Lecture 7 Flashcards
PNS
Cranial and spinal nerves
General functions of a neuron
Responding to chemical and physical stimuli, conducting electrochemical impulses, releasing chemical regulators, enabling perception of sensory stimuli/learning/memory/control of muscles and grands
Dendrites
Extend from cell body, receives impulses and conducts graded impulses towards the cell body
Axon
Conducts action potential away from cell body
Trigger zone
Axon hillock: Region where axon connects to cell body
AND
Axon initial segment where action potentials are generated
Tract
Bundle of fibers (axons) in CNS
2 types of PNS glia
Schwann and satellite cells
Schwann cells
Form myelin sheaths around peripheral axons
Satellite cells
Support neuron cell bodies within the ganglia of the PNS
CNS glia
Oligodendrocytes, microglia, astrocytes, ependymal cells
Oligodendrocytes
Form myelin sheath around axons of CNS neurons
Microglia
Phagocytose foreign and degenerated material through the CNS
Astrocytes
Regulate the external environment of neurons in the CNS
Ependymal cells
Line ventricles and secrete cerebrospinal fluid
PNS regeneration
Nerves in PNS can regenerate if cell body isn’t damaged because Schwann cells form a regeneration tube and release growth factors that stimulate growth of axon sprouts within the tube
CNS regeneration
Very limited ability for nerves to regenerate, death receptors form that promote apoptosis of oligodendrocytes and inhibitory proteins in the myelin sheath prevent regeneration, glial scars from astrocytes also prevent regeneration
Most abundant glial cell
Astrocytes
Blood brain barrier
Formed by tight junctions between endothelial cells of brain capillaries, movement is transcellular (not paracellular)
Resting membrane potential in neurons
-70mv
Cause of resting potential
Large negatively charged molecules inside the cell, sodium/potassium pumps, permeability of the membrane to positive ions
Depolarization
From Na+ sometimes Ca2+
Hyperpolarization from
K+ leaving or Cl- entering cell
K+ channels
Leakage channels that are always open, voltage-gated only open when depolarization occurs closed @ resting potential
Na+ channels
Only voltage-gated, closed at rest
Threshold membrane potential
- 55 mV
At threshold membrane potential
When - 55mV the voltage-gated Na+ channels open, as the cell depolarizes more and more sodium channels open (positive feedback loop
@ 30 mV
Na+ channels close, K+ channels open causing repolarization (negative feedback loop)
- 85 mv
Caused by repolarization overshooting resting potential, voltage gated k+ channels are inactivated as the membrane potential falls- sodium/potassium pumps quickly reestablish resting potential
Action potential amplitude
All-or-none because of Na+ channel inactivation and k+ channel opening, amplitude about +30mV and duration 3msec for all APs
Stronger stimulus causes
Action potentials to occur more frequently (frequency modulated), as stimulation increases more axons will become activated (recruitment)
Absolute refractory period
Period after an action potential when the neuron can’t become excited again, occurs during the action potential when Na+ channels are inactive
Relative refractory period
When k+ channels are still open and only a very strong stimulus can overcome this to cause an AP
Cable property
Ability of neurons to conduct charges through their cytoplasm
Conduction of a nerve impulse down the axon
Action potential at given point on a neuron opens voltage gated Na+ channels as a wave down the axon, the action potential at one location serves as the depolarization for the next region, making the impulse one directional due to the refractory period in the preceding region
Conduction in unmyelinated neuron
Potentials are produced down the axon at every patch op membrane making the conduction rate slow because of the amount of action potentials produced, but each action potential has the same amplitude until the end of the neuron is reached (conducted without decrement)
Saltatory conduction
In myelinated neurons nodes or ranvier allow Na+ and k+ to cross the membrane every 1-2 mm, sodium channels are concentrated at the nodes and APs occur only at the nodes
Action potential speed increase by
Diameter of neuron and myelination
Axodendritic
Most common where a presynaptic neuron can signal the dendrite
Release of neurotransmitter
Action potential reaching end of axon causes voltage-gated Ca2+ channels to open, Ca2+ triggers the fusing of synaptic vesicles to the plasma membrane resulting in exocytosis of neurotransmitter
Graded potentials
Created when ligand-gated ion channels are opened, opening Na+ or Ca2+ ligand gated channels creates a graded depolarization EPSP, opening K+ or Cl- ligand gated channels causes a graded hyperpolarization IPSP
Determines whether AP occurs
Summation of EPSPs and IPSPs at initial segment of axon
ACh excitatory
In all somatic motor neurons
Nicotinic ACh receptors
Can also be stimulated by nicotine, always excitatory
Skeletal muscle cells, autonomic ganglia, some parts of CNS
Muscarinic ACh receptors
Can be stimulated by muscarine
CNS and plasma of smooth and cardiac muscles, glands innovated by autonomic
Agonists
Drugs that can bind to and activate a receptor
Antagonists
Drugs that reduce the activity of a receptor
Antagonist for muscarinic
Atropine
Antagonist for muscarinic
Curare
Nicotinic ACh mechanism
Receptor is a ligand-gated ion channel, binding of 2 ACh opens channel allowing Na+ to flow in and K+ out, na+ flowing in depolarizes creating EPSP that can lead to an AP
Muscarinic ACh mechanism
G-protein coupled, one ACh opens or closes k+ channels via the alpha or beta-gamma subunit dissociating and diffusing through the membrane to the K+ ion channel that it opens or closes
G-protein coupled in heart
K+ channels are opened by the beta-gamma complex creating IPSPs through hyperpolarization slowing heart rate
G-protein coupled in stomach smooth muscle
K+ channels closed by alpha subunit producing EPSPs and contraction of these muscles
Alzhiemer’s disease
Associated with loss of cholinergic neurons that synapse on the areas of the brain responsible for memory
Dopaminergic neurons
Concentrated in 2 areas of midbrain: nigrostriaial dopamine system (motor control) and mesolimbic dopamine system (emotional reward)
Substantia nigra
Part of basal nuclei, neurons from this part of the brain send dopaminergie neurons to the corpus striatum
Parkinson’s
Degeneration of dopaminergic neurons in the substantia nigra, treated with L-dopa and monoamine oxidase inhibitors
Major excitatory neurotransmitter in brain
Glutamate/ glutamic acid
Glutamate receptors
Also serve as ion channels, named according to molecules they bind, NDMA and AMPA receptors work in memory storage
Glycine
Inhibitory
GABA
Most common neurotransmitter in the brain used by 1/3 of brain’s neurons, inhibitory opens Cl- channels when it binds to receptor, involved in motor control
Huntington’s disease
Degeneration of gaba-secreting neurons in the cerebellum
Spatial summation
Convergence of signals onto one postsynaptic neuron
Temporal summation
Successive waves of EPSPs and IPSPs add together at initial segment of axon
Synaptic plasticity
Ability of synapses to change in response to activity
Long-term potentiation
When repeated high-frequency stimulation enhances excitability of a synapse, associated with insertion of AMPA glutamate receptors in post synaptic neuron, found in hippocampus
Long-term depression
Prolonged periods of low-frequency stimulation of glutamate releasing presynaptic neurons that stimulate release op endocannibinoids, results in removal of AMPA receptors
LTP and LDP depend on
Rise in calcium in postsynaptic neuron, rapid rise leads to LTP, smaller prolonged rise leads to LTD
Synaptic plasticity involves
Enlargement or shrinkage of dendritic spines, more or less room for receptors
