Cognitive & Behavioural Neuroscience Week 1

Neurons, Action potential, Synaptic transmission, Synaptic Plasticity

CNS & PNS

CNS: Brain & spinal chord. PNS: all nerves that relay info between CNS and rest of the body

Soma

nucleus + machinery for life processes, shape depend on type

Dendrites

Receivers of messages transmitted across synapse

Axon

long, slender tube covered by myelin sheath. Outer surface carries info from soma to terminal buttons

Terminal buttons

knobs at end of axon branches, little special function, secrete neurotransmitters either excites/inhibits receiving cell. Neuron receives info from terminal buttons of axons of other neurons

Axon hillock

site in soma where axon originates & AP 1st triggered

Synapse

gap between axon terminals (aka synaptic boutons), many types: synapses on soma, synapses on spines of dendrites

Action potential

brief change in electrical potential across membrane. Inside of neuron becomes + charged. Depends on summation of signals EPSPs & IPSPs to reach threshold of excitation

Excitatory postsynaptic potential (EPSP)

temporary change in membrane potential which makes a neuron more likely to fire an AP

Inhibitory postsynaptic potential (IPSP)

temp. change in membrane potential makes neuron less likely to fire and AP

Action Potential steps

1.EPSPs trigger resting membrane to increase to -55 mV (threshold of excitation). 2. Sodium-potassium pump opens Na+ ions enter cell (depolarising it) triggering the electrical signal. 3. Reaches a peak at +40mV. 4. Sodium ion channels become deactivated and K= ions return cell to hyperpolarised state - how quickly depends on amount of K+ active in cell & efficiency of sodium-potassium pump

What is responsible the duration of an AP?

Current through K+ channels (usually open)

Why do we want to know about APs?

Electrical APs arise because of stimulus - interested in how we respond to stimuli and how drugs can block receptors /cause more receptors to form/speed up enzymes breakdown of neurotransmitters (delay reuptake/diffusion)

Synaptic transmission

how an electrical signal in 1 neuron becomes a chemical signal in the next

Synaptic transmission Steps

1. depolarisation opens Ca2+ channels. 2. Ca2+ triggers synaptic vesicles to move to/fuse with presynaptic membrane. 3. Fusion releases neurotransmitter molecules into synaptic cleft. 4. Neurotransmitter binds receptors on the postsynaptic membrane opening ion channels and changing neuron voltage

Synaptic plasticity

ability of synapses to strengthen/weaken over time in response to increase/decrease in firing activity - causality only occurs if Cell A fires just before Cell B (temporal contingency).

Where does synaptic plasticity cause changes to?

SP happens at synapse, several underlying mechanisms cooperate (more CA+ = better). Can cause changes in presynaptic axon terminals

Kandel: Habituation

Can learn to ignore large # of innocuous (non essential to survival) stimuli. Homosynaptic. HR and respitory rate decrease when concentrating

Habituation in Aplysia (sea slugs)

Withdrawal reflex habituated recorded from SN & MN to categorise how synapses changed - weakened level of EPSPs called long term depression (LTD)

Long term depression (LTD)

fewer neurotransmitters released by each AP, LT habituation due to inactivation of connection + structural changes: LTD decrease in connections (synaptic boutons) at axon terminals

SP can cause more connections to form at axon terminals due to diff receptors being activated at the synapse. 2 receptor types:

linked to glutomate: ionotropic (AMPA) and (NMDA) receptors and metatropic receptors (mGLuRs)

Sensitisation

learning about noxious stimuli, results from increased synaptic strength, more complex form of declarative memory.

Longn term potentiation (LTP)

more connections (synaptic boutons) at axon terminals and dendrites. Heterosynaptic. Dendrites grow new spines/increase their spine density

How does sensitisation cause changes to axon terminals?

Ionotropic/metatropic receptors present on presynaptic terminals work similarly as on post-synaptic membrane - cause LT activation → activation of 2nd messenger system to cause LT changes to axon terminals. Cyclic AMP activates cell metabolism (protein kinase) in combo with Ca works to enhance vesicle mobilisation/release and close K+ channels. e.g. sea slugs -electrical shocks SN/MN

ST alterations

due to transmitter vesicles mobilisation and release (presynaptic facilitation)

LT alterations

through regulation of protein synthesis and growth e.g. cyclic AMP-response element binding protein (CREB) regulatory role in changes, activates genes in neuron’s nucleus that initiate new synaptic growth

2 types of plasticity

synaptic: change in strength of existing connections between neurons. Neural: ability of neural networks to change through growth/reorganisation. When brain rewired to function differently to previously