The neuron: electrical properties week 5 Flashcards
What do EMG’s record? What are they useful for?
Electromyogram (EMG) : electrical activity of muscles; useful to detect neuromuscular disorders and differentiate diseases involving peripheral nerves, muscles and the neuromuscular junction
the giant motor unit potential (in attached pic) recorded from a muscle provides evidence of loss of motor neurons and sprouting of adjacent motor neurons.
What do nerve conduction studies record? What are they useful for?
Nerve conduction studies: conduction of action potentials in peripheral nerves; useful to identify peripheral nerve disease and to differentiate axonal disease from demyelinating disease
-see attached pic: Stimulating the ulnar nerve at various points along the left and right arm yields compound muscle action potentials in the hypothenar muscle. The sudden drop in amplitude and increase in latency at stimulation points above the elbow on the right indicates an ulnar neuropathy at the elbow on that side. Nerves can also be assessed for and sensory and motor conduction separately.
What are sensory evoked potentials and motor evoked potentials used for?
Sensory evoked potentials : summed action potentials and/or synaptic potentials in each of the sensory systems may be used for clinical diagnosis, prognostication in comatose patients, or for intraoperative monitoring during surgeries that put sensory pathways at risk
- Somatosensory Evoked Potentials (SEP)
- Visual Evoked Potentials (VEP)
- Brainstem Auditory Evoked Potentials (BAEP)
Motor evoked potentials (MEP):assess the pathway from the cerebral cortex to individual muscle groups. Used primarily for intraoperative monitoring during surgeries that put motor pathways at risk
How are electroencephalograms (EEGs) generated? What diseases are they specifically useful for the diagnosis of?
Electroencephalogram (EEG) generated by summed synaptic activity in large numbers of nerve cells of the cerebral cortex immediately beneath the scalp. The EEG is particularly useful in the diagnosis of epilepsy and coma. Certain patterns of activity are characteristic of epileptic seizures and contribute to a specific diagnosis.
See attached: EEG shows generalized three-per- second spike and wave discharges of a patient with petit mal (Absence) seizures.
What 5 factors determine resting membrane potential (RMP)?
RMP is established by
- Selective resting permeability of plasma membrane to ions: PK>PCl>PNa
- Impermeant anions
- Concentration gradient for permeant ions: Ki >Ko, Nao>Nai
- The ability of the plasma membrane to maintain a separation of charges: this is membrane capacitance
- Concentration gradients for sodium and potassium are maintained by the electrogenic sodium pump (Na-K ATPase), which actively transports sodium ions outside the cell for every 2 potassium ions into the cell, against their concentration gradients. Agents that block the sodium pump produce depolarization and seizures
What equation determines membrane potential if the membrane is permeable to only one ion?
What equation determines membrane potential if a membrane is permeable to multiple ions?
Why is the resting membrane potential near the K+ equlibrium potential?
If the plasma membrane is permeable to only one ion (X), the membrane potential is determined by the concentration gradient and the charge of that ion, as described by the Nernst equation, and electrical and chemical forces on the ion are in balance. This is referred to as the Nernst (or equilibrium) potential Ex= (RT/ZF) ln ([X]out/[X]in C.
If the membrane is permeable to more than one ion, the contribution of each ion’s Nernst potential to the membrane potential is weighted by the relative permeabilities (P) of the ions. This is reflected in the Goldman equation (see attached).
The resting membrane potential is near the potassium equilibrium potential due to the relatively high permeability of the membrane to potassium, but deviates from it due to the partial permeability to sodium. At the resting membrane potential there is no net current flow across the membrane, i.e. the sum of inward currents is equal and opposite to the sum of outward currents.
During an action potentia (AP), the permeability of what ion dominates?
During excitatory synaptic potentials, the permeabilty of what ion dominates? During inhibitory?
Resting potential: K permeability dominates
Action potential: Na permeability dominates
Synaptic potentials
- Excitatory (depolarizing) Na (or Ca) dominate
- Inhibitory (hyperpolarizing) K (or Cl) dominate
What is passive conduction?
Relatively, what distance can this type of conduction relay information and why?
PASSIVE MEMBRANE PROPERTIES: Electrotonic conduction provides intracellular communication across short distances: a few mm.
Passive conduction (electrotonic conduction): ionic current flows through the cytoplasm and changes the potential of adjacent patches of the plasma membrane. The membrane potential at each successive patch of membrane is less due to current “leaking” out of the cytoplasm across the membrane. This occurs most noticeably in the spread of excitatory and inhibitory synaptic potentials spread within the dendritic tree, but also in demyelinated axons.
What is the length/space constant (lambda)?
What property of neurons affect this constant? Compare this property in dendrites vs axons.
Length (or space) constant (lambda): the distance in which a change in membrane potential declines to 37% of the original value. Equal to the square root of the ratio of membrane resistance to cytoplasm resistance. Cytoplasm resistance is a function of diameter of a neuronal process (axon or dendrite). The larger the diameter, the further the potential will reach. Dendrites tend to be thicker than axons; they rely primarily on passive membrane properties for conduction to the soma. This contributes to spatial summation between dendrites and the axon hillock. Axons are so thin that they would not conduct more than a millimeter or two by passive conduction. The action potential mechanism developed to address this limitation, and it provides repetitive amplification along the length of the axon. There are even scattered voltage gated sodium channels in dendrites to amplify the small EPSP signals from distant dendrites.
What is the time constant? What does it mean for a membrane to have a long time constant?
Compare the time constants btwn axons and dendrites.
Time constant (tau): the time (in milliseconds) it takes to charge the membrane to 63% of the final membrane potential. Equal to the product of membrane resistance times membrane capacitance. Membranes with long time constants change voltage slowly. Dendrites and the cell body (soma) generally have long time constants. This allows for temporal integration of synaptic activity (temporal summation). Myelinated axons have lower capacitance (and thus shorter time constant) than unmyelinated axons. This contributes to the faster conduction velocity in myelinated axons.
How does lidocaine work?
How do phenytoin and carbamazepine (anitepileptics) work?
Voltage gated sodium channels are the target of many drugs, including anesthetics, analgesics and antiepileptics.
- The anesthetic lidocaine blocks sodium channels in damaged pain fibers, without depressing central nervous system excitability.
- The antiepileptic drugs phenytoin and carbamazepine prevent epileptic seizures by blocking voltage gated sodium channels in a use dependent manner, having much greater effect on rapidly firing neurons than slowly firing neurons.
