Neuroscience Basic Terms And Phrases

Front 1

Structure of Gap Junctions

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1 gap junction = 2 connexons

1 connexon = 6 connexins

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Structure of classic chemical synapses

Back 2

Presynaptic axon terminal with transmitter vesicles. Postsynaptic membrane with transmitter receptors and a small synaptic cleft.

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Types of chemical synapses

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axosomatic, axodendritic and axo-axonic

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Chemical synaptic target types (with features)

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Gray Type 1: round synaptic vesicles, large active area, wide synaptic cleft, axodendritic and axosomatic, glutamate.

Gray Type 2: flattened synaptic vesicles, small active area, narrow synaptic cleft, axosomatic, GABA.

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Steps for signal processing in chemical synapses

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Synthesis, storage, release, receptor binding, inactivation

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Type(s) of neurotransmitter(s) formed by cleavage of propeptides by enzymes within vesicle

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Neuropeptides (non-classical neurotransmitter)

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Type(s) of neurotransmitter(s) formed by reaction of precursor molecule reacting with an enzyme that then breaks down the propeptides (vesicle already dissolved by enzyme)

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GABA and ACh (classical small molecule transmitters)

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Neurotransmitters already found in the body, no extra synthesis necessary

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Glutamate and glycine (classical)

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Some examples of ionotropic receptors

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nicotinic AChR, AMPA glutamate receptor, NMDA glutamate receptor, GABAAR and GlyR.

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Agonists

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substances that bind to neurotransmitter receptors and mimic their actions. E.g. nicotine, AMPA and NMDA

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Antagonists

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Substances that bind to, but do not activate, transmitter receptors. Block actions of neurotransmitters or agonists

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Reversal (potential) Equilibrium (IPSP or EPSP reversal)

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The mem. pot. of a post-synaptic neuron (or other target cell) at which the action of a given neurotransmitter causes no net current flow. These and threshold potentials determine postsynaptic excitation and inhibition.

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General rule for postsynaptic actions in terms of reversal potential

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If the reversal potential is more positive than threshold = excitation (EPSP)

If it's more negative than threshold = inhibition (IPSP)

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Some examples of metabotropic receptors

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ACh (muscarinic AChR)

Glutamate

GABA (GABAR)

Noradrenaline/ adrenaline

Neuropeptide (all receptors)

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Inactivation mechanisms

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Re-uptake of neurotransmitters by transporters.

Binding of neurotransmitters to autoceptor at presynaptic membrane.

Diffusion out of synaptic cleft.

Uptake of neurotransmitters by Glial cells

Internalisation of postsynaptic receptors

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Length of short- and long- term plasticity

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Short<1ms

Long = minutes-hours

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Homosynaptic plasticity (plus types)

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synaptic strength change due to own activity. Synaptic depression/facilitation

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Synaptic depression cause

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Depletion of available transmitter. Depletion of vesicles in presynaptic terminal -> desensitization of post-synaptic receptors. Saturation of postsynaptic receptors leads to activation of autoreceptors = negative feedback

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Synaptic facilitation cause

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Accumulation of residue Ca2+ in presynaptic axon terminal = increase in releasable vesicles - Calcium channel facilitation.

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Heterosynaptic plasticity

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Strength change due to activity in another pathway.

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LTP (synaptic plasticity)

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Long Term Potentiation: persistent strengthening of synapse based on recent patterns of activity.

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LTD (synaptic plasticity)

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Long term depression: long-lasting decrease in synaptic strength.

Underlies memory? Memories as a modification in signal strength.

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Hebbs General Rule

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Those that fire together, wire together; those that fire apart, wire apart.

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Between neuron signal transmission stages

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1. 1 motor neuron spike -> many boutons, produces compound EPSP

2. Each bouton - many release sites

3. Each site release 1 vesicle activating many receptors
4. each receptor opens in an all-or-none manner (summated = muscle EPSC)

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Quantum Release Theory

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Vesicles = quanta. One quantum generates miniature end plate potential (MEPP). Summation of the total MEPPs = end plate potential (EPP)

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Transition mediated by glial cells

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Glial cells have receptors to be activated by transmitters released from neurons. They can also release transmitters to act on neurons.

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Retrograde signalling

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Process by which a retrograde messenger, such as nitric oxide, is released by a postsynaptic dendrite or cell body and travels 'backwards' across a chemical synapse to bind to the axon terminal of a presynaptic neuron

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Endocannabinoids role in retrograde signalling

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Suppress transmitter release in a transient or long lasting manner, at both excitatory or inhibitory synapses. Mediates synaptic plasticity. Also a plastic system: postsynaptic activity -> eCB production that move across the synapse and bind to presynaptic receptors = suppress neurotransmitter release

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Calciums role in retrograde signalling

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Calcium influx through NMDARs. Ca2+/calmodulin activate NO synthase. NO released and diffuses. NO activate GC. cGMP enhances vesicle release

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Typical synaptic connection in terms of function: presynaptic inhibition

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axo-axonal synapse: C indirectly inhibits B via A.
C activates receptors on A terminal. A terminal Cl- conductance increases which makes the AP smaller. There is then less Ca2+ entry into A terminal = less transmitter release from A terminal.

= smaller EPSP in B. (usually caused by GABA)

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Typical synaptic connection in terms of function: presynaptic facilitation

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axo-axonal synapse: C indirectly excites B via A.

C activates receptors on A terminal, causing depression of the K+ current = A terminal AP becomes longer. More Ca2+ entry into A terminal. More transmitter release from A terminal. Bigger EPSP in B.

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Typical synaptic connection in terms of function: Reciprocal inhibition

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Tapping patellar tendon activates IA fibres from the muscle spindles. IA excites motoneurons controlling quadriceps. IA fibres also excite inhibitory interneurons, that inhibit motoneurons innervating the hamstring muscle. (negative feedback)

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Typical synaptic connection in terms of function: Reciprocal excitation

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Neurons excite each other in a positive feedback fashion. It may be a mechanism

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Chemical synapse features

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Fast but with synaptic delay. Signal transmitted in one direction. Normally only transmit APs. Can have gain, transmitted signal can be amplified (spike numbers). Highly plastic.

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Electrical synapse features

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Fast, little delay. Most gap junctions are bidirectional. Graded, transmit both APs and synaptic potentials. Do not have gain, transmitted signal is always smaller than the original. Close to lowered cytoplasm pH or elevated cytoplasmic Ca2+. Can be modulated by chemical synapses.

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Sensory modality and submodalities

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A main type of sense, such as vision, hearing, taste.

Major modalities have several constituent qualities (taste types)

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Labelled line code

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specific sensory receptors and neuronal pathways for each modality

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Features that are encoded by sensory systems

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Modality. Amplitude. Temporal detail. Spatial info.

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Sensory pathway as an analogue-to-digital converter

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Converts graded waveforms of sensory neuron signals into all-or-none digital action potentials.

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Basic sensory neuron response type to skin touch in vertebrates

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Slowly adapting
Rapidly adapting

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Range fractionation

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different cells fire for different ranges of signals

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Convergent excitation

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receptive field of a single 2nd order sensory neuron is made up of receptive fields of many 1st order sensory neurons = successively more complex sensory info.

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Receptive fields

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Stimulus space in which stimulation leads to firing of a particular sensory neuron

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Mechanoreceptors in our hands

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Merkel cells (slowly adapting, small RF)

Ruffini endings (slowly adapting, large RF),
Meissner corpuscles (rapidly adapting, small RF),

Pacinian corpusles (rapidly adapting, large RF)

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Two-touch discrimination test

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Two jabs or one? Measures density of touch receptors on the skin. The higher the acuity, the smaller the receptive field size of the receptor.

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Basic sensory pathway from touch to brain

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Skin cells/sensory receptors -> thalamus -> somatosensory cortex.

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Finger receptive field types

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Excitation only. Replacing inhibition. Surround and replacing inhibition.

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Lateral inhibition

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Inhibition of surrounding neurons when one is excited - cause of edge detection in the visual system. Achieved by horizontal cells depolarising the central photoreceptor that synapses the bipolar cell - helps produce centre surround receptive field

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Lamination

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Division of functional layers - seen in the structure of human retina

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Cell types of the retina

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photoreceptors, bipolar cells, ganglion cells, horizontal cells, amacrine cells

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Centre surround receptive fields of bipolar cells

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Less glutamate released = hyperpolarised horizontal cells. Less inhibition of central photoreceptor by horizontal cells = depolarisation. Central photoreceptor activates Off pathway, giving the synapsing off-bipolar cell and off centre and on surround.

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LGN

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6 layers, P-type ganglion cells project to parvocellular LGN cells and M-type cells project to magnocellular LGN cells. LGN projects to primary visual cortex (V1).