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Flashcards in Neurotransmission Deck (37)
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CNS inputs

All connections between peripheral afferents and CNS neurons are excitatory
requires balance by CNS inhibition
processing often involves removing unwanted inputs


Presynaptic inhibition

more selective than post-synaptic
- lower effectiveness of one or a few inputs to an euron
- does not affect other inputs or postsynaptic membrane potential
major pathway in spinal cord

GABA is the major NT
GABAa receptors: Chloride conductance, shunting of AP
GABAb receptors: long -acting; G-protein coupled modulation of K and Ca channels

Axoaxonic, and dendroaxonic interaction


Recurrent inhibition

Autoregulation of motor neuron firing rates
Modulation of motor output by its own activation
Glycine dominant NT, but also GABA
Convergent synaptic input from descending pathways
Renshaw cells involved


Renshaw cell

recurrent inhibition of motor neurons
spinal interneurons
Excited by collaterals from motor neurons, and then inhibit those same motor neurons --> negative feedback
Regulates motor neuron excitability and stabilizes firing rates


Golgi tendon organ

GTO stretch (contraction of muscle) --> afferent axon compressed by collagen fibers --> rate of firing increases
Disynaptic GTO inhibition and the Ib inhibitory interneuron = inverse myotactic reflex, "clasp knife reflex"
Ib feedback from GTO inhibits contraction of agonist, and facilitates antagonist



~ 1 million fibers, mostly myelinated
lateral fibers decussate at midbrain (not all cross)
projects to alpha and gamma motor neurons, interneurons
Monosynaptic connections
Also indirect pathways (rubrospinal, reticulospinal)


Reticulospinal tract

Innervates LMN, affected by supraspinal projections
Activity controls posture and strength of reflexes
Interruption in pathway leads to deficits


Interruption of descending input

"releases" spinal interneurons, of which many are inhibitory
Unrestricted flow of excitation reaches motor neurons
- hyperreflexia
- can also affect the sign of reflexes (e.g. Babinski, Bing)


LMN disorder characteristics

flaccid weakness or paralysis
decreased or absent monosynaptic reflex
muscle denervation, atrophy
affects single muscles or small groupw innervated by common nerve
cutaneous reflexes normal


UMN disorder characteristics

spastic weakness (increased velocity sensitivity)
exaggerated monosynaptic reflex
clonus (5 Hz)
no signs of denervation, atrophy
large groups affected, organized by halves or quadrants of the body
reversed (Babinski) or absent cutaneous reflexes



more pronounced in anti-gravity muscles: flexors in the arm, extensors in leg


UMN lesion treatment

Diazepam (Valium)
- antispastic action by increasing frequency of GABAa receptor channel openings, enhancing postsynaptic inhibition in spinal cord

Baclofen: reduces spasticity by activating presynaptic GABAb receptors, inhibiting glutamate release from afferent fibers



Ischemia --> glutamate release --> activation of glutamate receptors --> Na influx --> activation of VaC channels --> influx of Ca --> neuronal injury


Neuronal body vacuolation

cytotoxic edema (failure of pumps, water influx)
Prion diseases (spongiform encephalopathy)



byproduct of catecholamine synthesis
in neurons of substantia nigra and locus cereleus
differs from skin melanin



pigment of aging
in many neurons


Axonal reaction/central chromatolysis

Response of nerve cell body to axonal transection
Swollen cell body with displaced nucleus, dispersed Nissl substance
increased mRNA synthesis --> increased protein synthesis


Wallerian degeneration

degeneration of distal fragment of axon after axonal transection


Axonal retraction balls

damming up of organelles conveyed by axonal transport to proximal stump of axonal transection site


Axonal spheroids

seen in neuroaxonal dystrophies
certain locations in aging
light microscopically similar to, but ultrastructurally different from, axonal retraction balls


Dendritic reactions

abnormalities in number, shape, and size of dendritic spines in mental retardation/epilepsy


Astrocyte function

"scar" cell of CNS
support and structure
syncytium throughout CNS
Energy from glycolysis
Glutamate and GAPA uptake
pH, osmolarity regulation
spatial buffering of K+
glutamine for glutamate synthesis
gray matter: protoplasmic
White matter: fibrous


Gliosis changes

early: hyperplasia, hypertrophy, upregulation of GFAP
Late: fibrillary gliosis


Astrocytic swelling

Rosenthal fibers
- linear/corkscrew hyaline inclusions
- seen in long-standing gliosis


Astrocytic inclusions

Corpora amylacea
- round inclusions of glycoprotein
- in astrocytic foot processes
- particularly around blood vessels, or near surfaces of CNS


Ependyma reactions

lining of ventricles
destruction of ependymal cells probably not replaced with other ependymal cells
Subventricular glial nodule (Granular ependymitis): non-specific reaction of subventricular astrocytes to ependymal injury/loss


Microglial reactions

CNS cells originally derived from bone marrow
Phagocytic function
Antigen presenting

Activated in response to CNS injury in absence of parenchymal destruction
Turns into macrophages in response to CNS injury with parenchymal destruction


Immune response in the CNS

Class II MHC-controlled
Class I cMHC controlled

Often don't see T and B cells due to immunological priviledge


Class II MHC-controlled immune response

Normally minimal constitutive Class II MHC in white matter microglia
CD4 TCR recognizes Ag in the context of Class II MHC on the APC
Need other co-stimulatory molecules and receptors
T-cell + APC --> proinflammatory cytokine profile --> immune response to antigen initiated
OR immunomodulatory cytokine profile --> immune response to antigen suppressed


Class I MHC-controlled immune response

Interaction between cytotoxic T-cell and target/APC --> lysis/apoptosis of target cell
Normally constitutive class I MHC on endothelial cells and probably some glia and perivascular cells in the CNS
CD8 TCR recognizes antigen (peptide) in context of Class I MHC on target cell
no intermediary cell to carry out target destruction