Spinal Reflexes Flashcards

1
Q

Neural Communication- How is resting membrane achieved?

A

A nerve will remain inactive when the resting membrane potential is maintained.

Potasssium must be continually regulated for this to happen - RM is achieved when the movement of K out of the cell equals K movement into the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What happens as the Synapse?

A

Depolarisation of presynaptic terminal causes Ca influx.
Ca require for vehicle fusion and release.

[The Action Potential AP in the presynaptic nerve reaches the calcium receptor - this then causes a calcium influx which causes the vesicles to release the neurotransmitters.
Neurotransmitters are proteins, they then randomly hit the receptors on the post synaptic nerve which causes a channel to open up]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the seven steps neurotransmitters go through at the synapse?

A
  1. NT are synthesised from precursors under the influence of enzymes
  2. NT molecules are stored in vesicles
  3. NT molecules that leak from their vesicles are destroyed by enzymes
  4. Action potentials cause vesicles to fuse with the presynaptic membrane and release their NT molecules into the synapse
  5. Released NT molecules bind with autoreceptors and inhibit subsequent NT release
  6. Released NT molecules bind to postsynaptic receptors
  7. Released NT molecules are deactivated either by reputable or enzymatic degeneration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

At they synapse - What is ‘gating’?

A

In nerve cells, the channels that open to allow ions to flow through are ‘gated’
Switching from closed-open-closed is caused by the binding of a transmitter [ligand-gated], a change of voltage [voltage gated] or phophorylation of the channel protein.

NT influence ligand-gated channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

NB - What is an IONOTROPIC RECEPTOR [IR]?

A

When the channel opens at the synapse it causes a flow of positive ions, i.e. Current flow, to change the membrane potential = IR [pertains to ions]

Once a potential difference across the membrane changes in the post-synaptic neurone [often dendrites], this is transmitted along the membrane.
Done by an AP [active process], or passive spread due to flow of current.
Input arriving at dendrites is transmitted passively to Axon Hillock and AP may be initiated: depends on totally excitatory or inhibitory input.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Synaptic Integration - what can influence the transmission between neurones?

A

The number of connections received by a neurone
The type of NT, receptor and current flow
And the size of the response in postsynaptic cell

Thus, an AP in a presynaptic neurone rarely elicits AP in the post synaptic neurone,
AP in postsynaptic neurone requires integration of all inputs that it receives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Synaptic Integration - What are the 2 types of currents that can change the polarisation of a membranes potential?

A
  1. Excitatory postsynaptic potential (EPSP)
  2. Inhibitory postsynaptic potential (IPSP)

These refer to the channel itself not the orgin of the NT

The type of current depends on the type of ion channel gated by a NT - not the transmitter itself

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which transmitters almost always have excitatory or inhibitor effects?

A

Excitatory - Glutamate in the SC

Inhibitory - GABA & glycine in the brain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Synaptic Integration - what is Temporal summation?

A

Temporal summation of the EPSPs moves the membrane potential closer to the threshold due to synapases of cell bodies often being inhibitory - which makes the neurone less likely to fire

Therefore it needs more impulses [temporal summation] and/or impulses from multiple sources and closer to Axon Hillock [spatial summation]

Remember- there’s no myelin in dendrites or cell bodies, so the amplitude of a potential will decrease with distance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Synaptic Integration - What 2 things does a post synaptic neurone depend on to discharge?

A
  1. Amplitude and sign [excitatory/inhibitory] of postsynaptic potential.
  2. Location of the synapse relative to Axon Hillock.

Remember - a neurone can synapse at the dendrite, cell body or axon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Second Messengers - what are they?

A

In addition to IONOTROPIC RECEPTORS, there as also METABOTROPIC RECEPTORS

Indirectly gate ion channels via second messengers [e.g. G protein-coupled]

METABOTROPIC RECEPTORS can open/close ion channels, but act through one or more metabolic steps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Second Messengers - What is a G-protein? NB

A

As example. - cAMP activates an intermediate molecule - G protein [Guanine nucleotide-binding protein]

G protein stimulates other processes to enhance or, more often, reduce the membrane potential rise.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Second Messengers - What do METABOTROPIC RECEPTORS influence?

A
  • resting membrane potential
  • input conductance [how strongly current is drawn through an ion channel]
  • voltage threshold
  • dendrite/neurone propagation ability

And thus influences = action potential duration & discharge characteristics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Persistent Inward Currents [PICs] - Explain the action of PICs

A

Dendrites contain METABOTROPIC receptors for serotonin [5-HT] & noradrenaline [NA]
These are called MONOAMINES: their released by presynaptic neurones emanating form the brain stem [and also in the SC itself]

5-HT = Caudal Raphe Nucleus
NA = Locus Coeruleus

5HT and NA activation causes second messengers to open voltage gates Ca & Na channels.
This creates long-lasting inward currents called Persistent Inward Currents/ PICs.

Numerous 5HT & NA receptors on dendrites = causes influx of positive charge [PIC] via METABOTROPIC/second messenger system.

Na = very quick
Ca = very long lasting effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

PICs - Where do the axons originate that use 5 HT?

A

Caudal Raphe Nucleus

Activation of this brainstem region increases descending activity in the ‘monoaminergic system’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

PICs - Where do the axons originate that use NA?

A

Locus Coeruleus

Activation of this brainstem region increases descending activity in the ‘monoaminergic system’

17
Q

Persistent Inward Currents [PICs] - Postsynaptic neurones and membrane potential

What effect does the IONOTROPIC CHANNEL change have on membrane potential?

A

PS neurones have lots of channels - included Na & Ca = influx through these channels changes the membrane potential.

When IONOTROPIC channel opening occurs with monoamine release [METABOTROPIC input] the membrane is further depolarised and IONOTROPIC input is amplified.
If IONOTROPIC input stops, the PIC continues [plateau potential] which may even allow continued action potentials [self-sustained firing].

Monoamine release therefore modulates the neurone firing in response to IONOTROPIC input.

18
Q

Summary of 5HT, NA, & PIC

A

Motor neurones have receptors for 5HT & NA, which typically increase excitability
Interneurones also have such receptors but they typically decrease excitability

Monoaminergic [serotonin & noradrenaline] drive from 5HT & NA neurones emanating in the brainstem stimulate these receptors - causes influx of positive charge [inward current; PIC]

PIC tend to amplify synaptic [particularly sensory] inputs: Increase muscle force
Once PIC is activated, there needs to be a significant drop in input to deactivate it.

19
Q

What is Neuromodulation?

A

5HT dependent activity tends to occur during repetitive motions such as walking/locomotion and increases with contraction force [even in non-contracting muscles - broad effect]

No need for fear or arousal, therefore ‘emotional brain’ not required

Arousal has significant effect on NA release
Both 5HT & NA activities are suppressed during sleep - essential

Activity through these systems is needed even for the low levels of motor output req for posture.
Increases in ‘gain’ of 5-[5HT] to 10 fold [NA] with activation - otherwise may produces only 40% of Max force!
Achieving recruitment of FT fibres would likely be nearly impossible without this influence.

20
Q

Neuromodulation - How to control it?

  • reciprocal inhibition
  • recurrent inhibition
A

Effects of these inputs are very general - so motor unit pools over the body will increase excitability.

Need for ‘regulatory’ system
Reciprocal inhibition probably provides this regulatory system- Ia reciprocal inhibitory synapses are close to the soma so have a significant effect.

Recurrent inhibition has also been shown to deactivate PICs - in the SC, motor neurones signal to Renshaw cells, which mediate recurrent inhibition of the same motor neurones [prevent over-revving] and also the Ia inhibitory interneurone

21
Q

What is Reciprocal inhibition?

A

Describes the process of muscles on one side of a joint relaxing to accommodate contraction on the other side of that joint. Joints are controlled by two opposing sets of muscles, extensors and flexors, which must work in synchrony for smooth movement.

22
Q

Neuromodulation [NM] and SC injury - What occurs with the motor neurones?

A

Complete spinal transaction reduces motor neurone excitability; almost complete loss of reflex response [more in extensor groups]

Interneurones increase in excitability because released from monoaminergic inhibition

Monoaminergic agonists restore motor neurone excitability in animals
Desperately wanting to walk increases response to chronic exercise training in rats - 5HT & NA response?

After a period of time, humans exhibit spasms, suggesting chronic motor neurone adaptation
Loss of NM with SC injury, but rapid increase in continually active 5HT receptors occurs in weeks/months!
Na & Ca PICs more than double at 8 weeks, despite low 5HT/NA [hint=spasticity]

No significant change in resting membrane potentials, so it seems only PIC affected?

Most drugs appear to work by increasing 5HT activity to reduce the influence of sensory stimuli

23
Q

NB - PRESYNAPTIC INHIBITION [PI]- 3rd way of shutting off PIC - NB

What is Presynaptic Inhibition? How does it occur?

A

PI : interneurone reduces transmitter release by presynaptic (sensory) cell

May occur by:

  • METABOTROPIC receptor activation closes Ca channel so transmitter release is minimised
  • METABOTROPIC receptor directly inhibits processes of NT release
  • IONOTROPIC receptor influences the [GABA-gated] chloride channel

Therefore- sensory feedback can reduce central/efferent drive by presynaptic inhibition

24
Q

NB - Presynaptic Inhibition: What is the H reflex?

A

Sensory afferent synapse or descending motor neurones can be blocked through axoaxonic transmission

Influence reflex activity [e.g. Muscle stretch or pain may influence descending drive]

Maybe test the efficiency of the type Ia reflex arc as ‘indicator’ of Presynaptic inhibition

25
Q

NB - Presynaptic Inhibition: what are some sensory inputs that can produce presynaptic inhibition?

A

-pain, pressure and other sensory inputs [including type II ligament receptors]

These factors can reduce our capacity to produce force [i.e. Work to decrease membrane potential - opposite to PIC]

26
Q

What is the H reflex?

A
  • Electrical stimulation of the nerve activates both afferent and efferent tracts
  • Afferent volley returns through monosynaptic reflex arc to muscle
  • Get both motor wave [M-wave] and reflex wave [Hoffman/H reflex]
  • Less inhibition [greater excitability = greater H reflex amplitude]

H reflex unregulated in spasticity due to hyperexcitability of facilitatory interneurones or inhibition of inhibitory interneurones.
H reflex depressed after spinal injury - and PIC amplitude reduced, therefore less reflex excitability