Neuronal Synaptic Transmission Flashcards
Difference between orthodromic and antidromic conduction
Ortho moves in the right direction and always gets to its destination no matter the hurdles it has to cross
Anti goes the wrong way and dies out fast
Rough ER can be found in which parts of a neurone
Soma and dendrites but not axon
Structure of synapse in the cerebral and cerebellar cortex
Axodendritic
Structure of synapse in the cerebellum and autonomic ganglia
Axosomatic or axodendritic
Chemical synapse increase or decrease based on use or experience
T/F
T
How many synapses are in the CNS
2 x 10^14
Division of the synapses in cerebral cortex
98% on dendrites (received 8k nerve endings)
2% on soma ( receives 2k nerve endings)
Examples of dense vesicles
NE, EPI, dopamine
Location of active zones on the presynaptic nerve terminal
On the subsynaptic membrane
Location of Ca channels on the presynaptic nerve terminal
Active zones of the subsynaptic membrane
Size of synaptic cleft in EPSP
20-40nm
Contents of the synaptic cleft of EPSP
Enzymes that breakdown NTs
By-products of NTs
CSF
Location of receptors on the post synaptic cell
Subsynaptic membrane of post synaptic cell
- -+ -= post synaptic density
Receptors , enzymes, proteins
Function of neurexins
bind pre terminal to post cell;protein to receptor
What guides and binds the vesicle to the cell membrane
V-snare protein synaptobrevin
T-snare protein syntaxin
What’s the kiss-and-run discharge in neuronal transmission
contents leave through a small hole in the active zones and this hole closes up immediately after NT passes through
Relate one EPSP to threshold and rmp
It’s above rmp but below threshold
Time between:
Stimulation and response
To reach peak
To crash
0.5
1.5
3 msec
EPSP obeys all or none law
T/F
F. It doesn’t
Spatial summation of EPSP
Temporal summation of EPSP
S: more than one adjacent knobs needs to be stimulated at the same time
T: just one adjacent knobs need to be stimulated repititively
Lesser the duration of EPSP the less the opportunity for summation
T/F
T
What causes slow EPSP
Closure of K gates
Reducing conduction of K
Latency period of slow EPSP generally
100-500msec
Duration is a few seconds
Latency period of slow EPSP in sympathetic ganglia
5sec
Duration is 30mins
Slow EPSP is noticed in?
corticalneurones,autonomic ganglia,cardiac, and smooth muscles
Physiology significance of IPSP
Used to reduce excess signals and abolish unwanted signals
NT in IPSP is?
Glycine
When does IPSP peak?
1.5msec and crashes exponentially in constant time
Reason for slow IPSP
K’s influx
Increase in conductance of K
Presynaptic inhibition can be found only in?
CNS
Inhibitory NT in presynaptic inhibition is ?
GABAa or GABAb
Gamma amino butyric acid
How long can N1 in presynaptic inhibition transmission release gaba for
100msec
Gaba agonists can be used to treat?
Multiple sclerosis and spastic spinal cord injury
Examples of gaba blockers
picrotoxin,strychnine,bicchulin
NT in presynaptic facilitation is?
Serotonin
What causes schizophrenia
No one fucking knows
Symptoms of schizophrenia
Disordered thinking, reduction in gray matter
Schizophrenia effect on dopamine receptors
They increase drastically
Treatment for schizophrenia
Dopamine receptors blockers
Multiple sclerosis is caused by?
due to formation of plaque by the demyelination of the nerves in the cns without affecting the axons
Treatment of multiple sclerosis
treatment is by treating the symptoms
Rational treatment
Symptoms of multiple sclerosis includes?
Paraesthias, optic neuritis, motor and sensory disability etc
Define paraesthias and optic neuritis
abnormal sensation caused by damage or pressure to peripheral nerves, inflammation of optic nerve
Cause of epilepsy
abnormal focus of excitation in cns
Treatment of epilepsy
Anticonvulsant
Epilepsy involves one or both hemispheres
T/F
T
Characteristics of epilepsy
loss of consciousness, systemic jerking of the limb, convulsions,sustained contraction of limbs, momentary loss of motor response
Cause of Parkinson’s disease
caused by lesion on the nerve terminal of the nigro -striatum pathway of the substantial nigra
-making the substantial nigra to not produce enough dopamine to inhibit the striatum of basal ganglia leading to
Low inhibitory dopaminergic function and
Excess excitatory cholinergic function
Symptoms of Parkinson’s disease
muscle rigidity, gait disturbance,bradikinesia, impaired autosomal postural
Treatment of Parkinson’s disease
injection of L-dopa because dopamine can’t cross the blood brain barrier
Brain stem divisions are 3.
List them from top to bottom
Mid brain
Pons
Medulla
Anti-choline esterases slow down the progression of Senile Dementia significantly
T/F
F. F
Senile Dementia is Alzheimers. Even though the condition is related to a reduced concentration of Acetylcholine within the CNS and anticholine esterases would otherwise increase the concentration of Ach by preventing its degradation, it has been shown to not have any effect on the progression of Alzheimers.
Alzheimer’s is caused by too much or too little ach??
Too little
Citrulline is a by-product of the synthesis of Nitric Oxide from Serine
T/F
F
