HISTOLOGY Flashcards
NEURONS
classification
FORM + NUMBER OF THEIR PROCESSES
bipolar
unipolar
multipolar
NEURONS
Nissl substance
Clumps or rough ER (endoplasmatic reticulum) with bound polysomes
sites of protein synthesis
(also are free polusomes in cytoplasm)
NEURONS
Cytoplasmic Inclusions in CNS disease
(2)
LEWY BODIES
- in degenerating neurons
- Parkinson’s - pars compact of the substantia nigra
- Dementia - cortical and brain-stem neurons
NEGRI BODIES
- eosinophilic in degenerating neurons
- Rabies - hippocampus and cerebellar cortex
NEURONS
Cytoskeleton
NEUROFILAMENTS
+
MICROFILAMENTS
+
MICROTUBULES
NEURONS
Neurofilaments
(where and why)
Most numerous in the axon and dendrites (proximal part)
+
structural support
NEURONS
Microfilaments
(where and why)
form matrix near the periphery of neuron
+
growth cones (add motility)
and
dendrites (specializations at synaptic membranes)
NEURONS
Microtubules
(where and why)
In ALL parts of the neuron
+
axonal transport
NEURONS
NEUROFIBRILLARY TANGLES
(Cytoskeleton)
DEGENERATIVE NEURONAL DISEASES
(Alzheimer’s, Amyotrophic Lateral Sclerosis, Down Syndrome)
tau protein becomes more phosphorylated and microtubules form helical filaments
(also senile plaques are formed in dendrites e in the cell body)
NEURONS
Dendrites
may contain spines
+
provide major surface for synaptic contacts
\+ highly branched (the pattern is used to define cell type)
NEURONS
Axon
(diameter, collateralls and proximal part)
uniform diameter
+
may branch at right angles into collaterals (90º)
+
proximal part is marked by axon hilllock
(lacks of Nissl substance)
+
trigger zone
(sodium ion channels)
NEURONS
Axon
(myelin sheath)
CNS
Oligodendrocyte can myelinate individual segments of many axons
PNS
Schwann cells (each one can myelinate only single internodal segment of a single axon) - also phagocyte debris after PNS injury
(node of Ranvier - saltatory conduction)
NEURONS
Axon
(cytoplasm)
Entire axon lacks
polysomes
+
Nissl substance
+
Golgi apparatus
(only contains mitochondria and smooth ER)
NEURONS
Anterograde axonal transport
(fast and slow)
cell body → synaptic terminal
- fast (100-400 mm/day) transport is dependent on kinesin (motor molecule) - deliver precursors of peptide NT
- slow transport (1-2 mm/day) is the movement of soluble cytoplasmic components (isn’t dependent of ATP or microtubules) - cytoskelon proteins, enzymes and precursos of small NT
NEURONS
Retrograde axonal transport
synaptic terminal → cell body
(material returns to recycle or be digested)
(trophic factors go to cell body)
- microtubules
- slower than anterograde (60-100 mm/day)
- dynein (ATPase) - dependent
NEUROPATHIES AND AXONAL TRANSPORT
DIABETES
hyperglicemia → alterations in proteins of microtubules → disrupt axonal transport
long axons
glove-and-stocking pattern
(altered sensation and pain)
NEUROPATHIES AND AXONAL TRANSPORT
Other causes
- Anoxia (mitochondria) and anticancer agents (depolymerize microtubules) - disrupt fast anterograde transport
- Polio, herpes, rabies and tetanus (only the toxins) - disrupt retrograde transporte of SKELETAL MUSCLE