2704658
| Question | Answer |
| What are main afferent pathways? | - posterior column: fine touch, pressure, vibration, proprioception (crosses in medulla) -> thalamus - anteriolateral (spinothalamic): l: pain/temperature, a: crude touch, pressure (crosses in the sc) - spinocerebellar: proprioception (cross two times, so stays at the same side) |
| Size of the brain, number of neurons/synapses? | ~1400ml, 150ml blood/csf; ~1700mg; ~86billion neurons (3-4 as much glia), 16bil neocortex, 69bil cerebellum, 30000 synapses in the cerebellum, average in neocortex ~7000, loss after 25: 1/second, length of myelinated axons - 150000-180000km in total |
| What are the three layers of the embryo? What do they develop into? | Endoderm (inner organs), mesoderm (muscles, sceleton), ectoderm (nervous system, skin) |
| What is gastrulation? | When blastula is reorganized into a three-layered gastrula |
| What is neurulation? Describe it! | Folding process from the neural plate to the neural tube; tissue thickens, borders differentiate from ectoderm (become neural crest when neural plate folds to neural groove), neural tube closes, neural crest layer over it (PNS) |
| How are neurons being created in the embryo? | proliferation in ventricular zone of the neural tube; neural stem cells -> slightly more differentiated neuroblasts/glioblasts(precursor cells/immature neurons/glia cells), asymmetric division -> nb/gb -> nb/gb + a postmitotic neuron; |
| How do neuroblasts migrate? | From inside to outside (excp: cerebellum), guided by radial glia (not only for scaffold but also progenitors for the actual glial cells), some take other route -> resulting horizontal dispersion migration to nuclei and PNS -> cell adhesion molecules; each group of stem cells in the ventricular zone -> column of closely interrelated neurons in the cortex |
| Brain vesicles? | 3 primary vesicles (prosenc, mesenc, rhombenc) -> 5 secondary (telenc: cortex, basal ganglia, subcortical white matter; dienc: thalamus, mamilary bodies, optic nerve, optic vesicles; mesenc: tectum, tegmentum, cerebral peduncles; metenc: cerebellum and pons; myelenc: medulla) |
| Neurons/glia? | neurons: stellate (interneurons), pyramidal (projection neurons), limited capacity to proliferate (DG, olfactory bulb); astrocytes (support, nourishment, BBB), microglia(immune system), oligodendrocytes/Schwann cells (insulation), ependyma (production of CSF) |
| Synaptic transmission? | AP arrives, triggers opening of Ca+ channels -> Ca+ makes vesicles fuse w/the membrane, NT bind with the receptors, postsynaptic receptors make channels open/close, receptor activation -> postsynaptic current causes EPSP or IPSP, their sum decides whether postsynaptic AP; some NT associated w/ certain effect, but the final effect determined by postsynaptic signaling cascade |
| GM/WM? | GM: 95% of the oxygen, cerebral cortex, nuclei WM: bundles of axons, glia cells, projection tracts: away from cortex; comissural tracts: to cortex in other hemisphere, association: cortex of the same hemisphere |
| Cortex layers? | allocortex = 3-4 layers (archicortex, oldest, 3: hippocampus, olfactory cortex, subcallosal area; paleocortex, 3-5: parahippocampal area, olfactory bulb), mesocortex (3-5, CG), isocortex (6, neocortex), different cell types in every layer, regional differences in the laminar features -> functionally specific, diameter gives insight in connectivity |
| Connectivity/Structure of the layers? | Layer I: molecular level, synapses, few cell bodies Layer II: modulatory input (densely packed stellate cells -- interneurons), extragranullar layer Layer III: small pyramidal cells, corticocortical connections --> those 3 layers are supragranular level (intracortical connections) Layer IV: stellate cells, main input from thalamus (pulvinar -> parietal, medial dorsal nuclei -> frontal), most prominent in primary sensory regions, no pyramidal cells (internal granular layer) Layer V: pyramidal and giant benz cells, main output to subcortical structures, most developed in motor areas, pulvinar also gets some Layer VI: main projections to the thalamus, feedback on what thalamus projected to the layer 4 (morphologically diverse) (5 and 6: infragranular levels) motor areas: agranular cortex bc granular layers II and IV less developed; subcortical modulation to all layers -> learning, motivation, arousal |
| Brodmann? | areas based on cytoarchitecture/cellular composition in cortex/layers, corresponds very well with functional mapping of the cortex |
| how does myelin serve faster signal communication? | current doesn't leak out, electrical insulation, increases membrane resistance and length constant (= distance before AP decreases); AP elicited at Nodes of Ranvier flow passively to the next one where they initiate another AP, no need to open sodium channels at every step along the axon (a way to increase velocity without myelin would be to increase diameter to decrease internal resistance) |
| oligodendrocytes/schwann cells? | CNS/PNS, processes wrapping up to 50 axons/1:1 correspondence (lies directly on an axon) |
| what do I know about astrocytes? | most abundant, structural/metabolic support (nourishment), detoxification, clearance of neurotransmitters, reaction to injury, tripartite synapse (can react to NT in an integrated way and modulate the synaptic transmission by releasing NT itself), part of BBB (wraps around blood vessels), protoplasmic in GM, fibrous in WM |
| microglia? | brain immune cells, normally scanning the environment, sensing on/off signals -> change form, gather around the injury site, produce immune response molecule, proliferate; if cell death -> phagocytosis |
| what are seven basic parts of the nervous system? | caudal to rostral: spinal cord, medulla, pons, cerebellum, midbrain, diencephalon, cerebrum |
| Telencephalon (cerebrum/forebrain)? | - interhemispheric cleft, connected by CC, AC and PC - some lateralized specialization (language...) - contralaterality since majority of sensory/motor connections cross below forebrain - primary sensory (main input/output for a given modality)/ higher association (integration, cross-talk within the brain, cognition) cortices |
| Gyri and sulci? | serve the extension of surface, 2/3 of the cortex surface are in sulci, primary sulci identical across humans, secondary/tertiary -- highly individual; Sulci: - Interhemispheric cleft - sylvian fissure (=lateral sulcus; insula hidden within covered by opercula) - central sulcus (dominant motor hand area - omega shaped knob; pre-/postcentral gurys = motor/somatosensory) - calcarine sulcus (between temporal and occipital lobe) - intraparietal sulcus (superior/inferior parietal lobule on both sides) - Heschl gurys (primary auditory cortex, lies deep in sylvian sulcus, runs mediolaterally) |
| Lobes? | frontal, parietal, temporal, occipital, (insula), (limbic); prefrontal cortex: lies anterior to premotor cortex; lateral, medial, orbital; executive functions, highest relative increase in evolution |
| different prefrontal lobe functions? | general: selection, planning, execution of appropriate behavior dlpfc (not an anatomical structure, rather functional): end point of the dorsal stream, working memory, supervisory attention system ("what is consolidated?") vmpfc: processing of risk and fear, decision making+reward processing (adaptive decisions), planning, social restraint mpfc: learning auditory and verbal associations, spatial memory, self-referential activity, ofc: limbic, emotional responses |
| executive functions? | decision-making, action initiation, planning, mental flexibility, impulse control and inhibition, monitoring, error detection, working memory, sustained attention |
| dysexecutive syndrom?/problems with prefrontal lobes? | - problems with executive functions - difficult assesment: a lot of possible reasons to fail tests ("hot": disinhibition, high impulsivity/ "cold": preservation, inflexible thinking) - early prefrontal lobe disease: social/cognitive impairment (lack of willpower etc) - bilateral advanced symptoms: severe cognitive impairment - dlpfc lesions: apathy, hypokinesia, indifference - ofc lesion: hyperkinesia, increased instinctual drives |
| Ways to access dysexecutive syndroms? | Wiskonsin card sorting test (mental flexibility, goal-monitoring, working memory); nonverbal working memory (preservation, errors), go/no go tasks (error rates and reaction times), frontal assesment battery (to differentiate between alzheimers and frontoparietal dementia) |
| What is basal ganglia? | group of subcortical nuclei (caudate (association) + putamen (sensorimotor)= dorsal striatum, separated by internal capsule; N.Acc = ventral striatum; external and internal Globus pallidus, substantia nigra pars compacta and pars reticulata), subthalamic nucleus |
| Circuitry and connectivity of the basal ganglia? | main input structure: dorsal striatum from cortex (putamen: rather motor, caudate: frontal association, frontal eye fields) main output structures: GPi and SNr --> only to thalamus, superior colliculus, and pedunculopontine nucleus (what?); all nuclei are inhibitory except STN; |
| Direct/indirect pathways? | Direct: facilitation of appropriate movements (striatum gets excited by cortex and inhibits the tonic inhibition of GPi/SNr -> vetral lateral/ventral anterior thalamus is freed from inhibition and excites cortex back) Indirect: inhibition of inappropriate movements (striatum inhibits inhibition of GPe, its inhibitory effect on STN is decreased and STN starts to excite GPi and SNr to perform their inhibitory effects on thalamus); SNr synapses directly in superior colliculi for quicker eye movements |
| Role of dopamine in BG? | nigrostriatal projection from the substantia nigra pars compacta to the striatum; direct pathway striatal neurons: D1 receptor, activate striatum indirect pathway striatal neurons: D2 receptor, inhibit striatum DA increases the excitatory effect of the direct pathway (causing movement) and reduces the inhibitory effect of the indirect pathway (preventing full inhibition of movement) --> motivational influence on the motor performance (more D1 activation -> shorter RT or quicker movement) |
| BG and cognition? | involved in selecting and enabling cognitive, executive, or emotional programs stored in the cortex (prefrontal and limbic); trial-and-error based learning (select a rewarding action guided by dopamine, stereotyped firing pattern with time), stimulus-reward-learning (non-motor, incremental learning of stimulus–response associations, take turn A if stimulus A etc -> fire at the end and beginning), adequacy of behavior and pathology (gambling, Tourette, selecting wrong cognitive schemas or not being able to suppress inappropriate); |
| Function of BG? | - modulation of activity anticipating and during movement; help to switch between movement commands, movement selection - action selection: which of the actions cortex might be planning gets executed (DA - reward-based learning) - coordination: support the needed action (arm up), suppresses opposing action (arm down), turn up commands when it's their turn and turn them down when not; when behaviour learned: enable the appropriate motor/cognitive plan, then evaluating the reward at the end, - coordination of multi-joint movements - regulation of stance, posture, gait (highly automatized movements) |
| Parkinson? | slowness or absence of movement, resting tremor, loss nigrostriatal DA neurons, tips the balance in favor of activity in the indirect pathway, GPint neurons are abnormally active, keeping the thalamic neurons inhibited, without the thalamic input, the motor cortex neurons are not as excited, and therefore the motor system is less able to execute the motor plans in response to the patient’s volitio |
| Huntingtons? | involuntary, continuous movement of the body, selective loss of striatal neurons in the indirect pathway, the balance between the direct and indirect pathways becomes tipped in favor of the direct pathway. Without the normal inhibitory influence on the thalamus that is provided by the indirect pathway, thalamic neurons can fire randomly and inappropriately, causing the motor cortex to execute motor programs with no control by the patient |
| OCD (just for me) | worry inputs from OFC inhibit inhibition of thalamus --> hyperactivation back to the cortex; hyperexcitability, too much "error detection" although there is no error --> excessive erroneous messages about the problem and needing to act on it --> initiating of the "appropriate behaviour" |
| Structure of thalamus | - large mass of GM, a lot of subnuclei; relay + filtering - rough division: medial, lateral, anterior - important for consciousness - LGN: vision, MGN: auditory, ventrolateral+ventroanterior: to motor cortices (input from BG), mediodorsal: prefrontal (input from BG), ventralposteriolateral and medial: to somatosensory, different processing for different somatosensory modalities), anterior: input from mammilray bodies, projects to CG (regulates what input is redistributed to the cortex), pulvinar is driven by cortical input and provides input to the association cortices, intralaminar/midline nuclei: diffuse nonspecific projections to the cortex (widespread modulation) |
| Limbic system? | term still widely used although not a uniform circuitry, two subsystems (emotions/memory), OFC, CC, amygdala, hippocampus, parahipocampal gurys, |
| Hippocampus? | - retrocomissural part (primates), (supracomissural in rodents), body, head, tail, archicortex (3 layers), contains of dentate gurys (inner C) -> adult neurogenesis (formation of memories) is sucpetible to the release of glucocorticoids, CA1-4 |
| Hippocampal circuitry? | Input from sensory cortices & association cortex comes into enthorinal cortex (interface between cortex and hippocampus) -> DG -> CA3 -> CA1 (trisynaptic circuit); connections (fimbria and alveus) fornix -> MB -> anterior nucleus of the thalamus -> CG -> cortex |
| Functions of hippocampus? | encoding and starting the consolidation of declarative memories; combining external representations with internal motivation etc -> complex representations (memory), creating context; space cells help to create episodic memories; combines traces in the brain to one coherent memory; after the process of consolidation is complete memories are stored in the neocortex; procedural memory dependant on BG, amygdala, sensory cortices |
| categories of memory? | qualitative: declarative/procedural temporal: immediate memory, working memory, long-term memory |
| Amygdala? | almond-like nucleus essential for decoding emotions, and in particular stimuli that are threatening to the organism (emotional significance of the stimulus), conditioned fear response (emotional learning), fear reaction to threatening stimuli, anterior temporal lobe, adjacent to hippocampus, http://www.centersite.net/poc/view_doc.php?type=doc&id=48376&cn=1408 |
| Klüver-Bucy Syndrom? | removal/lesion of amygdala -> unable to distinguish fearful stimuli, recognize socia hierarchy, hypersexuality, abnormal oral behavior, reduced aggressiveness |
| Anatomy of amygdala? | - basolateral: receives majority of cortical input, projects to OFC and mpfc and mediodorsal thalamus (conscious perception of emotional states) - medial: olfaction - central group: projects to hypothalamus (physical expression of emotional states) |
| Addiction? | reward process spinning out of control, DA neurons fire in response to unexpected reward making striatal neurons more responsive to the cortical/amygdaloid input (stronger connection, rather chosen program, "repeat what you just did to get a reward"), decrease of receptors with repeated drug exposure, less drug effect http://neuroscience.mssm.edu/nestler/brainRewardpathways.html http://nutritionwonderland.com/2009/07/understanding-our-bodies-dopamine-rewards/ |
| LTP? | in NDMA receptor cells, especially powerful in DG, when enough AMPA receptors are activated (enough depolarization) Mg goes out -> NDMA is activated, Na+ AND Ca+ go in, Ca+ causes more AMPA receptors to be built, glutamate synthesis --> more synaptic strength |
| Parts of cerebellum? | - cerebrocerebellum (neo..) - hemispheres - spinocerebellum (paleo..): vermix - vestibulocerebellum (arci..): flocculus and nodulus, posture and equilibrium - deep cerebellar nuclei (dentate nucleus, interpositus x2, fastigius) (output), middle peduncle : cerebellar input through pons, inferior: output to medulla (spinal cord), superior: output to thalamus and SC |
| Inputs/outputs of cerebellum? | input (relayed in pons, crosses midline again -> ipsilateral): from cerebrum, spinal cord -> vermix (posture, head rotation, asceleration/desceleration, audiovisual input about position and motion), inferior olivary complex (current concepts place it as an "error detector", feedback loop) output: deep cerebellar nuclei -> superior peduncles -> ventrolateral thalamus -> M1, only 2,5% connections are efferent -> high convergence |
| Cerebellar circuitry? | https://www.dartmouth.edu/~rswenson/NeuroSci/chapter_8B.html#Circuitry input through mossy fibers to the granule cells in the deepest level (also exciting deep nuclei on the way) + climbing fibres from olivary nucleus, granule cells -> parallel fibres, A LOT of parallel fibers synapse with (and excite) each Purkinje cell, PC synapse on deep nuclei inhibiting them (to produce an appropriate output, inhibiting unwanted activity in the deep nuclei), simple spikes; climbing fibers -> individual relationship, powerful excitation, complex spike after which simple spikes are suppressed (error detection, when comparing intention and action yields an error -> powerful immediate inhibition, then deep nuclei are released) |
| Functions of cerebellum? | posture, balance, motor correction (feedback on ongoing movement, correction while movement being executed, dysfunctions: ataxia, hypo/hypermetria), motor learning (next time the movement is performed, it is performed more accurately from the beginning --> plasticity of the synapse between the PF and the PC (climbing fiber -> making all PF that were active undergo LTD, synapses that were active around the time of CFr input will be weakened, so that the next time the specific PF is active, it will have less of an excitatory effect on the PC -> each synapse can be adjusted during a process of learning to produce the correct cerebellar output, allows for procedural learning, where each time an action is performed, it becomes somewhat more accurate since the "right synapses" are contributing to the response, language (coordination of laryngeal muscles, dysfuction: scanning speech) |
| Elements of brainstem? | Midbrain (tectum/tegmentum), pons, medulla, cranial nerves |
| Cranial nerves? | Olfactory (nose) s -- smell Optic (retina) s -- vision Oculomotor (midbrain) m -- lid and eye movement, pupils Trochlear (midbrain) m - eye movement Trigeminal (pons) b - chewing + facial sensation Abducens (pons) m - some eye muslces Facial (pons) b - control of facial muscles, some taste (anterior) Vestibulocochlear (pons) s - hearing and vestibular Glossopharyngeal (medulla) b - salivation, sensation of skin, pharynx and taste (posterior) Vagus b - motor control of heart and viscera, sensation from thorax, pharynx, viscera Acessory m - control of shoulders and thorax Hypoglossal m - motor control of the tongue and some skeletal muscles |
| biogenic amines? | NT synthesized in the brainstem nuclei from AA tyrosine (dopamine, serotonine, norepinephrine, epinephrine, histamin) serotonin: raphe nucleus norepinephrine: locus coreulus (blue spot), implicated in arousal, attention, sleep |
| Reticular formation? | clusters of neurons in BS, positioned rostrocaudally ARAS: damage leads to coma or disturbance in vigilance, sleep-wake cycle rostral: modulatory function (biogenic amines), periaqueductal grey modulates pain perception (enkephalin-producing cells that suppress pain) caudal: premotor function node between upper lower MN and cerebellum, control of circulation and breathing |
| Deep cerebellum nuclei? | Dentate: to thalamus and premotor, parietal (and M1?), cross before thalamus interposed: spinal cord and M1 through thalamus (from spinocer) fastigial: brainstem and M1 directly (from spinocereb) (vestibular nuclei: from vestibulocerebellum to lower motor neurons, balance and vestibuloocular coordination) |
| Dysfunctions of cerebellum? | Ataxia (loss of order in movement), hypo/hypermetria, dysmetria (inability to judge distance) decomposition of movements dysarthria (slurred speech) lateral nystagmus |
| Photoreceptors? | Rodes: 90 mln, highly sensitive to light of every wavelength --> color insensetive, vision in dim light cones: 4.5 mln, lower sensitivity for light, mostly in the fovea (point of highest resolution), color-sensitive (specific for different wavelength) |
| how does visual information flow? | from retina -> optic nerve -> optic chiasm (TEMPORAL part stays, NASAL part crosses -> right visual field goes to left retina and left hemisphere) -> optic tract -> to hypothalamus (circadian control), SC (saccades), pretectum (pupils) and LGN -> through optic radiation (meyers loop - temporal lobe, inferior retinal quadrants, represents the superior visual field quadrants, upper loop - through parietal, upper rettinal quadrants, inferior visual field) to the V1 |
| Primary visual cortex? | simple cells -> bars of specific preferred orientation |
| secondary visual cortices? | V4 (color), MT (motion), complex, hypercomplex cells dorsal stream: how to interact with the object/where is the object/how does it move? ventral stream: complex object recognition, connects to semantic knowledge in temporal lobes |
| disorders of higher order visual processing? | achromatopsia (no perception of colour), cortical blindness (sometimes with blindsight), agnosia (no object recognition), prosopagnosia (no face recognition), alexia (impaired reading), akinetopsia (no perception of movement) Balint syndrome (no binding of a visual scene), hemispatial neglect |
| Parts of the ear? | outer ear (distortion of sound waves according to where they came from -> localization), middle ear (amplification of the sound by tiny bones), inner ear (translation of the sound waves into electric signals in cochlea) |
| Auditory processing? | information proceeds from the Organ of Corti to the cochlear nuclei, many fibers crossing in the trapezoid body to the superior olive in the brain stem (bunaural input -> localization on horizontal level, loudness, pitch, time). Then all ascending fibers stop in the inferior colliculus in the midbrain (lateral lemniscus = fibers from both SOC and contralateral cochlear nuclei, Ncl. of the lateral lemniscus projects to both IC --> frequency-specific lamination, cells are spatiotopic - sensitive to the position of the sound, av integratin between IC and SC) and the medial geniculate body in the thalamus, before reaching the cortex in the superior temporal gyrus (tonotopic organization); monaural information: both horizontal and vertical localization, accuracy varies depending on where the stimulus is and its nature |
| Motor system? | M1: precentral gurys, layer V contains giant benz cells, somatotopic, upper and lower motor neurons premotor areas: rostral to M1, rather planning of the movement |
| Somatosensory system -- receptors? | thermoreceptors, nociceptors, mechanoreceptors (Merkels, Ruffini - SA, Pacinian, Meissner - FA), free or encapsulated, especially a lot on hairless skin, density varies with bodyparts (2point discrimination) |
| Somatosensory cortex? | primary: postcentral gurys, somatotopic secondary: connections to amygdala and hippocampus (tactile learning) |
| How to classify a neuron? | neurites: (pseudo)unipolar, bipolar, multipolar, dendrites (spiny as pyramidal or stellate, aspinous as some stellate), connections (primary sensory, motor, inter) axon length (golgi type I - long, type 2 - short) NT |
| 5 fundamental types of neurons? | inhibitory local (Gabaergic interneurons)/distant (Purkinje) excitatory local (stellate cortical cells)/distant (pyramidal cortical cells) modulatory (influence neurotransmission, often at large distances) |
| 5 steps in the neuron? | intrinsic activity reception integration encoding output |
| active/passive electric signals? | AP (active response): summary of passive responses (de-/hyperpolarization, central role in AP propagation) |
| explanation of the membrane potential? | 1. differences in concentration (more potassium inside, more sodium outside) 2. difference of permeability (high for Ka+, low for Na+) permeability determines which ion contributes most -> membrane potential is close to Ka+ reversal potential --> there is a chemical and electrical gradient at the electrochemical equilibrium |
| why is there a difference in the ion concentration? | active transporters (can move ions against concentration gradient) |
| why is there different permeability? | selectively permeable ion channels (down the concentration gradient) |
| what if you change ion concentration? | if you increase Ka+ concentration outside resting membrane potential will decrease (slow depolarization) bc Ka+ ions dont have this much pressure to go outside now, so not so much negativity because of ions who have left; if you decrease Na+ concentration outside: lower AP amplitude (why? less ions to get in? less concentration gradient?), no effect on resting potential (bc of low permeability) |
| AP? | - consists of a rising phase, overshoot, falling phase, undershoot - comes into being because more sodium ions diffuse into the cell than potassium ions diffuse out of it (bc pf NT and opening of receptor channels)-> opening of the sodium channels -> increase in permeability, AP when Na+ permeability bigger than Ka+ permeability, Na+ influx bigger than Ka+ influx, falling phase: Ka+ goes out bc too much positivity inside, needs to achieve equilibrium -> membrane potential starts to go to normal, repolarization when only Ka+ channels open (continue to diffuse out until the equilibrium is reached), hyperpolarization: potassium permeability is unusually high driving the membrane potential even closer to potassium reverse potential (the increased potassium ion permeability lasts slightly longer than the time required to bring the membrane potential back to its resting level), after that Na+/Ka+ pump reestablishes the resting membrane potential; |
| AP II? | all or nothing (depolarization increase results in the increase of frequency, maximum frequency is limited by the absolute refractation period), That is to say that the absolute refractory period limits the maximum number of action potentials generated per unit time by the axon. |
| Propagation of the AP? | The entry of positive charge during the AP causes the membrane just ahead to depolarize to threshold (passive flow to the next node of ranvier, decreases with distance (length constant) -> active conduction, stable intensity), hops from one node to another (saltatory conduction); velocity of propagation depends on internal resistance (axon diameter, less resistance in the cytoplasm if diameter bigger) and membrane resistance (leakage/isolation of membrane, less resistance -> bigger length constance, less leakage along the way) velocity can be a clinical marker |
| electric synapse? | pre- and postsynaptic element, gap junctions made out of connexoms, ionic current flows through them, also other molecules like ATP can pass, can be bidirectional, extremely fast -> precise synchronization |
| Criteria of a NT? | 1. substance present in the post-synaptic neuron 2. release calcium-dependent 3. according receptors post-synaptically |
| Two types of NT? | small molecule transmitter (small clear core vesicles): synthesized in the synaptic terminal, enzymes needed are transported with slow transport (Ach, GABA), low frequency stimulation large molecule transmitter/prepeptides (large dense-core vesicles): being transported from soma, larger vesicles because enzymes cleave them to the ready peptides on the way (fast transport) (enkephalin, substance P), high-frequency stimulation |
| Two types of the receptors? | Ionotropic (ligand-gated ion channels. fast processing) Metabotropic (slower processing, G-protein coupled receptors, causes a chemical cascade) |
| example of a muscle weakness disorder? | lambert-eaton syndrome: there are unwanted antibodies to the ca+ ion channel proteins at theneuromuscular endplate (too little Ca+ goes inside, to little Ach released) |
| postsynaptic potentials? | EPSP -> NT open ion channels permeable for cations, influx IPSP -> open ion channels permeable for anions --> increase or decrease the likelihood of the AP, sum determines whether firing or silence, active or passive response |
| nernst and goldman equation? | Nernst: which membrane potential will be established for this one ion based on its concentration and valence (given that only those channels are present)? -> the potential at which the ion is at equilibrium Goldman: same but when multiple ions contribute to the membrane potential, also considers permeability, the one with the largest one contributes most |
| five somatosensory modalities and their receptors? | - touch (discriminative) (merkel, ruffini (+stretch), meißner, hair) - vibration (Pacinian) - temperature (free nerve endings) - nociception (free nerve endings) = cutaneous mechanoreceptors - proprioception (muscle spindle detect the length of the muscles + golgi tendon organ detects changes in tension) |
| rapidly and slow adapring receptors? | SA: Ruffini and Merkel (stretch and tactile discrimination + slow vibration) RA: Pacinian and Meissner (high-frequency vibration, skin motion (the reason we don't feel our clothes) |
| S I ? | - somatotopic organization - 1, 2, 3a, 3b, each body region in every SI region, different szbmodalities in every SI region - 1: RA from skin - 2: complex touch from skin, deep tissue (pressure and joint position) - 3a: deep tissue (muscle stretch) - 3b: SA and RA from skin - columnar organization (SA/RA), - layers --> functional segregation and localization |
| Corticocortical connectivity of S1 and S2? | - main thalamic input to S1 goes to 3b - input from S1 convergently goes to S2 and posterior parietal cortex (attentional modulation, sensorimotor integration) - S2 connects to amygdala and hippocampus (tatcile learning) - parietal cortex strongly connects to the motor areas (as most input to parietal is from 3a and 2 -> pathway to connect proprioception to the motor -> link between current state and the goal, my joints are like that, i need to move them this and this much to reach this motor goal) |
| motor cortex/pathways? | corticospinal (cc -> sc -> muscles) through internal capsule and cerebral peduncles modulatory: through cerebellum and BG to thalamus and back both BG and cerebellum project to SC SC has the final common path; M1 somatotopic, precentral gurys, upper and lower motor neurons, anterior horn of spinal cord |
| does M1 code for muscles or movements? | rather movement synergies (individual muscle representations distributed over cortex (because different neurons can synapse on the same muscle, like if it's involved in different movements) + overlap of eg shoulder and wrist muscles) firing isnt correlated with isolated muscles but whole movements, M1: higher level of abstraction topographic representation = behaviorally relevant categories of motor behaviour Movements of individual muscles are correlated with activity from widespread parts of the primary motor cortex. Similarly, stimulation of small regions of primary motor cortex elicits movements that require the activity of numerous muscles. Thus, the primary motor cortex homunculus does not represent the activity of individual muscles. Rather, it apparently represents the movements of individual body parts, which often require the coordinated activity of large groups of muscles throughout the body. |
| SMA and PM? | PM: selection of appropriate motor plans for voluntary movements/preparation and planning, guidance of movement, more related to visually guided, PMd (eye movements, reaching) PMv (mirror neurons, sensory guidance of movement planning, sequential motor actions) - information from other brain regions to choose an action appropriate to the context - understanding actions of others - connections to cingulate: emotional somatic behaviour - selection of action based on external events SMA: more related to internally guided more planning of self-initiated movements coordinating both sides of the body, postural stability SEF: saccadic movements pre-SMA: action selection, task-switching, inhibition, no direct projection to M1 but to dlpfc (Whereas the premotor cortex appears to be involved in selecting motor programs based on visual stimuli or on abstract associations, the supplementary motor area appears to be involved in selecting movements based on remembered sequences of movements.) |
| Pyramidal/extrapyramidal syndromes? | - hemiparesis (corticospinal tract) - hemmiballism or hyperkinesia (STN - hyperdirect pathway -> thalamus overexcited) - hyper/hypokinesia - disbalance in direct/indirect pathway - |
| examples of plasticity? | - removal of one digit --> other digits take over the space, -- sensory substitution (processing of non-visual information in V1 as a result of perceptual deafferentiation in V1, V1 lights up when reading braille in congenitally blind) -- changes in S1 bc of experience, learning -- changes of a movement representation in M1 if movement excessively trained, seen in fmri (bigger activated area for a trained digit or a trained sequence, Motor skill learning induces functional plasticity not only in M1!) |
| LTP features? | - state-dependent (postsynaptic cells must be depolarized enough) -- specificity: only the synapse that fire together wire together, not other synapses from those two cells -- associativity: if one synapse is weakly active when a neighbouring synapse is strongly active, they both undergo LTP -- timing |
| LTP/LTD? | - different calcium cascades: LTP - high-frequency stimulation, high-amplitude rise in Ca+ concentration leads to activation of protein kinases -> new AMPA receptors, LTD - low-frequency, low-amplitude rise of Ca+ concentration, protein phosphatases, AMPA receptors are internalized, less responsive to glutamate |
| spike-timing dependent plasticity? | efficiency of a synaptic connection between two neurons may be regulated by the precise timing of the joint activity of the neurons; if an input spike to a neuron tends to occur immediately before that neuron's output spike, then that particular input is made somewhat stronger. If an input spike tends to occur immediately after an output spike, then that particular input is made somewhat weaker. Thus, inputs that might be the cause of the post-synaptic neuron's excitation are made even more likely to contribute in the future, whereas inputs that are not the cause of the post-synaptic spike are made less likely to contribute in the future. BUT depends on even more things! |
| BCM theory/homeostatic plasticity? | capacity of neurons to regulate their own excitability relative to network activity; to prevent excessive potentiation/ depression; compensatory changes; http://synapses.clm.utexas.edu/lab/harris/lecture20-21/sld044.htm -> Prior history of high neuronal activity reduces the amount of LTP, threshold saying whether the synapse will be potentiated or depressed slides according to prior activity |
| structural plasticity? | - new synapses can be formed, e.g. in an enriched environment (Functional and structural changes typically go hand in hand) - Learning-induced structural plasticity enhances the turnover of subpopulations of new and pre-existing synapses specifically in excitatory neurons involved in the learning, and leads to the selective stabilization of some learning-induced spines (better in enhanced environemnt, The enhanced structural plasticity baseline levels underlie improved behavioural learning upon enrichment) |
| adult neurogenesis? | in subventrical zone in lateral ventricles and subgranular zone in hippocampus --> a role in learning and memory? |
| what does neuroplasticity involve? | changes in synaptic transmission: LTP and LTD (timing and prior states matter -> spike timing-dependent and homeostatic plasticity); structural changes: new dendrites/synapses (modulations of spines led to a change in the FC), neurogenesis |
| Learning-related structural plasticity in humans? | juggling: significant changes in GM between controls and subjects even after training, also changes in WM, aerobic exercise training increases the size of the anterior hippocampus, leading to improvements in spatial memory, learning-related structural plasticity even in a pathophysiological disease state such as in PD (compensatory in the cerebellum?) |
| TMS? | TMS: electromagnetic induction for weak electric current, induces action potentials, can measure intracortical/hemispheric exhibition/inhibition, rTMS modifies excitability (low/high frequency, effects outlast stimulation), can be used for diagnostic & rehabilitation, TBS (TBS after-effects are NMDA receptor dependent!), PAS (multimodal LTP production + plasticity induction, follows STDP rules and homeostatic plasticity), BUT a lot of determinants |
| tDCS? | modifies neuronal activity by a tonic de- or hyperpolarization of resting membrane potential (no APs!), Combining training with brain stimulation facilitates learning outcome! Effects are relatively short-lasting though! (approx. 30 min) |
| hypothalamus? | - coordinates somatic and visceral response: homeosthasis (body temperature and blood composition) - periventricular zone: SCN, regulate the outflow of (para)sympathetic regulation, neurosecretory (to the anterior and posterior putiitary) |
| putiitary? | - posterior (part of the brain): large magnocelullar neurosecrotory cells --> release neurohormones into bloodstream (oxytocin involved in interpersonal communication, lactation, bonding and vasopressin checks blood volume and salt concentration), both peptides - anterior: an actual gland, cells synthesize and secrete a wide range of hormones, master gland, parvocellular neurosecretory cells release hypophysiotropic hormones into bloodstrem (hypothalamopituitary blood circulation), travel to pituitary cells, make them suppress or produce hormones |
| example of the control by the pituitary? | - pC cells decide whether a stimulus is stressful, release CRH, it reavles to the antrrior, provokes release of the ACTH, it travles to the adrenal gland and stimulates cortisol release, self-regulating feedback |
| ANS? | - part of PNS, para- and sympathetic, widely coordinated control, commands every other tissue other than muscles that is innervated (glands, smooth muscle, cardiac muscle), disynaptic pathway (pre/post ganglion) - sympathetic: ganglion cells close to the spine (chain), (or synapse on ganglions in abdominal cavity) widespread effects, -parasympathetic ganglia -> close to the organs - preganglionic neurons of both release ACH - postganglionic: Ach in PARA (mostly muscarinic), norepinephrine in SYM (far-reached, even in the blood) - enteric division embedded in the lining of the organs like stomach... - HYPOTHALAMUS is the main regulator of the preganglionic autonomic function - nucleus of the solitary tract: in medulla, integrates information from internal organs and cooperates output of the autonomic brainstem nuclei |
| drugs used in ANS? | -sympathomimetic: promote NE or block the muscarinic actions of ACh -parasympathomimetic: other way round |
| modulatory systems of the brain? | - widespread diffuse connections, core is a small set of neurons in the BS, each axin can influence up to 10000 others |
| NE? | - locus coerulus, attention, arousal, sleep-wake, mood, anxiety, pain - more active: general arousal by interesting events in the outside world, making brain more responsive to the salient stimuli, more efficient |
| 5-HT? | - nine raphe nuclei - fire most rapidly during wakefulness, when an animal is aroused and active - sleep-wake, arousal, mood |
| DA? | - vta and sn - sn: fasciliating the voluntary movement initiation (shift towards indirect pathway) - vta: assigns value (reinforces) adaptive behaviors |
| ACh? | - basal forebrain complex (nuclei scattered): probably arousal, one of the first to die in ALZ - pontomesencephalotegmental complex: mostly acts on dorsal thalamus: excitability of sensory relay nuclei |
| what happens after and before food? | - brain needs glucose as much as oxygen, body is programmed to store energy - after food - prandial state, energy replenished as glycogen (muscles/liver) and triglycerine (fat) -> anabolism - between food: postabsorbic state, they are being broke down into glucose (catabolism) - there must be a mean of regulation to compare the energy ressources and its consumption (long-term regulation to maintain body's fat reserves and short-term regulation to control frequency and size of meals) --> lipostatic homeostasis |
| elevated peptin levels? | - feeding is stimulated when detects a drop in hormones released by fat cells (leptines, "satiety hormone") - leptine tells you to decrease appetite and increase energy expediture - lesion of lateral H - anorexia - lesions of ventromedial H - obesity - leptin -> receptors of arcuate nucleus -> anorectic peptides (number according to leptin) -> periventricular nucleus (humoral response -> release of hypophysiotropic hormones as TSH and ACTH into anterior puitary), controls activity of the sympathetic system, inhibiting feeding by projecting into lateral H |
| decreased leptin levels? | - turning off the anorectic peptide response AND stimulating another type of neurons in the arcuate nucleus (with orixogenic peptides Y and Agrp) -> inhibit the secretion of ACTH and THS, activate the parasympathetic division, stimulate feeding behavior activation of a receptor in the lateral h -> decreased feeding, blocking -> increased feeding |
| lateral hipothalamus? | - a group of cells receiving peptid input from arcuate nucleus releases melanin controlling hormone and orexin that partly has monosynapses to the neocortex -> motivates us to eat |
| short-term regulation of feeding? | during a meal: cephalic (anticipation, parasympathetic and ANS activated), gastric (saliva and digestion responses more intense when actually eating), substrate(nutrients begin to be absorbed), ghrelin: hormone released when hungry, activates Y and Agrp |
| how does the meal end? | - gastric distension (feeling full -> nucleus of the solitary tract) - cholecystokinin (present in some cells of stomach and enteric lining), also act on the vagus - insulin (to transport glucose into cells, anabolic and catabolic), glucose elevated when low insulin --> rise in glucose levels AND insulin signals to stop eating |
| reinforcement and reward? | - dopamin will reinforce the behavior that causes its release (response decreased by dopamine receptor blockers) - dopamine depleted animal behaves as it likes food but doesn't want food |
| serotonin and food? | - levels in hypothalamus are olw in the postabsorbic period, rise in anticipation, peak during eating (especially carbs), lower serotonine levels reduce satiety |
| what stimulates drinking? | - decrease in blood volume -> volumethric thirst, vasopressin reduces urine production - increase in the concentration of the dissolved substances in the blood -> osmomethric thirst |
| inhibiting rules for behavior? reversal learning? | - pre-sma, dlpfc, ifg - ofc: change of context, persistance of previously relevant behavior |
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