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87 Cards in this Set
- Front
- Back
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Identify: CNS, PNS, ANS |
Central Nervous system: brain + spinal cord Peripheral Nervous system: everywhere else Autonomic Nervous system: part of PNS, influences internal organs |
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afferent vs efferent neurons |
afferent: PNS --> CNS efferent CNS --> PNS interneurons <--> |
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CNS consists of? (3) |
Cerebral hemispheres: white matter, gray matter (thalamus, basal ganglia, cortex) brainstem: gray matter, white matter spinal cord: gray matter, white matter |
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gyri and sulci |
gyrus: faised fold sulcus/fissure: groove |
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what make up gray matter and white matter? |
gray matter: cell bodies white matter: bundles of axons |
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what protects the brain? (4) |
skull meninges cerebrospinal fluid blood-brain barrier |
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layers of meninges from outside to inside |
dura mater arachnoid mater pia mater |
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what does cerebrospinal fluid do? (4) |
keeps brain buoyant absorbs shock delivers nutrients clears waste |
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what produces CSF? |
choroid plexus which lines ventricles |
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where is the CSF? |
subarachnoid |
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lumbar puncture (spinal tap) |
important way to sample what's happening in the brain (used clinically and in research) |
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blood-brain barrier (2) |
protects brain from foreign substances in blood that could harm brain and from other neurotransmitters and hormones in the rest of the body maintains constant environment in brain |
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corpus callosum |
(area around the lateral ventricle)facilitates much of the communication between the 2 hemispheres; main function is to allow communication between the brain's left and right hemispheres |
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severed corpus callosum |
'split brain'when the corpus callosum connecting the 2 hemispheres is split to some degree |
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synapse |
a structure that permits a neuron to pass an electrical or chemical signal to another neuron |
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neurotransmitter (2) |
endogenous chemicals that enable neurotransmission transmit signals across a chemical synapse |
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synaptic vesicle |
store various neurotransmitters that are released at the synapse |
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chemical synapse |
biological junctions through which neurons signal to each other and to non-neuronal cells such as those in muscles or glands |
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electrical synapse |
a mechanical and electrically conductive link between two neighboring neurons that is formed at a narrow gap between the pre- and postsynaptic neurons known as a gap junction |
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characteristics of an electrical synapse (5) |
cells are linked electric current flows across synapse bidirectional fast less common, but often found in neural systems that require fastest response |
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characteristics of a chemical synapse (4) |
chemicals flow across synapse gap between cells undirectional still very fast, but not as fast |
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chemical synapse steps (7) *check to make sure this is chemical synapse |
1. action potential travels to axon terminal 2. depolarization of terminal --> Ca2+ channels open 3. Ca2+ enters into cell --> vesicles fuse with presynaptic membrane 4. neurotransmitter released into synaptic cleft 5. neurotransmitter binds to receptors on postsynaptic membrane 6. postsynaptic changes --> generating EPSP or IPSP 7. if input strong enough, action potential fires |
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If action potential is all-or-none, how does the neuron code the intensity of a stimulus? |
through frequency and duration of action potentials |
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When voltage-gated calcium channels which are generally closed, open in response to sufficient depolarization in step 2 of the chemical synapse, which way does the calcium want to go? |
electrostatic: Ca2+ wants to go outside cell (+ --> -) diffusion: wants to go inside cell (many --> few) diffusion is stronger, so Ca2+ goes into the cell |
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In a chemical synapse, if there is greater frequency of action potentials, there is...? |
grater amount of neurotransmitter released at synapse |
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describe step 5 of a chemical synapse (neurotransmitter binds to receptors on postsynaptic membrane) in 4 steps |
1. action potential arrives 2. vesicle fuses with plasma membrane 3. neurotransmitter is released into synaptic cleft 4. neurotransmitter binds to receptor |
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what are the 2 types of receptors? |
ionotropic metabotropic |
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characteristics of ionotropic receptors (4) |
forms an ion channel pore ligand-gated channels neurotransmitter binds to receptor --> ion channel opens fast-acting |
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characteristics of metabotropic receptors (4) |
indirectly linked to ion channels on the plasma membrane of the cell aka G-protein-coupled receptors slower acting potential for modulation |
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EPSP |
excitatory post-synaptic potential -activates excitatory synapse -diffusion + electrostatic forces: Na+ wants to go inside cell -influx of sodium --> depolarization -excitatory input causes the cell to fire |
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IPSP |
inhibitory post-synaptic potential -activates inhibitory synapse -diffusion > electrostatic forces: Cl- wants to go inside cell -influx of chloride --> hyperpolarization |
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role of axon hillock |
integrates post-synaptic potentials excitation from EPSP --> makes cell want to fire inhibition from IPSP --> makes cell want to not |
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how do EPSPs and IPSPs affect likelihood of an action potential? |
EPSPs increase likelihood (mv increases) IPSPs decrease likelihood (mv decreases) |
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Some neurons are always firing action potentials. In these cases, what effect may stimuli have? |
in these cases, stimuli change the rate of action potentials: excitatory inputs might lead to their firing APs more frequently, while inhibitory inputs might slow the rate of AP firing |
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how does the AP process stop? (5) |
action potentials stop firing voltage-gated Ca2+ channels close Ca2+ concentration inside cell decreases vesicles stop fusing with presynaptic membrane neurotransmitter no longer released |
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What about the neurotransmitter left in the synaptic cleft (when the AP process stops)? How do we stop neurotransmitter activity? (4) |
-diffusion: neurotransmitter can passively diffuse out of synaptic cleft -enzymatic degradation/deactivation: enzymes in the synapse can break down neurotransmitter -active transport: reuptake pumps in presynaptic membrane that can bring neurotransmitter back into axon terminal and recycle it -astrocyte endfeed: astrocytes near synapse can also have pumps that take in neurotransmitter to be broken down or recycled |
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neurotransmitters (3 facts) |
molecules that communicate information between neurons and target cells +60 known types of neurotransmitters often categorized based on their molecular structure |
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types of neurotransmitters |
small-molecule neurotransmitters: -monoamines (eg dopamine) -amino acids (eg glutamate) -others (eg acetycholine) neuropeptides (eg oxytocin, insulin, endorphins) |
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dopamine (DA) what type of neurotransmitter is it? what does it do? what can affect it? |
-monoamine (catecholamine) -important for a wide variety of behaviors -DA dysregulation underlies a variety of neurological and psychiatric disorders (eg Parkinson's disease, schizophrenia) -many drugs (eg cocaine, amphetamine) exert their effects by affecting DA transmission |
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dopamine pathways (3) |
mesolimbic: VTA (ventral tegmental area) --> nucleus accumbens mesocortical: VTA --> frontal cortex nigrostriatal: substantia nigra --> striatum |
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agonist |
chemical that binds to a receptor and activates it to produce some response |
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antagonist |
blocks or dampens activity of agonist |
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example of endogenous agonist |
transmitter |
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example of exogenous agonist |
drug |
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what does a competitive antagonist do? |
binds to receptor and blocks other agonists from binding to receptor |
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what does a non-competitive antagonist do? |
binds to a receptor, allows other transmitter to bind, but the other transmitter does not (can not?) activate |
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what are MAOIs and what do they do? |
monoamine oxidase A inhibitors prevent monoamine oxidase A from degrading monoamines |
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what are SSRIs and what do they do? |
selective seretonin reuptake inhibitors (eg Prozac) bind to serotonin reuptake transporter and prevent reuptake |
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2 categories of perturbation methods |
behavioral and neural |
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behavioral brain perturbations function and example |
-measure cognitive functioning eg accuracy, reaction time |
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what can be measured with neural perturbations? give examples |
examine brain tissue and structure (histology, MRI) observe how brain activity relates to function (fMRI, PET, EEG) perturb brain and measure effects on function (eg lesions, DBS, drugs) |
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what are the ways that typical brain activity can be disrupted by? (4) |
lesions electrical/magnetic stimulation pharmacological manipulations optogenetics |
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lesions |
neuropsychological approach: compare those with legions to those without and look for preserved and impaired cognitive functions |
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what does lesion evidence from HM suggest? |
his hippocampus and surrounding medial temporal lobe areas are important for the formation of new declarative memories |
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limitations of lesion studies (6) |
-"localizationist" -- ignores networks, parallel processing -relies on the "serendipity" of someone getting injured -single or few case studies -damage might be diffuse -cognitive function might be globally impaired -given brain plasticity, connections might be modified following injury |
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stimulations define identify 2 types |
alter electrical transmission in brain and examine effects on cognition intracranial stimulation: inside skull extracranial stimulation: outside skull |
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strengths of intracranial stimulation (3) |
can stimulate different areas and see how it affects behavior patient already having surgery can vary strength of stimulation and see effects |
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limitations of intracranial stimulation (5) |
-invasive -limited to studies in humans who require neurosurgical interventions -stress of being in OR and/or medications might affect behavior -time constraints limit experimental paradigms -retesting usually not possible |
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strengths of extracranial/transcranial (5) |
-can stimulate different areas and see how it affects behavior -can create inhibitory and excitatory effects -can create short-acting lesions and examine within-subject effects -can be performed in healthy people -can be combined with other imaging, e.g. fMRI |
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limitations of extracranial/transcranial (2) |
-not as localized as we might like -- typically a large area of the brain is stimulated -can only stimulate areas of the brain near the surface of the skull |
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what are the ways to examine how drug manipulation can affect typical brain activity? (3) |
1. look at people with history of use or abuse 2. administer drugs to humans (agonists: enhance neurotransmitter effects; antagonists: block neurotransmitter effects) 3. administer drugs to animals |
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strengths of drug manipulations (1) |
can provide data about specific chemical systems in the brain and how they relate to cognition |
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weaknesses of drug manipulations (4) |
possible selection bias systemic (whole brain & body) effects neurotransmitters often interact with each other ethical considerations |
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optogenetics |
biological technique which involves the use of light to control cells in living tissue, typically neurons, that have been genetically modified to express light-sensitive ion channels |
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brain observation methods (4) |
direct electrophysiological recording of neuron activity in animals electrophysiological recording in humans structural brain imaging (SMR) functional brain imaging (fMRI and PET) |
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describe direct recording of neural activity (4) |
-insert electrodes into brain of animal -record electrical activity (action potentials), usually of groups of neurons -usually extracellular activity -have the animal perform a task while neuron activity is recorded |
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limitations of direct recording of neural activity (3) |
can usually record from only 1-2 places in brain quite difficult to do, very invasive almost always in animals, so limits on types of tasks |
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describe EEG recording |
electroencephalographic recording place electrodes in specific locations on the scalp record electrical activity of large groups of neurons in each region |
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strengths of EEG (2) |
electroencephalography high temporal resolution relatively direct measure of brain activity |
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weaknesses of EEG (2) |
low spatial resolution different sensitivity to different regions, e.g., fairly insensitive to signals in deep brain |
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spatial resolution |
tells you what the smallest feature you can see based on the detector (smallest detectable distance, like .001 mm) |
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temporal resolution |
tells you how quickly you can measure things frames per second |
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what does sMRI stand for? |
structural magnetic resonance imaging |
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what can MRI tell us? (2) |
structure: -high-resolution images of fluid, fat, bone, etc -evaluate tissue density, cortical thickness, size, differences, etc |
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what can't MRI tell us? (3) |
-brain activity/function -blood flow -neurotransmitter activity |
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what can fMRI tell us? (2) |
function: indirect measure of brain activity brain activity specific to certain tasks, conditions, and mental states |
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what can't fMRI tell us? 2) |
neurotransmitter activity actual neuron activity |
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what does PET stand for? |
positron emission tomography |
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what can PET tell us? (2) |
brain function: measures of metabolic processes can measure multiple neurotransmitters, glucose, etc, depending on the ligand |
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what can't PET tell us? (2) |
more rapid changes in brain activity relatively low temporal and spatial resolution |
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converging evidence |
every experimental method has limitations these limitations are different converging evidence using multiple methods that all point to the same conclusion help to overcome individual limitations |
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gyrification |
process and extent of folding of cerebral cortex (i.e. creation of gyri and sulci) during brain growth |
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migration |
migration occurs inside-out -first-formed (oldest) neurons form deepest layer of cortex -last-formed (newest) neurons form outermost layer |
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what is myelination? when does it begin and when does it end? |
formation of myelin sheath around nerve fiber begins ~29 weeks gestation many major tracts not fully myelinated until adolescence or beyond |
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gestation |
process of carrying or being carried in the womb between conception and birth |
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synaptogenesis |
elaboration or formation of synapses (connections between nerve cells and target cells) occurs from birth to about 2 years? |
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synaptic pruning |
reduction of synapses leaving more efficient synaptic configurations (occurs during age 4 and 6?) |
