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79 Cards in this Set
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- 3rd side (hint)
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NEUROTROPHIC FACTOR HYPOTHESIS: Soulble molecules secreted by target cells promote the survival of neurons past a critical period of development (Neurotrophins, TG-F B class of growth factors, IL- 6 class of cytokines)
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Neurotrophins have scepcific receptors and are expressed by unique populations on neurons that require these factors to survive during critical period of developmental cell death.
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How do the neurons from the retina know how to line up properly in the back of the brain to form a correct image? What theory can help explain this?
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The CHEMOAFFINITY HYPOTHESIS:
axon-target recognition relies on the matching between complementary chemical markers on axons to their targets. Often these markers are expressed in gradients |
Ephrins and eph Kinases are required for formation of the retinotopic map in the optic tectum
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How DO neuron cells decide how many neurons are needed for a specific structure? What does it need for this to happen?
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Developmental "Programmed cell death" (via apoptosis)
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initially, there is an OVERPRODUCTION of neurons and axonal connections in a target region as a failsafe toinsure that a sufficient # of connections develope for a specific strucutre. There is a CRITICAL PERIOD during embryonic or early postnatal development when the excess number of neurons innervating the target undergo active cells death
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What are the 4 major processes that regulate the final specificity of synaptic connections
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1. development of transient axonal targets
2. axon collateral elimination 3. synapse elimination 4. synaptic rearrangement |
-all occur during development
- many are ACTIVITY DEPENDENT -synapse elimination & rearrangement occur continuously in mature nervous system as part of normal learning process and memory storage. |
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how do EPHERINS help line up connections within the nervous system?
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What are the different factors that act on a developing growth cone?
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Contact Attraction
Substrate Bound Cues: e.g. laminin, cadherins, and fibronectin Cell Surface Interactions: e.g. NCAM, L1, fasciculin, EphB receptors/ephrin-B Contact Repulsion Substrate Bound Cues: e.g. chondroitin sulfate proteoglycans Cell Surface Interactions: e.g. EphA receptors/ephrin-A, semaphorins, NOGO, MAG Chemoattraction Diffusible Factors: e.g. netrins, Wnts, Shh Chemorepulsion Diffusible Factors: e.g. netrins, soluble semaphorins, slit, Wnts, Shh |
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How does SHH help guide axons in the spinal chord?
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Helps mediate midline crossing and longitudinal extention of axons. (Commisural attraction)
Hedgehog interacting protien (HIP) |
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What does this molecular guidence system help ensure?
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axons relaying pain and temp in AL pathway cross midline at appropriate levels of spinal chord and remain on the contralateral side until they reach their targets in the thalamus.
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This is usually the case for attractants & repellents, but what is special about Netrin-1 (attractant) for axonal development of the TROCHLEAR NERVE (CN4) ?
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What type of disease are linked with these genetic polymorphisims and disorders?
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Autisim Spectrum Disorder
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Although a large number of candidate genes have been identified as candidate risk factors for ASD, many of these variants have been found in only a very small subpopulation of individuals and families with ASD. However, many of these genes can be grouped into several broad functional categories: 1) known genetic syndromes, 2) genetic abnormalities affecting synaptic proteins or synaptic function (especially glutamate, GABA and serotonin), 3) calcium-related genes, 4) growth regulating genes, genes affecting chromatin regulation, genes associated with neuronal migration, and subfamilies of cell surface tyrosine kinase receptors.
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INDICATE what criteria a molecule must fulfill to be a neurotransmitter.
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DESCRIBE the rate-limiting steps and the principal precursors required for the synthesis of the following neurotransmitters:
a. acetylcholine b. cathecholamines c. 5-HT d. glutamate e. GABA |
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IDENTIFY major nuclei in the CNS with high concentrations of selective neurotransmitters (e.g. ACH, dopamine, norepinephrine, 5-HT, histamine).
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LIST the major neurotransmitters and DEFINE their classification based upon their chemical structure:
a. Biogenic amine (e.g. acetylcholine, catecholamines, 5-HT) b. Amino acids (e.g. GABA and glutamate) c. Neuropeptides (e.g. Opioid peptides) |
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The 5 major steps involved in chemical synaptic transmission are all targets for drugs. DEFINE the inactivation of neurotransmitter action by cellular uptake mechanisms and DISCUSS the mechanism of action of antidepressant drugs and CNS stimulants.
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*Fluoxetine= highly selective for seratonin
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Describe the enzymatic degradative pathways involved in the termination of neurotransmitter activity (e.g. MAO, COMT, GABA-T).
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Degradative Pathways of CA:
1. MAO: monoamine oxidase 2. COMT: catechol-O-methyl transferase Inactivation of catecholamines occurs by both degradation and active transport back into the presynaptic vesicle or postsynaptic terminals. Enzymatic inactivation occurs by monamine oxidase (MAO) located primarily in the outer membrane of the mitochondria, or catechol-O-methyltransferase (COMT), localized in the postsynaptic membrane. Inhibitors of MAO and compounds that block the reuptake of NE into presynaptic terminals have been used to treat depression. |
**how does alpha-keto relate to GABA?
GABA is the major inhibitory neurotransmitter in the CNS. Approx.25-40% of all nerve terminals contain this transmitter. GABAergic neurons contain glutamic acid decarboxylase (GAD) which converts glutamate to GABA. GAD is rate limiting in the synthesis of GABA. A specific pathway exists for the metabolism of GABA known as the GABA shunt. The shunt is a closed loop that acts to conserve the supply of GABA. Glutamate is then converted to GABA by GAD. GABA can be transaminated by GAB A-T to form succinic semialdehyde only if a-ketoglutarate is acceptor of the amine group. This reaction also transforms a-ketoglutarate into the GABA precursor glutamate. GABA is removed from the synapse by reuptake in both GABA nerve terminals and glial cells. In glial cells GABA is converted to glutamine which is transported to neighboring neurons to serve as a GABA precursor. |
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CONTRAST the synthesis and release of peptide versus small molecular weight neurotransmitters.
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Which enzyme is found in GABA neurons only?
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GLUTAMIC ACID DECARBOSYLASE
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DEFINE receptor, binding site, agonist, antagonist, allosteric modulation.
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DEFINE ionotropic and metabotropic receptors. What are the differences between the two?
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A.Ionotropic Receptors
Ligand binding results in the regulation of intrinsic ion channel activity therefore also named ligand-gated ion channels. Activation of ionotropic receptors produces a postsynaptic potential (PSP) change in the target neuron or cell. This is in contrast to the voltage sensitive channels which are opened by changes in membrane potential, e.g. Na+ channel. B. Metabotropic Receptors Ligand binding results in the activation of an enzyme resulting in the induction of an intracellular signal transduction cascade that is mediated by second messengers and/or phosphorylation. This results in the indirect gating of ion channels as well as longer duration of effects on cellular metabolism. |
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Which IONS do these IONOTROPHIC receptors use?
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Whats so special about the structure of the glutamate receptor compared to other ionotrphic receptors?What are the differences between AMPA, NMDA, and Kainate receptors?
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Structurally distinct from nACH and GABAA receptors
Do not conform to the typical 4 transmembrane-spanning structure seen with nACHR. Only 3 subunits completely transverse the membrane and one forms an incomplete pore loop Tetramers or pentamers composed of 2 different subunits NMDA receptors are unique ligand gated ion channels since they are also voltage dependent |
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What does Ach have to bind to on its receptor in order to be activated?
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2 ACH molecues bind on the 2 alpha-subunits
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What 4 things are required for a IONOTROPHIC Glutamate NDMA receptor to become activated?
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DEPOLARIZATION DUDE!!
Both LIGAND GATED and VOLTAGE SENSITIVE |
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Where can CNS depressents act on a GABA receptor? How do they work?
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Why do we need both AMPA and NMDA glutamate receptors to be present on the same synapse?
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Since the NMDA receptors pass cations only when the Mg++ block is removed by depolariza-tion, the NMDA receptor is both a ligand gated and voltage-sensitive channel. AMPA and NMDA receptors often co-exist on the same post-synaptic membrane in the CNS synapse.
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For DORSAL COLUMN MEDIAL LEMINISCUS tract: What are the 3 neurons involved in this (ascending) pathway?
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What happens if we damage these colums?
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for ANTERIORLATERAL SYSTEM: What are the 3 neurons involved in this (ascending) pathway? Where are their cell bodies located?
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What happens if you damage ALS? How would it be different from damaging DCLM tract?
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Damage to controlateral side? Ipsilateral side? (harder to tract down exactly where the lesion is...
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Think about what in a stroke would cause the mixed up pathology
(can't travel up through the lesion). |
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IDENTIFY the 2 (ascending) pathways that transmit unconscious proprioception to the cerebellum (upper half vs. Lower half).
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Clarkes nucleus only appears from C8 to L2
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Just muscle spidles and golgi tendon organ. remain more medial in spinal chord.
2nd order axon. starts in clarkes nucles & travel out , join inferior cerebellar peduncle Type 1&2 fibers. stays in dorsal column, synapse in accesory cuneate nucleus |
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For CORTICOSPINAL TRACT What are the 2 neurons involved in this (descending) pathway? Where are their cell bodies located?
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most of what we focus on is in the lateral corticospinal tract. (medial is a little bit later)
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What happens if you damage one the of the pathways along the corticospinal tract? (lots going on in the internal capsule... whoa...) Why do different types of lesions behave so differently? do they present so differently ?
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upper motor neurons play important role of chronic inhibition (tonic control) of lower motor neurons)... we get spasticity
Lower motor neuron= atrophy of muscle/ flacid muscle upper motor neuron= increased reflex response. very violent kick.(no descending control) lower motor neuron= no reflex happens. |
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What are you losing with this and why?
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lose ALS on other side of body
lose coricospinal tract in throacic region |
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hydrocephalus of spinal chord... usually happens in cerival region. What would you lose and why? What do patients usually present with first
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CSF in region diffused through central canal... expansion
loss of 2nd order neurons in ALS. expands to different dermatomes severe burns of hands that they never feel |
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What would be lost Here?
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get degeneration of upper and lower motor neuons
degeneration of corticospianl tract and lower body neurons as well |
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fasciulus gracislis degeneerated
seletively lose our dorsal columns. |
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Where is the lesion?
entire right side of the spinal cord. dorsal columns and horns (bilaterally). the corticospinal tract (bilaterally). lower motor neurons. the ventral half of the spinal cord . |
lower motor neuron problem and problem with ALS
problem with ventral |
occulsion of anterior spinal artery (affecting both ALS and other column) gray and white matter affected.
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5. DRAW the cross-section profile of the white and gray matter in the cervical enlargement of the spinal cord and show the location of the major ascending and descending pathways in the white matter.
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Which scan is best for looking at Gray vs. white matter? Cerebral hemorrhages? Bone structure? What color would those all appear?
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T1= gray vs white/ anatomy
T2= better for infarts than T1 CT= bones |
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What are the differences between the T1 and T2?
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If youre gonna fcuk up and cut a nerve, why is it better to do it closer to the target than the cell body? And why is it especially important to maintain muscle activity after this happens?
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As close to target organ as possible. If it takes to long, cellular and molecular components at the target site disintegrate.... and full fxn regeneration may never happen.
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Cellular Response at the Neuromuscular Junction: After the presynaptic axon degenerates, Schwann cells remain at the original site of the presynaptic terminal. The basal lamina remains intact in the folds of the postsynaptic junction and AcH receptors and other postsynaptic proteins remain at the postsynaptic membrane. The cellular and molecular components that remain at the neuromuscular junction provide a guidance mechanism by which axons can successfully reinnervate their appropriate muscle at the original postsynaptic site. However, if the regenerating axon does not reach the target muscle for many months, then these guidance cues gradually disintegrate and full functional regeneration does not occur.
Effects of muscle activity: Maintaining muscle activity either by electrical stimulation or by mechanical exercise can prolong the integrity of the postsynaptic scaffold & associated guidance molecules located within the postsynaptic membrane & associated basal lamina. |
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What two things can happen that makes CNS injuries more catostrophic than just PNS injuries
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1-primary Injury response (irreversable necrosis in the area)
2- secondary injury response -massive influx of excited neruotransmitter--> massive influx of extracellurlar Ca++--> apoptosis---> "EXCITATORY NEUROTOXCITY" -no associated extracellular basal lamina (like in PNS Schwann cells) that seperate bundles of myelinated axons. |
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VERY IMPORTANT!! What are 4 important differences between CNS injury and PNS injury?
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1. SECONDARY INJURY PROCESSES beginning after CNS trauma contribute to a neurotoxic environment that results in more extensive tissue loss.
2. ABSENT OR WEAK UP- REGULATION OF AXONAL GROWTH PROGRAMS in injured CNS neurons that support axonal regeneration. 3. REACTIVE ASTROCYTES AND DEGENERATING CNS MYELIN CONTAIN INHIBITORY MOLECULES for axonal regeneration. 4. PRODUCTION OF NEUROTROPHIC AND NEUROTROPIC FACTORS needed to support neuronal survival and axonal growth is absence or not sustained in the CNS. |
Experimental therapeutic strategies to promote axonal regeneration:
Use of peripheral nerve grafts or stem cells to bridge the spinal cord lesion. Administration of exogenous growth factor to enhance neuronal survival and stimulate axonal growth. However, the axonal regeneration that has been observed using these approaches does not extend very far into distal spinal cord. Inhibit the intercellular and intracellular signaling pathways that contribute to aborted axonal regeneration. Unfortunately, the amount of functional regeneration that can be achieved so far has been very limited. |
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7. DESCRIBE the following aspects of the adrenergic receptor subtypes:
a. anatomical location b. physiological effects they mediate |
Receptor subtypes and activation by NE and EPI:
1. alpha-adrenergic receptors: (activated by EPI, NE) a) alpha1 receptors mediate excitatory smooth muscle responses: i. mydriasis – due to radial muscle contraction ii. constriction of blood vessels everywhere (smooth muscle contraction) iii. piloerection 2. beta-adrenergic receptors: a) beta1 receptors mediate: (activated by EPI, NE) i. increased heart rate and myocardial contractility (cardiac muscle contraction) ii. increased renin release b) beta2 receptors mediate: (activated by EPI only) (Beta2 receptors are not innervated by SNS neurons, they are stimulated by circulating EPI.) i. bronchodilation (smooth muscle relaxation) ii. vasodilation in skeletal muscle blood vessels (smooth muscle relaxation) iii. liver - increased glucose release |
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4. DESCRIBE the following aspects of the cholinergic receptor subtypes:
a. anatomical location b. physiological effects they mediate |
Acetylcholine (cholinergic) receptors:
A. Nicotinic receptors: 1. nicotinic neuronal (NN) receptors mediate: a) stimulation of postganglionic neurons of PNS and SNS b) stimulation of adrenal medullary cells to release EPI and NE 2. nicotinic muscle (NM) receptors located at the NMJ mediate: a) contraction of skeletal muscle fibers B. Muscarinic receptors (various subtypes): 1. end organs of PNS - mediate all the effects of PNS stimulation listed above 2. sweat glands – innervated by cholinergic fibers in the SNS |
A. Acetylcholine (cholinergic neurons):
1. preganglionic neurons of SNS and PNS 2. preganglionic neurons of the SNS that innervate the adrenal medulla 3. postganglionic neurons of PNS 4. postganglionic neurons of the SNS that innervate sweat glands - sympathetic cholinergic fibers (special case) 5. alpha-motoneurons of the Somatic NS that innervate skeletal muscle B. Norepinephrine (adrenergic neurons) and Epinephrine: 1. postganglionic neurons of the SNS release norepinephrine 2. adrenal medulla secretes: norepinephrine - 20% epinephrine - 80% |
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Why would DIRECT ACTING CHOLINOCEPTOR (AcH) STIMULANTS (mostly parasympathetic effects) also cause an increase in sweat gland secretion?? WTF is happening?
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Sweat glands have a muscarnic receptor
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What is the difference between awake, non-REM sleep, and REM sleep on an EKG?
Where do Sleep spindles occur? Sharp wave ripples (and delta waves)? |
Stage one-- loss of alpha rythym= drowsiness
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The waking state is characterized by high-frequency, low-amplitude activity, whereas descent into non-REM sleep is characterized by decreasing frequency and increasing amplitude of EEG waves.
, rapid eye movement sleep is characterized by the reappearance of low-voltage, high-frequency activity that is remarkably similar to the EEG activity of individuals who are awake. |
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Why can't we just party all the time? Why even sleep?
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-critical role in memory consolidation
-rhythmic brain activity can cause changes in the post synaptic portion of excitatory synapses that are linked to enhanced synaptic function -homeostatic plasticity of the brain (tune down activity, while maintaing circuts) -metabolic clearance of metabolites |
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Accumulation of ADENSOINE can make you sleepy! why does this happen?
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wakefulness is associated with the accumulation of various brain metabolites such as adenosine, prostaglandins and cytokines, as well as of inhibitory amino acids such as GABA and glycine. Sufficient accumulation of such metabolites leads to inhibition of wakefulness promoting centers (like the SUPRACHIASMATIC NUCLEUS!
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Where exactly are the neurons located that stimulate wakefulness (AROUSAL oooo... sexy?)?
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Wakefulness and arousal appear to reflect activation of the reticular activating system, particularly a group of cholinergic nuclei near the pontine midbrain junction (Fig. 4). Many neurons in this region show high rates of discharge during wakefulness as well as during REM sleep, but not during non-REM sleep. Moreover, stimulation of these regions produces EEG patterns that simulate wakefulness. Activity within these nuclei is associated with initiation of wakefulness or REM sleep, whereas inactivity of these neurons is related to non-REM sleep. However, other nuclei and neurotransmitters also appear to be involved, particularly noradrenergic neurons within the locus coeruleus and serontergic neurons of the raphe nuclei.
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What things help you wake up and stay awake? (4 things in particular)
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-ascending projections from the brainstem are though to activate thalamo cortical networks
-suprachiasmatic nucleus -lateral hypothalamus -medial prefrontal cortex |
wakefulness in particular, ascending projections from the brainstem are though to activate thalamo cortical networks. Wakefulness may also involve activation of cells in the suprachiasmatic nucleus (SCN; both glutamatergic and neuropeptide-Y cells), lateral hypothalamus (LH where hypocretinergic/orexinergic cells synthesize hypocretin/orexin), and medial prefrontal cortex (mPFC; glutamatergic cells which could also directly activate the entire cortex
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Narcolepsy is a condition in which individuals go directly into REM sleep from wakefulness, rather than the normal process of prior non-REM sleep. This may be associated with cataplexy What the F is CATAPLEXY? Why does it happen? What are ways we could treat narcolepsy? AKA WHICH PATHWAY (KNOWN FOR WAKEFULNESS) COULD BE USEFUL in treatment?
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CATAPLEXY= a sudden loss of postural time while awake – which may be stimulated by strong emotional stimuli
The HYPOCREATIN (OREXIN) PATHWAY stimulates wakefulness. |
Narcolepsy is a condition in which individuals go into REM sleep from wakefulness, rather than the normal process of prior non-REM sleep. This may be associated with cataplexy – a sudden loss of postural time while awake – which may be stimulated by strong emotional stimuli. Other symptoms may include sleep paralysis and hypnogogic hallucinations. There is a genetic component in the human form of the disease, relating to a particular form of the HLA gene. In canine models, there is a mutation of the orexin (hypocretin) receptor 2 gene. In humans, the major pathophysiological basis of narcolepsy appears to be loss of lateral hypothalamic neurons that produce hypocretin (Dauvilliers and Zeitzer) Treatment includes frequent naps, use of stimulants, such as amphetamines, treatment with certain antidepressant drugs (which suppress REM sleep). More recently available drug treatments include the non-amphetamine compound modafinil or the short acting sedative sodium oxybate. Newer drug
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What is REM sleep disorder? Sounds kinda scary...
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REM SLEEP DISORDER - a condition in which patients enact their dreams. Males are affected more often than females and the condition is often associated with pathology in the brainstem. It can be a harbinger of neurodegenerative disease in that a higher percentage of affected than non affected individuals go on to develop Parkinson’s disease and possibly Alzheimer’s
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Everybody hurts... sometimes... why?
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What is the difference between delta and C fibers? Which pain do you feel first?
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Which receptors are important for our NOCICEPTORS?
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There are two ascending pathways for pain. One we already know (Spinothalamic/ anteriolateral system). What is the pathway for the trigeminal pain (on the face). It is also a 3 order neuron signal. Where does it start/ where does it synapse? End?
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ALS for review
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Pain has a very emotional aspect to it? How?
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Where does modulation of pain begin?
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AT THE LEVEL OF THE SPINAL CHORD (substantia gelatinosa is essential site of control)
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For gateway control theory, what are some examples of things that can open the gate? Close it?
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What are the three families of endogenous opioids that are in our bodies? What do they do?
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What exactly is happening in the brain with the placebo effect?
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Acute pain is useful but chronic pain SUCKS (causes more suicide than depression. What are three types of chronic pain that our patients may have?
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NSAID and sterioids work by helping to block prostaglandins after tissue damage. But stronger pain meds like opiods are different. How do these pain medications (opiods) work?
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Normal pain (Nociceptive pain) is different from neuropathic pain. What are examples of neuropathic pain?
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Looking at this slide, based on location alone if you had to guess....
What types of muscles (extensor/flexor) does the RUBROSPINAL TRACT INNERVATE? LATERAL VESTIBULAR Tract? |
RUBROSPINAL= lower motor neuron distal Limb FLEXORS
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Rubrospinal + corticospinal= flexors
Reticulospinal +Vestibulospinal= extensors |
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Lateral corticospinal and rubrospinal tract both provide control of distal limbs (both DORSOLATERAL motor pathways), but what is the ONLY INPUT TO THE FINGERS?
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LATERAL CORTICOSPINAL TRACT= fine motor control
Good piano players have this. people, apes that have a problem with this tract lose fine motor control of fingers.... need to palm things instead. |
For the DECORTICATE rigidity case, this phenomenon is a manifestation of activity in brain stem flexors facilitation centers such as the red nucleus, which most strongly influence flexion in the upper limb. These examples of lesions in the brain stem suggest that the rubrospinal and corticospinal tracts in humans influence strongly the activity of distal muscles (limb) and are solely responsible for the very skilled movements of the individual fingers.
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These are two abnormal postures that may result from a brain lesion.What is causing the FLEXED ARMS in the DECORTICATE RIGIDITY?
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The obvious major difference between the two is in the arms. The elbows are extended in decerebrate rigidity, but they are flexed in decorticate rigidity. Remember that the rubrospinal tract innervates the flexors of the distal limbs (but not the digits!). If you have a lesion above the red nucleus the rubrospinaltract is spared. The distal flexors remain in tact and the patient presents with bent elbows (decorticate, B). If the lesion is below the red nucleus, innervation to these flexors is lost and the patient presents with extended elbows.
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How can we explain the differences in limb rigidity in these patients? The extensor posturing in decerebrate rigidity is thought to occur because of the impairment of the extensor inhibition normally exerted on the reticular formation by the cerebral cortex. In addition, the lesion releases the inhibition of the reticulospinal and vestibulospinal tracts leading to the hyperactivity of the extensor muscles and muscle tone. Thus, in this lesion, we see the combined effect of tonic activity of the vestibular and pontine reticulospinal neurons which activate both alpha and gamma motoneurons innervating extensor muscles. As a result, stretch reflexes of extensor muscles are hyperactive and muscle tone in these muscles is increased (be aware of the fact that the lateral reticulospinal tract receives axons from various motor structures while the medial reticulospinal tract is more dependent on cortical inputs).
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These brainstem nuclei are associated with which descending motor control pathways?
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What is the area of the brain that can make a cat without a brain.... be able to walk by itself....
(probably why zombies can still walk) |
Mesencephalic motor region
Initiation and termination= motor cortex, but flexors and extensors can be controlled automatically after (you don't have to think about it unless something catches your attention) |
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Riding a bus and and the bus decelerates quickly... your head moves forward, and you're leaning forward and your lower legs tense up to stop you from falling.... is this brainstem or motor cortex working? Why?
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ALL BRAINSTEM REFLEXES!! We don't even have to think about it! yay!
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What are the key difference between the MEDIAL (pontine) reticulospinal tract and LATERAL (medullary) reticul0spinal tract in where they decussate? Which starts in pons, is bilateral, and does all PROXIMAL muscles?
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MEDIAL reticulospinal= pons, bilateral and proximal muscles
LATERAL reticulospinal=medulla, ipsilateral, distal muscles |
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Which descending motor pathways are VENTROMEDIAL
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Tectospinal, vestibulospinal, and reticulospinal
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Whats the differnce between the LATERAL vestibulospinal tract and MEDIAL vestibulospinal tract in terms of
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Where do the fibers of the RUBROSPINAL TRACT decussate?
What other tracts are near it? What happens if you stimulate the red nucleus? |
VENTRAL TEGMENTAL DECUSSATION
Runs in pons/medulla close to ANTERIOLATERAL system |
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What happens when you stimulate the red nucleus?? What does it receive projections from?
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Stimulation of the red nucleus results in a) excitatory postsynaptic potentials in contralateral flexor alpha motor neurons, and b) inhibitory postsynaptic potentials in contralateral extensor alpha motor neurons
Receives projections from: cerebellum, cerebral cortex (precentral and premotor cortex) and inferior olive |
just think about how it mightbe related to this.... food for thought... very interesting
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Brain stem nuclei and their spinal projections are of limited use in localizing focal lesions. However, their activity (or inactivity) may be used as indicators of the levels of brain stem impairment in comatose patients with brain stem compression or lesion. Why would the DECORTICATE position mean that the red nucleus is working?
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When brain stem impairment occurs BELOW the red nucleus, but ABOVE the vestibular nuclei,--> DECEREBRATE rigidity. This syndrome is known for its characteristic rigidity. In fact, the upper and lower limbs extend when comatose patients with such lesion receive an appropriate stimulus. The feet exhibit plantar flexion.
Decorticate rigidity instead presents different clinical and anatomical features. It occurs when the lesion is located in the brain stem ABOVE the red nucleus (internal capsule or the cerebral hemisphere). It is characterized by flexion of the arm, wrist, and fingers with adduction in the upper extremities; the lower limbs extend, the feet rotate internally. |
For the decorticate rigidity case, this phenomenon is a manifestation of activity in brain stem flexors facilitation centers such as the red nucleus, which most strongly influence flexion in the upper limb. These examples of lesions in the brain stem suggest that the rubrospinal and corticospinal tracts in humans influence strongly the activity of distal muscles (limb) and are solely responsible for the very skilled movements of the individual fingers.
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How do these all decussate? Same side, both sides or contralateral?
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