block 4 synapses Flashcards

1
Q

why is synaptic integration important?

A

-Neurons make contact with
multiple neurons and receive
100-1000s of synaptic inputs
-synaptic integration enables
information processing in the
CNS
-integration of synaptic inputs
determines nervous system
function.
therefore synpases and there contacts are important because of the complexity of the neurone, and their ability to reach 100’s of neurones

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2
Q

two aspects of synaptic integration

A

-Single EPSP: A tiny positive signal in a neuron that briefly makes it more likely to send action potential
-Spatial Integration: Adding up signals from multiple neurons sending inputs to one neuron at the same time.
-t
temporal Integration: Adding up repeated signals from the same neuron over a short period of time.

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3
Q

parameters that effect synaptic integration

A

b -The neuron needs multiple signals from synapses, both from different places (spatial summation) and over time (temporal summation), to generate a large enough signal to “fire” and send a message. The structure of the neuron and its connections affects how these signals combine

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4
Q

spatial synaptic integration

A

A single neuron can receive signals from multiple synapses at once. When several neurons are active at the same time, they send signals to the same target neuron. The combined effect of all these signals from different synapses determines the electrical state of the target neuron’s cell body (soma). If the combined signals are strong enough, the neuron will fire and send its own signal.

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5
Q

purkinje cells= intergrators in the cerebellum

A

urkinje cells are special brain cells that receive two types of input, like getting messages from two different messengers:

Climbing fibre (big messenger):

Each Purkinje cell talks to just one climbing fibre.
That climbing fibre makes many, many connections to the Purkinje cell, so it sends a strong, focused message.
Parallel fibres (small messengers):

Each Purkinje cell gets messages from thousands of parallel fibres.
But each parallel fibre only makes one small connection with the Purkinje cell, so their messages are weaker individually.
Together, the climbing fibre gives one strong signal, while the parallel fibres work together to provide lots of small signals.

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6
Q

purkinjie cells-two types of synaptic inputs summary

A

Parallel fibre input:
Single contact
- small synaptic
current & potential
Climbing fibre input:
Many contacts
- large synaptic current & potential,
-triggers complex spike

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7
Q

spatial synaptic intergration and length constant

A

synaptic potentials spread passively from site of synapse
- The amplitude of synaptic potential change reduces with distance from synapse
- The decline in synaptic amplitude with distance from the synapse is determined by length constant
- Synaptic potential decline is
described by length constant 
(lambda) and the exponential (see lecture)
- make a maths sheet block 4 lecture 2

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8
Q

whats the purpose of chemical synapses

A

-information transfer between cells: excitation, inhibition, modulation
-amplification of signals
-intergration of multiple inputs
-plasticity- learning and memory

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9
Q

inotropic mechanisms

A
  • ligand-gated ion channels. When a neurotransmitter binds to the receptor, it directly causes the ion channel to open or close, altering the flow of specific ions across the membrane.
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10
Q

metabotrophic

A

Metabotropic receptors are G-protein-coupled receptors (GPCRs) that do not directly control ion channels. Instead, they initiate a cascade of intracellular signalling through second messengers.

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11
Q

what are the 3 ways to classify synpases:

A
  • transmitter chemistry=e.g. acetylcholine
    -transmitter mechanisms: iontropic or metabotropic
    -transmitter functions: inhibitory or excitatory
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12
Q

what describes weather a synapses are excitatory or inhibitory?

A
  • depends on the change in postsynaptic membrane permeability caused by the neurotransmitter
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13
Q

resting membrane potential

A

Resting Membrane Potential:

The resting membrane potential (Vm) is approximately -60 mV.
This is due to ion concentration gradients and higher permeability for K⁺ over Na⁺ (about 50 times more permeable).
Typical ion concentrations:
K⁺: Inside = 135 mM; Outside = 3 mM.
Cl⁻: Inside = 7 mM; Outside = 120 mM.
Na⁺: Inside = 18 mM; Outside = 145 mM.
Ca²⁺: Inside = 0.0001 mM; Outside = 1.5 mM.

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14
Q

how do neurotransmitters work?

A

Neurotransmitters affect the postsynaptic cell by opening ion channels, altering membrane permeability, and changing the membrane potential.
Excitatory Postsynaptic Potential (EPSP)

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15
Q

what happens if you make the membrane potential more permeable for K+

A

-more k + leaves the cell as we are making the cell more positive shifting the ratio
-therefore the membrane will become more negative causing a slight hyperpolarisation
-A more negative cell is less likely to “fire” a signal to the next cell.
-causes an inhibitory postsynaptic potential ( the nerve is less like;y to send a action potential)

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16
Q

what happens when the cell becomes more permeable to Na+ and or Ca+ ions

A

-Na+ and Ca+ ions enter the cell
-membrane potential becomes less negative
-excitatory postsynaptic potential

17
Q

what happens when the cell is more permeable to Cl- ions

A
  • Cl- ions enter the cell
    -membrane potential becomes more negative
    -inhibitory postsynaptic potential
  • however, this only cases for Adult neurons
    -young neurons have a transporter called NKCC1, which pumps chloride into the cell and so cl- leaves the cell
    -Adult neurons: Develop a different transporter called KCC2, which pumps chloride out of the cell. This keeps the inside low in chloride. When chloride channels open, chloride flows in, making the neuron less likely to fire (inhibitory).
18
Q

summary. what is the ionic basis of Excitatory Postsynaptic potential (EPSPs) ,Inhibitory Postsynaptic Potential(IPSPs)

A

-positive ions influx (cations)= more positive membrane= depolarisation =epsp
-negative ions influx (anions)= more negative= hyperpolarisation=ipsp

19
Q

the cys-loop receptor family

A

-includes nicotinic ACh (excitatory)GABAa receptors (inhibitory),glycine receptors (inhibitory)
- the excitatory receptors have a glutamate group which is negatively charged so maybe repels negatively charged ions
-the inhibitory group have a arginine receptors which are positively charged and so attract negative ions
-so mutating this receptor can change the selectivity of them
-receptors are on the intracellular surface of the receptor

20
Q

temporal synaptic intergration

A

-short time constant = no temporal summation as by the time the second signals comes along the first one would have already decayed
-long time constant= temporal summation as the postsynaptic potentials add up (PSP)

21
Q

time constant

A

-the time it takes for PSPs to decay. see equation again block 4-L2

22
Q

LECTURE 3

A

WATCH

23
Q

paired-pulse facilitation- a presynaptic model

A

Residual Calcium Build-Up:
When the first pulse arrives, it causes calcium ions (Ca²⁺) to enter the presynaptic terminal, triggering the release of neurotransmitters from primed vesicles (vesicles that are ready to release their contents). After the first pulse, not all the calcium is cleared out immediately; some “residual calcium” remains in the presynaptic terminal.

Boosted Neurotransmitter Release:
The second pulse arrives shortly after the first, and the leftover calcium adds to the calcium influx caused by the second pulse. This extra calcium helps to quickly prepare (prime) more vesicles and enhances the release of neurotransmitters, making the response to the second pulse larger.

Short Timescale:
This facilitation only occurs if the second pulse comes within a few milliseconds of the first. If too much time passes, the residual calcium is cleared, and the effect disappears.

24
Q

synaptotagmin 7

A

-calcium sensors important for synaptic vesicle release

25
Q

spike broadening

A

Spike broadening refers to an increase in the duration of an action potential (the “spike”) in a neuron. This means that the action potential becomes wider or lasts longer than usual.
- ca ion channels stay open for longer

26
Q

Synaptic depression

A
  • at some synapses repeated firing of presynaptic neuron leads to progressively weaker postsynaptic responses
27
Q

release probability of synapses

A

-synapses with a low probability are when a single action potential only releases a small number of vesicles most likely to undergo synaptic facilitation
-high probability= first action potential releases a high number of vesicles and then the second one is less as it it takes time to replenish the vesicles. therefore more likely to under synaptic depression

28
Q

heterosynaptic modulation of synapse function

A

-post synaptic modulation= modulatory inputs alter sensitivity of postsynaptic membrane to presynaptic transmitter release. (means that certain signals can change how sensitive the receiving cell (the “post-synaptic membrane”) is tothe chemical messages sent by the sending cell (the “presynaptic transmitter release”).

-presynaptic modulation= modulatory inputs alters presynaptic transmitter release

29
Q

example f postsynaptic modulation

A
  • activated G-protein coupled receptors e.g. serotonin receptors activate protein kinase which leads to the phosphorylation of GABAa receptor.
    -alter of GABAa can either enhance or suppress receptor function
30
Q

presynaptic inhibiton

A

-a process where the activity of the neuron sending signals (presynaptic neuron) is reduced. leads to a reduced transmitter release, reduced receptor activation and reduced EPSP.
-occurs when Presynaptic inhibition occurs when inhibitory inputs decrease the amount of neurotransmitter released, even if there is an excitatory input trying to make the presynaptic neuron release neurotransmitters

31
Q

synaptic plasticity- long term potentiaon (LTP) and learning.

A

-where the connection between two neurons becomes stronger after they are repeatedly activated together (e.g. repeated firing). It’s a form of synaptic plasticity, which means that the brain’s synapses (the connections between neurons) can change and adapt over time.
- a form of facilitation
-usually synapse

32
Q

tenus stimukation to show long term potentiation

A
  • before tenus esps is lower
    -after tenus refers to a brief but intense burst of stimulation that can cause the synapses between neurons to become stronger
    -afyer tenus ESPS is increased
    -very long lasting affect
33
Q

why is long term potentiation important in memory

A

-plays a central role in memory by strengthening the connections between neurons that are involved in encoding, storing, and recalling memories. When neurons repeatedly fire together, their synaptic connection becomes stronger, making it easier to activate the same neural pathways in the future. This process helps the brain encode new information, consolidate memories, and reinforce learning, all of which are key to forming both short-term and long-term memories.