Lectures
Neuroanatomy
Neuroanatomy I & II
Recap
The ‘grote hersenen’ are the cerebrum and the ‘kleine hersenen’ are the cerebellum. In the
cerebellum, there are however more neurons than in the cerebrum. A neuron consists of a
dendritic tree (sensors/receptors), the soma (cell body) and the axon (axon hillock and
synaptic terminals). Action potentials travel along axons and their presence is signaled to the
next neuron at the synapse. Neurotransmitters convey the message at the synapse.
The axonal conduction:
Action potential: Is an all-or-none signal. No attenuation (verzwakking). The rest
potential is around -70mV. When there is a stimulation, there will be natrium influx
and there will be depolarization. If this crosses the threshold potential (-50mV), there
will be an action potential that goes to +25mV.
The natrium channels will close and the
potassium channels will open leading to
repolarization. However, the channels close a
bit too late so there is hyperpolarization. Always
the same signal for a specific neuron.
Saltatory conduction: Mediated by the myelin
sheath. Signal is transduced at nodes of
Ranvier. At a node, there will be sodium influx.
This diffuses along the axolemma to the next
node. Then there will be excitation of the
voltage gated channels over there to generate
the next action potential. To increase the
velocity.
Synaptic transmission:
Neurotransmitters: Can be both excitatory and inhibitory. Excitatory will lead to
sodium influx. Inhibitory will lead to potassium or chloride influx (further from
, threshold). Change in membrane potential (postsynaptic potential, PSP). Is not
the same as the action potential. Depends on the kind and amount of
neurotransmitters, kind and amounts of receptors/channels etc.
Calcium influx at a synapse (because of action potential) will lead to release of
the neurotransmitter containing vesicles.
Postsynaptic potential (PSP) Can be both excitatory and inhibitory. One PSP is
never enough to generate a new action potential. PSP also attenuates, in contrast
to action potentials.
Flow of information is from the dendrites, to the soma, to the axon. Information carriers are
the postsynaptic potential (PSP), then the action potential and at the end the
neurotransmitters.
A sensor can sent signals to afferent neurons. Are smell, taste, touch (somatic and visceral),
hearing and vision. Go to the brain. Efferent neurons are the effector systems. Somatomotor
system for the striated muscles (often connected to the skeleton). Visceromotor systems for
the smooth muscles and the glands. Brain can only activate either muscles or glands.
There can be an interruption of the flow of information. Sensory deficits will lead to a loss of
sensory functions. Black box (brain) deficits leads to complex changes of cognitive functions.
Complex because sensory and motor system are often close together. Effector deficits can
lead to loss of somatomotor functions (paresis, paralysis) or of the visceromotor functions
(visceral dysfunctions).
The axons of afferent and efferent neurons are often colocalized (for peripheral nerves) or
located in close proximity (in the spinal cord and brain stem). The type and location of the
lesion determines what combination of deficits there will be. With knowledge of the
neuroanatomy the location of the lesion can be deduced from the symptoms. Can also
explain/predicts the symptoms by the found lesion.
The perikaryon is the cell body and is important for the protein synthesis. After a lesion, only
parts that are still connected to the perikaryon will survive. Regeneration can occur.
Cells of the nervous system
Neuroanatomy
Neuroanatomy I & II
Recap
The ‘grote hersenen’ are the cerebrum and the ‘kleine hersenen’ are the cerebellum. In the
cerebellum, there are however more neurons than in the cerebrum. A neuron consists of a
dendritic tree (sensors/receptors), the soma (cell body) and the axon (axon hillock and
synaptic terminals). Action potentials travel along axons and their presence is signaled to the
next neuron at the synapse. Neurotransmitters convey the message at the synapse.
The axonal conduction:
Action potential: Is an all-or-none signal. No attenuation (verzwakking). The rest
potential is around -70mV. When there is a stimulation, there will be natrium influx
and there will be depolarization. If this crosses the threshold potential (-50mV), there
will be an action potential that goes to +25mV.
The natrium channels will close and the
potassium channels will open leading to
repolarization. However, the channels close a
bit too late so there is hyperpolarization. Always
the same signal for a specific neuron.
Saltatory conduction: Mediated by the myelin
sheath. Signal is transduced at nodes of
Ranvier. At a node, there will be sodium influx.
This diffuses along the axolemma to the next
node. Then there will be excitation of the
voltage gated channels over there to generate
the next action potential. To increase the
velocity.
Synaptic transmission:
Neurotransmitters: Can be both excitatory and inhibitory. Excitatory will lead to
sodium influx. Inhibitory will lead to potassium or chloride influx (further from
, threshold). Change in membrane potential (postsynaptic potential, PSP). Is not
the same as the action potential. Depends on the kind and amount of
neurotransmitters, kind and amounts of receptors/channels etc.
Calcium influx at a synapse (because of action potential) will lead to release of
the neurotransmitter containing vesicles.
Postsynaptic potential (PSP) Can be both excitatory and inhibitory. One PSP is
never enough to generate a new action potential. PSP also attenuates, in contrast
to action potentials.
Flow of information is from the dendrites, to the soma, to the axon. Information carriers are
the postsynaptic potential (PSP), then the action potential and at the end the
neurotransmitters.
A sensor can sent signals to afferent neurons. Are smell, taste, touch (somatic and visceral),
hearing and vision. Go to the brain. Efferent neurons are the effector systems. Somatomotor
system for the striated muscles (often connected to the skeleton). Visceromotor systems for
the smooth muscles and the glands. Brain can only activate either muscles or glands.
There can be an interruption of the flow of information. Sensory deficits will lead to a loss of
sensory functions. Black box (brain) deficits leads to complex changes of cognitive functions.
Complex because sensory and motor system are often close together. Effector deficits can
lead to loss of somatomotor functions (paresis, paralysis) or of the visceromotor functions
(visceral dysfunctions).
The axons of afferent and efferent neurons are often colocalized (for peripheral nerves) or
located in close proximity (in the spinal cord and brain stem). The type and location of the
lesion determines what combination of deficits there will be. With knowledge of the
neuroanatomy the location of the lesion can be deduced from the symptoms. Can also
explain/predicts the symptoms by the found lesion.
The perikaryon is the cell body and is important for the protein synthesis. After a lesion, only
parts that are still connected to the perikaryon will survive. Regeneration can occur.
Cells of the nervous system
