2.2 - Cells of the Nervous System Flashcards

1
Q

What does the CNS consist of?

A
  • brain and spinal cord
  • two cerebral hemispheres, brainstem, cerebellum, spinal cord
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2
Q

Cerebral hemispheres

A
  • two cerebral hemispheres aka telencephalon - distinctive convoluted surface with ridges called gyri and valleys called sulci
    Each hemisphere is split into:
  • frontal lobe - executive functions like personality
  • parietal lobe - contains somatic sensory cortex responsible for processing tactile information
  • temporal lobe - contains hippocampus (short term memory), amygdala (behaviour) and Wernicke’s area (auditory perception and speech)
  • occipital lobe - processing of visual information
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3
Q

What does the brainstem consist of?

A
  • the midbrain, pons and medulla in descending order
  • these structures have a multitude of important functions (e.g. control of respiration and heart rate)
  • they are the target / source of all cranial nerves
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4
Q

Where is the cerebellum and what is its role?

A
  • located towards the dorsal region of the CNS and attached to the brainstem
  • important role in motor coordination, balance and posture
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5
Q

What is the spinal cord?

A

Extends down from medulla and acts as a conduit for neural transmission but can coordinate some reflex actions

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6
Q

Neuron morphology

A
  • unipolar - consists of a cell body with one axonal projection
  • pseudo-unipolar - single cell body with single axonal projection that bifurcates (forks into) 2 different branches
  • bipolar - single cell body with 2 projections - one is the axon, the other is the dendrite
  • multipolar - numerous projections from cell body - 1 is axon, rest are dendrites: e.g.
  • pyramidal cells - pyramid shaped cell body
  • Purkinje cells - GABA neurons found in the cerebellum
  • Golgi cells - GABA neurons found in the cerebellum
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7
Q

How can neurons be described?

A
  • excitable cells of the CNS - able to change their membrane potential to communicate with other cells
  • have heterogenous morphology - look different to each other
  • non-dividing cells (but there’s evidence of some dividing neurones in brain which can be important for growth)
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8
Q

What do all neurones have in common?

A

Soma (cell body, perikaryon)

  • contains nucleus and ribosomes
  • has neurofilaments which are important for structure of neurone and transport of proteins e.g. to end of axons/dendrites

Axon - single projection of cell body that originates from soma at axon hillock

  • can branch off into collaterals
  • usually covered in myelin - allows signals to be transmitted at faster rate
  • ‘voice’ of neuron - used to communicate

Dendrites - branches of cell body not covered in myelin

  • receive signals from other neurons
  • ‘ears’ - listens to communication from other neurons
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9
Q

What are astrocytes?

A
  • most abundant cell type in CNS
  • structural cells - have an important role in cell repair (neurotrophic factors), synapse formation (NT removal and reuptake), neuronal maturation and plasticity
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10
Q

What are oligodendrocytes and Schwann cells?

A
  • oligodendrocytes - glial cells that are the myelin-producing cells of the CNS
  • each cell body sends out numerous projections that form internodes of myelin covering the axon of neurons
  • capable of myelinating a number of neurons
  • Schwann cells are the myelin producing cells of the PNS - myelinates a single axonal segment
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11
Q

What are microglial and ependymal cells?

A
  • microglial - specialised cells similar to macrophages that perform immune functions in CNS
  • ependymal - epithelial cells that line fluid filled ventricles regulating the production and movement of CSF
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12
Q

What is the resting membrane potential?

A
  • caused by uneven distribution of ions inside and outside cell
  • 4 major physiological ions - K+, Na+, Cl-, Ca2+
  • cell membranes are impermeable to these ions –> transportation regulated by channels and pumps
  • this causes an uneven ion distribution: high extracellular Na+ and Cl-, low extracellular K+ = high concentration gradient for Ca2+
  • difference in concentration –> creates a potential difference across the membrane
  • neuronal cells - negative charge inside compared to outside
  • RMP of -40 to -90 mV = RMP -70 mV
  • positive and negative charges concentrated around membrane
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13
Q

Action potentials

A
  • at RMP, VGSCs and VGKCs are closed
  • when the membrane is excited and there is a change in potential, membrane is depolarised which opens VGSCs and causes Na+ influx into cells which causes further depolarisation
  • VGKCs open at a slower rate and cause efflux of K+ from cell - this causes membrane repolarisation
  • there is a local imbalance of Na+ and K+ that needs to be restored
  • Na+K+ATPase restores ion gradients
    1) in pump’s resting configuration - Na+ enters vestibule and upon phosphorylation, the ions are transported through protein
    2) in pump’s active configuration - Na+ removed from cell and K+ enters the vestibule
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14
Q

What is saltatory conduction?

A
  • AP spreads along the axon by ‘cable transmission’
  • myelin prevents AP spreading because it has high resistance and low capacitance
  • Nodes of Ranvier are small gaps of myelin intermittently along axon - contain high concentrations of VGSCs, VGKCs and Na+K+ATPase
  • AP jumps between nodes in saltatory conduction
  • AP is unable to jump across the synapse at the axon terminal which is where neurotransmitters come in
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15
Q

What is the synapse?

A
  • a junction consisting of a pre-synaptic nerve terminal (e.g. axon terminal) and a post-synaptic cell (e.g. dendrite of another neurone) by an extracellular space called the synaptic cleft
  • electrical signal can’t jump over synaptic cleft so is converted into a chemical signal to cross the synapse then back into an electrical signal on the post-synaptic cell
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16
Q

First step of synapse - propagation of the AP

A
  • AP propagated by VGSCs opening
  • Na+ influx –> membrane depolarisation –> AP ‘moves along’ neurone
  • VGKC opening –> K+ efflux –> repolarisation
17
Q

Second step of synapse - neurotransmitter release from vesicles

A
  • AP opens voltage-gated Ca2+ channels at presynaptic terminal
  • Ca2+ influx –> vesicle exocytosis (fuse with presynaptic membrane and release NT into synaptic cleft)
  • NT diffuses across synaptic cleft
18
Q

Third step of synapse - activation of postsynaptic receptors

A
  • NT binds to receptors on postsynaptic membrane
  • receptors modulate postsynaptic activity
19
Q

Fourth step of synapse - neurotransmitter reuptake

A
  • NT dissociates from receptor and can be:
  • metabolised by enzymes in synaptic cleft e.g. cholinesterase breaks down acetylcholine
  • recycled by transporter proteins
20
Q

Post-synaptic cell

A
  • communication between nerve cells - NT release
    Synaptic organisation:
  • axodendritic synapse - connection between presynaptic terminal –> neuronal dendrite
  • axosomatic synapse - connection between presynaptic terminal –> neuronal soma
  • axoaxonic synapse - connection between presynaptic terminal –> neuronal axon
21
Q

The neuromuscular junction

A
  • specialised structure incorporating axon terminal and muscle membrane allowing unidirectional chemical communication between peripheral nerve and muscle
  • communication between nerve and effector cells - paracrine (NT release)
  • NMJ: AP propagated along axon (Na+ and K+) –> Ca2+ entry at presynaptic terminal
  • Ca2+ entry –> ACh release into synapse
  • ACh binds to nicotinic ACh receptors (naChR) on skeletal muscle –> binding allows change in end-plate potential (EPP)
  • miniature EPP: quantal ACh release
22
Q

Neuromuscular junction - components

A

Sarcolemma:

  • skeletal muscle membrane - nAChR activation –> depolarisation = AP
  • T-tubules - continuous with sarcolemma and closely connected to sarcoplasmic reticulum
  • AP travels through T-tubules

Sarcoplasmic reticulum:

  • ER within muscle, contains Ca2+ allowing contraction to occur
  • location - surrounds myofibrils - contractile units of muscle
  • function - Ca2+ storage –> Ca2+ release following sarcolemma depolarisation
  • effect - Ca2+ –> myofibril contraction and muscle contraction
23
Q

Disorders of the neuromuscular junction

A
  • Botulism - Botulinum toxin (BTx) - irreversible disrupts stimulation-induced ACh release from presynaptic nerve terminal; affects face muscles
  • Myasthenia Gravis (MG) - autoimmune disorder (antibodies directed against ACh receptor = ACh has nowhere to act); causes fatigable weakness (difficult for muscles to contract, more pronounced with repetitive use)
  • Lambert-Eaton myasthenic syndrome (LEMS) - autoimmune disorder - antibodies directed against VGCC
  • all three have similar patient presentation - for BTx check patient history, MG and LEMS = blood test for antibodies