Neuro Physiology Flashcards

1
Q

Summary of Neurotransmitters-Acetylcholine, Glutamate, GABA, Dopamine, Noradrenaline/Adrenaline

A
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2
Q

Ionotropic Receptors

A

Ligand gated ion channels, where the binding of the neurotransmitter causes a conformational change in receptor pore proteins. Opens integral ion pore and allows ions to move across cell membrane. Rapid

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3
Q

Metabotropic Receptors

A

Sends messag to ion channel proteins, change in shape activates a signal transduction pathway. Receptor proteins do not have integral pore but activate G-proteins which acitvate effector proteins

Signalling cascade sends message to ion channel proteins. Slow acting changes

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4
Q

Cholinergic Receptors (Acetylcholine Receptors)

A

Either nicotinic (ionotrophic) or muscarinic (metabotrophic). Nicotinic found at nuromuscular juctions, muscarinic found in brain, heart, gut and broncial passageways.

Nicotinic receptors have 5 possible subunits arranged around a central pore.

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5
Q

Adrenergic Receptors (Noradrenaline Receptors)

A

All metabotrophic.

If binds to alpha 1 receptor, receptor changes shape, activates G protein, signals to enzymed which activates Ca2+ channels.

If binds to alpha 2 receptor, activates G protein, inacitvates enzyme, reducing intracellular cAMP and deactivating Ca2+ channels.

If binds to Beta receptors, activates G protein, activates enzyme, increase cAMP, phosphorylates and activates C2@+ channels.

Alpha 1 for smooth muscle contraction, alpha 2 smooth muscle contraction, beta heart contraction and smooth muscle relaxation.

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6
Q

Conditions of Neurotransmitters

A
  1. Synthesised endogenously within presynaptic neuron
  2. Available in sufficient quantity to affect post synaptic neuron
  3. Effects mimic endogenously released substance if externally administered
  4. Biochemical method for inactivation must be present
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7
Q

The Muscle Spindle

A

Are intrafusal muscle fibres arranged in parallel inside fusiform capsule with extrafusal muscle fibres. Contractile proteins at polar ends, but non in equitorial region. Polar end contractions stretches equitorial region. Afferent Ia (ijcrease firing when change in muscle length) and II nerves (sustained firing to constant muscle length) to CNS and efferent gamma motor nerves from CNS.

When whole muscle stretches, spindle also stretches to keep taut. When muscle fibre contracts, spindle shortens and afferent firing decreases.

Muscle spindle is sensory and tells CNS the state of the muscle. Rate of firing of Ia and II fibres is proportional to the length of muscle spindle, amount and rate of stretch.

Motor gamma efferent cause contraction of polar ends of spindle, keeps equitorial region under pressure when extrafusal muscle shortens.

Higher brain activity cause co-activation of alpha and gamma motor neurons. (alpha to extrafusal muscle) to ensure spindle is sensitive to all muscle lenghts.

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8
Q

Golge Tendon Organ

A

Golgi tendon organ is a type of stretch receptor formed from terminals of group Ib afferent fibres which have a large diameter and similar conduction speed to group Ia fibres. Terminals wrapped around bundles of collagen fibres in tendon, sensory endings arranged in series within muscle.

Each tendon organ has afferent sensory nerve which carries APs to CNS but has no motor innervation. Activated by increased muscle tension. When extrafusal fibres contract, tendon organ stretched, APs sent to CNS at frequency proportional to muscle tension.

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9
Q

Stretch Reflex

A

Occurs when muscles over stretch.

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10
Q

Golgi Reflex

A

Occurs when muscles contract.

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11
Q

Flexion Reflex

A
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12
Q

Pyramidal Motor Tracts

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Corticospinal tract - Lateral pathway directly excites motor neurons, reflex arcs, inolved in fine movements of distal limbs and supports musculature or proximal limbs. Interneurons are ipsilateral to allow fine and independent control of limbs. Pathway begins in cortex, descends through internal capsule, diencephalon, mesencephalon, pons, crosses over in medulla and ends in lower motor neurons contrlateral side of spinal cord.

Corticobulbar tract - similar but terminates in brainstem and influences brainstem LMN to head muscles.

Corticopontine-cerebellar tract - begins in cerebral cortex, descends to brainstem, synapses in pons with axons to ascend to contralteral cerebellum. Informs cerebellum of intended movement by cortex so adjustments can be made.

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13
Q

Extrapyramidal Motor Tracts

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Reticulospinal tract - begins in reticular activating system and ends on a diffuse population of spinal gamma LMN to proximal extensor muscles

Vestibulospinal tract - begins in medullary vestibular nuclei and ends on diffuse spinal alpha motor neurons

Tectospinal tract - begins in visual tectum and ends on LMN of rostral spinal cord

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14
Q

Skeletal Muscle Fibre Contraction

A
  1. Arrival of nerve impulse at neuromuscular junction stimulates ACh release, accelerated by by influx of Ca2+
  2. Increased permeability of Na+ on muscle cell elicits membrane depolarisation
  3. Impulse conducted to all parts of muscle fibre by sacrotubular system in clos association with sarcoplasmic reticulum
  4. Tubulaes of SR depolarise resulting in release of Ca2+ into sarcoplasm
  5. Ca2+ transmitted to contractile apparatus by troponin and tropomyosin on thin filaments
  6. Active sites on actin molecule uncovered, cross bridge formation
  7. Cross bridge heads bind with ATP and detach from active sites as ATPase hydrolyses ATP, increasing attachment of the heads
  8. Causes actin to slide toward myosin centre
  9. Process repeated until actin filaments pulled into centre
  10. Decrease in calcium causes relaxation in muscle
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15
Q

Smooth Muscle Contraction

A
  1. Ca2+ ions bind with calmodulin, a protein similar to troponin
  2. Myosin kinase activated, and myosin head phosphorylates
  3. Muscle contraction through attachment-detachment
  4. Relaxation
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16
Q

Learning Process

A

First perform behaviour and double check movement via cerebellum.

Then need to sensitise the neurological pathway. Interneuron releases serotonin onto presynaptic terminal which stimulates adenlycyclase and the build up of cAMP. Intracellular cAMP causes phosphorylation of K+ channels, decreasing K+ current. A broader presynaptic AP means greater neurotransmitter release and mobilisation leading to a larger response.

Prolonged APs at the end of the pathway mean more neurotransmitter release onto motor neurons which improves the sit pathway.

Long term sensitisation leads to increase in number of vesicle release sites, numbers of synaptic terminals and active zones and dendrites of post synaptic neurons expand.

17
Q

Voluntary Movement in Mammals

A
  1. Cerebral Cortex - decision made and motor programme in cortex is independent of muscles that execute movement. Executes movement via tracts to spinal cord.
  2. Pyramidal tract - directly from motor cortex to spinal cord, pass through medullary pyramids, direct voluntary movement. Cross over in medulla. Or extrapyramidal tracts indirect path to spinal cord, posture, balance and orientation.
  3. Spinal cord - motor neurons which cause muscle contraction, sensory afferent return feedback from stretch receptors and proprioceptors to cerebellum
  4. Cerebellum provides sensory feedback and other info from vestibular apparatus. This integration of signals outputs to cortex via thalamus to refine and adjust descending motor outputs.
  5. Effectors - alpha motor neuron stimulation causes extrafusal muscle fibre contraction. Muscle spindle feedback from afferent spindle fibres synapse onto gamma motor neurons to provide control via muscle spindle.
18
Q

Rod Excitation

A

Outer segment leaky to Na+ ions, inner segment continually pumps out Na+. A cAMP splint keeps Na+ channels open.

When rhodopsin exposed to light, it decomposes and breaks down Na+ splint decreasing its conductance to Na+ ions. Therefor ions are still pumped outbut fewer leak in resulting in an increase in electronegativity causing hyperpolarisation. The more light, the greater the electronegativity until there is an equilibrium potential of K+ ions across the membrane. Signal transmission in retinal neurons occurs via electronic conductance rather than APs.

Hyperpolarisation triggers release of glutamate, an excitatory neurotransmitter. This opens channels on the post synaptic membrane, causing an action potential.

This is different from traditional APs where depolarisation occurs.

19
Q

Neurophysiology of Audition

A
  1. Stereocilia of hair cells bend due to the shear forces set up by displacements of the basilar and tectorial membrane from the sound waves.
  2. Hair cells depolarises when stereocilia move towards tallest cilium, hyperpolarise when move in opposite direction.
  3. Change in membrane potential opens K+ channels, K+ ions move in from surrounding fluid causing depolarisation.
  4. Hair cells release excitatory neurotransmitter when depolarissed produces a generator potential which excites cochlear afferent nerves.
  5. Afferent location in the organ of Corti determines which discharge, given sound frequency causes different displacements along basilar membrane.
20
Q

Stimulus Coding of Sound

A

Discharge of primary afferent nerve fibres when stimulated by characteristic frequency of that fibre, duration of the stimulus is signalled by duration of the neural activity, intensity is signalled by the amount of activity and number of fibres.

21
Q

Activation of Nociceptors

A

Activation of Nociceptor terminal in receptor leads to release of substance P and calcitonin gene-related peptides.

Nerve impulse is established in nociceptor and spreads to other axon branches.

SP and CGRP are released into skin from branches causing vasodilation and increased capillar permeability leading to inflammation responses.

22
Q

Ways of Distinguishing Between Touch and Pain

A

Tract cells of spinothalamic tract are wide dynamic range meaning there is excitatory input from different receptor types activated by wide range of intensities and high threshold receptors activated only by noxious stimuli.

23
Q

Neurophysiology of Equilibrium

A
  1. Hair cells bent towards kinocilium, apical membrane conductance increases and cell is depolarised.
  2. Smallest hair to kinocilium tug stereocilia, opening channels in neuronal cell membrane, positive ions move incausing depolarisation.
  3. Hair cells release excitatory neirotransmitter tonically but when depolarised, more is released onto afferent fibres.
24
Q

Movement of Endolymph on Ampullary Crests

A
  1. When head rotates, endolymph remains stationary because of inertia but semi circular ducts move.
  2. When rotation stops, endolymph continues to rotate, ducts stop and cupula are bent in opposite direction.
  3. Hair cells stop discharging completely.
  4. When endolymph stops moving, discharge returns to normal tonic levels.