting that they are genetically different |
| how is taste info conveyed? | conveyed via several cranial nerves to nuclei in the brainstem and then to the thalamus |
| how do we convey perception of tastes | from the thalamus, a taste specific pathway projects to cortical taste areas |
| Parkinson's disease | - results in degeneration of the dopaminergic neurons of the Substantia Nigra - progressive disorder of the nervous system that affects movement |
| what are the symptoms of Parkinson's | slurred or soft speech, tremors, general motor deficits, inability to perform directed actions, and progresses to stiff and/or uncontrolled movement |
| what are symptoms of Parkinson's caused by? | reduced dopamine but exact causes of neural degradation are unknown |
| what medication is used for Parkinson's | Levodopa --> compound converted into dopamine in the brain can help attenuate symptoms |
| Alzheimer's disease | - most common form of dementia - neural changes including formation of beta amyloid plaques |
| plaques | deposits of a protein fragment (in the case of Alzheimer's beta amyloid) that build up in the spaces between nerve cells |
| Tangles | twisted fibers of another protein called tau that build up inside cells and disrupts transportation of essential nutrients |
| what are some symptoms of Alzheimer's? | - memory loss that disrupts life - challenges in planning or solving problems - confusion with time or place - trouble with visual images or spatial relationships - misplacing things, losing ability to retrace steps |
| What are some risk factors for Alzheimer's | - risk doubles about every 5 yrs after age 65 - family history - genetics - black and Hispanic adults |
| is Alzheimer's more prevalent in men or women? | women |
| what is the association between education and risk of dementia | each additional year of education decrease risk of developing dementia |
| what two genes are involved in Alzheimer's | risk and deterministic genes |
| risk genes | increase the likelihood of developing the disease but don’t guarantee it will happen (apolipoprotein E-e4, APOE-e4) |
| deterministic genes | directly cause a disease (amyloid precursor protein, APP; presenilin-1, PS-1) called autosomal dominant Alzheimer's disease |
| Depression | mood disorder that results in the persistent feelings of sadness and/or happiness and loss of interest in activaties |
| what are some symptoms of depression? | - feelings of sadness - angry outburst, irritability, frustration - sleep disturbances - tiredness - changes in appetite - feelings of worthlessness or guilt - trouble thinking about |
| what are some causes of depression? | biological differences, brain chemistry, hormones, inherited traits |
| what are some treatments for depression? | - Meds; SSRI's, SNRI's, NDRI's, MAOI's - others: counseling, changes in lifestyle, use of supplements (st. john's Worts) |
| Multiple Sclerosis | - CNS demyelinating disorder characterized by inflammatory plaques in white matter - disrupted neural transmission within the CNS |
| what are the phases of multiple sclerosis? | - Inflammatory phase: inflammation drives myelin loss - Neurodegenerative phase: chronic axonal degradation and gliosis |
| what do the loss of myelin insulation result in? | reorganization of ion channels, abnormal electrical conduction |
| what are the symptoms of multiple sclerosis? | - depends on the location but - issues with vision, weakness, numbness, tingling in limbs, dizziness, fatigue, balance problems, poor bladder control, altered mood changes |
| what are the causes of multiple sclerosis? | - unknown but could be immune mediated inflammatory disease, genetic susceptibility, Vit D deficiency |
| what are some treatments for multiple sclerosis? | Meds: immunotherapy (injection of either interferon, synthetic polypeptides, monoclonal antibodies) |
| what do interferons do? | reduce the frequency/severity of relapses |
| what do synthetic polypeptides do? | block immune attack on myelin |
| what do monoclonal antibodies do to VLA-4 adhesion molecule? | block movement of damaging immune cells form bloodstream to brain/spinal cord |
| autism spectrum disorder | - serious neurodevelopmental disorder that impairs a child's ability to communicate and interact with others - can cause significant impairment in social, occupational, and other areas of functioning |
| what are some symptoms of Autism? | - resisting cuddling or prefers to play alone - fails to respond to their own name - lack or delayed speech (can't start a convo or keep one going, speaks) - doesn't understand simple questions |
| What are some causes of Autism? | - several genes and genetic changes - other potential factors include viral infections, air pollutants, and/or high levels of testosterone in utero |
| what are some treatments of autism? | no cure but early treatments may include behavior and communication therapies, educational therapies, family therapies, medications |
| ADHD | characterized by combination of problems including difficulty sustaining attention, hyperactivity, and impulsive behavior |
| can ADHD persist into adulthood? | yes, but symptoms commonly attenuate as people age (chronic condition) |
| what are some causes of ADHD? | - Suspect hypoactivity of the dopamine and norepinephrine projections into the prefrontal cortex - in animal models, determined that testosterone may dealy maturation of dopaminergic and norepinephrine pathways critical for attention and reward |
| what are some treatments for ADHD? | - stimulant meds which boost and balance levels of neurotransmitters and improve symptoms of inattention and hyperactivity - some antidepressants have shown to be effective but take longer to take effect |
| OCD | - characterized by unreasonable thoughts and fears (obsessions) that lead you to repetitive behaviors (compulsions) - individuals feel driven to perform compulsive acts to ease stressful feelings |
| what are some obsessive symptoms? | - repeated, persistent and unwanted urges or images that cause distress or anxiety (fear of contamination by shaking hands or touching objects, doubts you locked the door, intense stress when objects aren't orderly) |
| what are some compulsion symptoms? | - repetitive behaviors you feel driven to perform in an attempt to reduce anxiety related to the obsession (washing hands until raw, checking doors repeatedly, counting in certain patterns, arranging items, silently repeating word or phrase) |
| what are causes or risk factors for OCD? | biology, family history, environment, stressful life events |
| what are some treatments for OCD? | - psychotherapy: exposure responsive prevention (ERP) which involves gradually exposing the patient to the feared object/obsession and learning healthy ways to cope with anxiety - meds: antidepressants/psychiatric meds |
| what is the most effective treatment for OCD? | exposure responsive prevention (ERP) |
| what do the cornea and lens do? | focus light |
| Refraction | bending of light accomplished by the cornea |
| what do the ciliary muscles do? | adjust focus by changing the shape of the lens |
| accomodation | process of focusing the lens |
| what muscles control eye movement? | extraocular muscles |
| light entering the eye is controlled by what? | the pupil (opening in the iris) |
| photoreceptor cells? | rods and cones |
| where does visual processing begin in? | the retina |
| what do the horizontal cells in the retina contact? | photoreceptors and bipolar cells |
| what happens after bipolar cells are contacted? | they receive input from photoreceptors and synapses on ganglion cells whose axons form the optic nerve and exit the eye |
| what cells do amacrine cells contact? | bipolar and ganglion cells |
| what are the two functional systems for photoreceptors? | photopic and scotopic |
| photopic system (cones) | requires more light and allows for color vision; good visual acuity (sharpness) |
| Scotopic system (rods) | works in dim light, low visual acuity |
| photons | quanta of light energy with visible wavelengths (triggers the receptors) |
| photoreceptors adaptation | ability of individual photoreceptors to adjust sensitivity to prevailing level of illumination |
| range fractionation | handling of different intensities by different receptors |
| visual acuity | measure of how much detail we see and is sharpest in the center of the visual field |
| where is the visual detail sharpest? | fovea because it's a high density of tightly packed cones and this region receives direct light input that does not pass through other cells or blood vessels |
| where are rods more numerous? | in the periphery; they're more sensitive to dim light |
| why does the pupil dilate under low illumination? | helps to let light in to activate the rods |
| optic disc | where blood vessels and the optic nerve leave the eye resulting in no photoreceptors |
| blind spot | due to lack of photoreceptors in the optic disc |
| what don't we see holes in our vision? | Saccades constantly shift the eyes so the adaptation doesn't cause the scene to disappear; constantly moving to get the most complete picture of info |
| lateral inhibiton | process where interconnected neurons inhibit their neighbors and produce contrast |
| optic tract | axons of the optic nerve after passing the optic chiasm |
| nasal hemiretina | portion of the retina closest to the nose or midline that projects its axons to the contralateral side of the brain |
| temporal hemiretina | lateral portion of the retina that projects its axons to the ipsilateral (same) side of the brain |
| where is information from the left visual field processed? | on the right side of the brain |
| what is the visual system pathway? | photoreceptor cells --> bipolar cells --> ganglion cells --> LGN of thalamus --> primary visual cortex |
| axons of the postsynaptic cells in the LGN form what? | optic radiations which terminate in the primary visual cortex (V1) or striate cortex of the occipital lobe |
| where does most visual info arrive first? | primary visual cortex of the occipital lobe |
| what does damage at the level of the retina cause? | prevents info about light coming into the brain (wouldn't be able to see anything) |
| what does damage at the level of the cortex cause? | light can come into the brain, but sense cannot be made of it or consciously detected (might see image but not know what it is) |
| Visual acuity | sharpness of vision best in the middle of the fovea but also where the visual fields overlap |
| visual field | whole area you can see without moving your head or eyes |
| do predators or preys have a smaller visual field? | predators |
| why do predators have a smaller visual field? | they need to be able to hunt more efficiently so visual acuity is more needed |
| the first stage of color reception concerns what photoreceptor cell | cones |
| trichromatic hypothesis | there are three different types of cones with different types of opsin/photopigment that respond to different parts of the light spectrum |
| what are the different types of cones? | - short (S): peak sensitivity 420nm - Medium (M): 530 nm - Long (L): 560 nm |
| does each cone respond to a single wavelength or a wide range of it? | wide range of wavelengths |
| color blindness | due to the absence of cones sensitive to medium wavelength (M cones) |
| why are more men color blind than women? | women have two X chromosomes, a defective gene encoding the medium wavelength pigment on one X chromosome is almost always compensated for by a normal copy on the other X; since males don't have 2 X's they can't make up for the defective gene |
| myopia | - occurs if the eyeball is too long - causes the image to be focused in front of the retina |
| amblyopia | reduced visual acuity not caused by optical or retinal damage and is usually due to misalignment of the eye |
| what happens if amblyopia is untreated | brain will ignore info from the weak eye and only connections in the strong eye will be saved |
| how can amblyopia be corrected | using the weak eye regularly with the good eye covered, vision can be preserved in both eyes (only if corrected early on) |
| reflex | - simple, unvarying, and unlearned responses to sensory stimuli such as touch, pressure, and pain - doesn't require cortical (brain) involvement - stimulation triggers motor neuron at spinal cord level |
| motor plan/motor program | set of muscle commands established before the action occurs |
| what do the skeletal system do? | attached to muscles to allow movement of |
| what does the spinal cord control | skeletal msucles |
| what does the brainstem contorl? | motor commands and relays sensory info; first place to fine tune things |
| what does the primary motor cortex do? | initiates commands for actions |
| what do the cerebellum and basal ganglia do? | modulates activities of these control systems sometimes via the thalamus in a loop back to the cortex |
| how do muscles work? | work solely through contraction (shortening or pulling) and in antagonistic pairs (one contracts other extends) |
| what are muscles that work together called? | synergists |
| what do motor neurons do? | transmit motor messages to muscles |
| what system are smooth muscles controlled by? | autonomic nervous system |
| what determines movement? | muscle attachments |
| what filaments do muscle fibers contain and what are they made of? | thick filaments (made of myosin) and thin filaments (made of actin) |
| striated muscles | the overlapping of filaments giving muscles it's striped appearance |
| what are the two main types of striated muscle fibers? | - fast twitch (contract rapidly but fatigue easily but don't maintain tension for longer periods of time) - slow twitch (contract more slowly but are resistant to fatigue - mainly postural muscles) |
| neuromuscular junctions | where the neuron terminates on the muscle fibers |
| motor unit | consists of a single motor neuron and all the muscle fibers it innervates |
| where do spinal motor neurons send their axons out the ventral roots to? | periphery |
| what neurotransmitter is released at the target of motor neuron axons? | acetycholine |
| what muscles are controlled directly by the cranial motor nuclei in the brainstem? | muscles of the head and neck |
| what are all other muscles controlled by? | spinal cord motor neurons that receive commands from the brain |
| pyramidal system/corticospinal system | consist of neurons in the cerebral cortex and their axons which pass through the brainstem and form the pyramidal tract to the spinal cord |
| where does the pyramidal tract cross the midline | in the medulla called the decussation |
| where do many of the axons form the pyramidal tract originate from? | neurons in the primary motor cortex (M1) |
| what does the primary motor cortex mainly consist of? | precentral gyrus |
| what does damage to M1 produce? | partial paralysis on the contralateral side of the body |
| what are the two main regions of the nonprimary motor cortex | - supplementary motor area (SMA) and premotor cortex |
| supplementary motor area (SMA) | important for planning movements that are internally generated |
| premotor cortex | directs movement in response to external cues |
| how can learning a new skill change motor representation in M1 | - can change electrical activities in M1 - early musical training results in an expansion of the width of M1 - as monkeys learn a skill, metabolic activity in M1 during the task declines as it becomes more efficient |
| mirror neurons are active when? | both when an individual makes a particular movement and when an individual sees another individual make that same movement |
| what are mirror neurons through tot be important in understanding? | what other people are doing and suggests a neural basis for empathy |
| what area contains mirror neurons | area F5 in the premotor cortex |
| what happens if area F5 gets dirupted? | it makes it difficult for participants to guess what actions are being mimicked |
| what is one reason for patients with autism to anticipate other's thoughts and actions? | they have a deficit in mirror neuron activity (have less activation in this region when trying to mimic an activity) |
| extrapyramidal system | includes motor tracts that do not run through the medulla |
| basal ganglia | forebrain nuclei that modulate movement and include the caudate nucleus and putamen and the globus pallidus |
| what does each structure that makes up the basal ganglia receive input from? | wide areas of the cerebral cortex that send output back to the cortex via the thalamus forming a loop |
| what is the basal ganglia important for? | determining amplitude and direction of movement and skill learning |
| what does the cerebellum affect? | programs, coordination, and learning of acts and guides movement through inhibition |
| what does the cerebellar cortex contain? | Purkinje cells which only send inhibitory messages |
| what does cerebellar damage cause? | impairments like ataxia (loss of coordination) of the legs, difficulty producing gestures, and problems tracking movement with the eyes |
| how two brainstem pathways are used by the extrapyramidal system to communicate with the spinal cord? | reticulospinal and rubrospinal tract |
| reticulospinal tract | originates in the reticular formation of the brainstem and modulates movmeent |
| rubrospinal tract | originates from the midbrain's red nucleus |
| learning | process that expresses itself as an adaptive change in behavior in response to experience |
| memory | encoding, storage, and retrieval of info about past experience and is necessary if learning is to take place |
| what did HM suffer from | severe epilepsy |
| what part of the brain did HM get cut out? | hippocampus |
| retrograde amnesia | loss of memories formed prior to onset of amnesia |
| anterograde amnesia | inability to form new memories after onset of disorder |
| declarative memory is | facts and info acquired through learning that can be stated or described (things you can tell others and is used to answer "what" questions) |
| what kind of new memory was HM unable to form? | declarative memory |
| nondeclarative (procedural memory) | shown by performance rather than recollection (things you know that you can show by doing and answers "how" questions) |
| how did HM perform on the mirror tracing task | his performance got better after every trial and every day even though he couldn't remember doing it --> built up muscle/procedural memory |
| hippocampal formation | composed of the hippocampus, Para hippocampal gyrus, subiculum, and entorhinal cortex |
| what is the hippocampus important for? | critical for declarative memory formation |
| Was HM able to remember things from early childhood | yes, so the hippocampus can't be for long term storage site of memories |
| what brain structures are procedural memories supported by? | basal ganglia and cerebellum |
| how can declarative memories be tested in animals? | - monkey presented with a sample object and finds food under it - after a couple seconds it's presented with original object and another one - over many trials with different pairs of objects, it learns that food is present under the diffent object |
| what brain regions did KC damage? | frontal and parietal cortex and severe shrinkage of the hippocampus and parahippocampal cortex |
| what type of memory could KC not retrieve | episodic memory |
| what type of memory did KC retain | semantic memory |
| what is the cortex essential for? | long term storage of memories once they are formed |
| semantic memory | generalized memory (facts and info) |
| episodic memroy | detailed autobiographical memory (memories about personal things in your life) |
| skill learning | learning how to perform a task requiring motor coordination |
| priming | change in stimulus processing due to prior exposure to the stimulus |
| associative learning | - association of two stimuli or of a stimulus and response - learning about a relationship or the process by which an association between two stimuli is established |
| classical conditioning (Pavlov's dogs) | - An unconditioned response (UR) becomes associated with a conditioned stimulus (CS) - Learned through repeated pairings of the conditioned stimulus (CS) with an unconditioned stimulus (US) to produce a conditioned response (CR) |
| Operant conditioning | association is made between a behavior (action) and a consequence (reward or punishment) ex: rats playing basketball |
| what is long term memory for and how long does it last for? | to allow us to record important events that we can use to shape our future behavior in adaptive ways; can last for days to years |
| what are the three stages for creating and retaining memories | encoding, consolidation, retrieval |
| encoding | when sensory info is brought into short term/working memory |
| consolidation | transferring info from short to long term memory/storage |
| retrieval | taking info out of long term storage |
| forgetting | pruning of unimportant memories to preserve cognitive resources |
| neuroplasticity | ability of neurons and neural circuits to be remodeled in response to exposure or the environment |
| how can physical changes in the brain be measured? | can be measured physiologically and may be presynaptic, postsynaptic, or both |
| what changes in the brain are possible? | increased neurotransmitter release and/or changes in neurotransmitter-receptor interactions |
| what are some structural changes that may occur at synapses due to an experience? | - new synapses could be formed with training/use or some could be eliminated with lack of use - training might also lead to synaptic reorganization |
| what idea did Hebb propose | if a presynaptic neuron repeatedly activates a postsynaptic neuron, the synaptic connection between them will become stronger and more stable |
| what is long term potentiation (LTP) and what does it cause | stable and enduring increase in the effectiveness of synapses which causes the addition of AMPA receptors on the postsynaptic membrane |
| what is long term depression (LTD) | weakening of a synaptic efficiency |
| cell assemblies | group of neurons that |
| what are three housing conditions for lab animals | - standard conditions (no interactive playground/activities) - impoverished condition (no social interactions, no interactive activities, just alone by itself) - enriched condition (has everything: social life, playground, spacious) |
| what are differences between animals housed in enriched conditions (EC) vs. impoverished conditions (IC)? | - heavier, thicker cortex - enhanced cholinergic activity - more dendritic branches with more dendritic spines suggesting more synapses |
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rach6774