215 revised exam terms

The ion that enters the axon terminal when an action potential arrives and triggers vesicles to release transmitter

Calcium (Ca2+)

Two ways a transmitter is cleared from the synapse

Reuptake (transporters) and breakdown by enzymes

Receptors on the sending neuron that sense the transmitter and regulate how much is made and released

Autoreceptors

What decides whether the receiving neuron fires

The sum of EPSPs and IPSPs reaching threshold (EPSP = toward threshold, IPSP = away from it)

Receptor type that is itself the channel; fast and brief

Ionotropic (AMPA, NMDA, GABA-A, nicotinic)

Receptor type that starts an internal chain reaction; slower, longer, amplified

Metabotropic (mGluR, muscarinic, dopamine, adrenergic)

The main excitatory transmitter in the brain

Glutamate

The main inhibitory transmitter, made from glutamate by the enzyme GAD; too little can cause seizures

GABA

Transmitters that tune how well the two main ones work instead of carrying the message themselves

Neuromodulators (dopamine, acetylcholine, serotonin)

Chloride-channel receptor where benzodiazepines, barbiturates and alcohol act

GABA-A receptor

Acetylcholine receptor that is a fast channel, activated by nicotine and blocked by curare

Nicotinic

Acetylcholine receptor that uses second messengers (slower) and is blocked by atropine

Muscarinic

Dopamine pathway whose loss causes tremor, rigidity and difficulty starting movement

Nigrostriatal (substantia nigra to striatum): movement

Dopamine pathway most linked to reward and drug reinforcement

Mesolimbic (VTA to nucleus accumbens, amygdala, hippocampus)

Dopamine pathway to the prefrontal cortex that supports planning and working memory

Mesocortical (VTA to PFC)

Brainstem source of noradrenaline that increases vigilance

Locus coeruleus

Brainstem source of serotonin, linked to mood

Raphe nuclei

Stimulant that reverses the dopamine and noradrenaline transporters so transmitter is pushed out

Amphetamine (and methamphetamine)

Stimulants that block dopamine reuptake; one is used to improve attention in ADHD

Cocaine and methylphenidate

Antidepressants that block serotonin reuptake and take weeks to work

SSRIs

Antidepressants that block the enzyme that breaks down monoamines

MAO inhibitors

Question to ask to decide if a drug is an agonist or antagonist

Does the transmitter system end up with MORE activity (agonist) or LESS (antagonist)?

Drug that activates a receptor only up to a ceiling, so lower overdose risk

Partial agonist (buprenorphine)

Precursor that gives neurons more raw material to make dopamine; treats Parkinson's

L-DOPA (agonist)

Toxin that stops acetylcholine release so muscles can't contract

Botox (antagonist at release)

Drug that fits the same receptor site as acetylcholine and copies it

Nicotine (direct agonist at nicotinic receptors); causes both reward and aversion

Dopamine-receptor blocker used to reduce psychotic symptoms

Chlorpromazine (direct antagonist)

Drug that binds a different GABA-A site, boosts GABA and reduces anxiety

Diazepam / Valium (benzodiazepine, indirect agonist)

Hallucinogenic anaesthetics that block the NMDA channel from a separate site

PCP and ketamine (indirect antagonists)

Drug that blocks adenosine receptors; more brain energy use but less cerebral blood flow

Caffeine (antagonist)

Drug that boosts GABA and suppresses glutamate, causing relaxation and poor balance, memory and judgement

Alcohol

Cannabis compound that is an agonist at CB receptors; high at low doses, anxiety or paranoia at high doses

THC

Cannabis compound that doesn't strongly activate CB receptors, so no high

CBD

Needing more of a drug to get the same effect

Tolerance (the brain compensates to keep homeostasis)

Opposite effects when a drug is stopped, because the brain's compensation is now unopposed

Withdrawal (a sign of physical dependence)

Repeated doses giving a bigger effect; e.g. more anxiety with each cup of coffee in one day

Sensitization

An inactive substance that works through expectation, conditioning and context

Placebo

Barrier of tight capillary junctions, supported by astrocytes, that limits what enters the brain

Blood-brain barrier

Fastest route of drug administration, reaching the brain in seconds

Intravenous (IV)

Why alcohol overdose can be fatal

Brain areas controlling breathing, heart rate and temperature begin to shut down

Brain regions whose circuits are especially vulnerable to THC in adolescence

Prefrontal cortex and hippocampus

Receptor that opens first when glutamate binds, letting sodium in and depolarising the neuron

AMPA

Receptor that opens only with glutamate (plus glycine) bound AND depolarisation removing a magnesium plug

NMDA (a coincidence detector)

The ion through NMDA that acts as a second messenger

Calcium

The lasting change in LTP that makes a synapse stronger

More AMPA receptors inserted into the postsynaptic membrane

Long-lasting strengthening of a synapse, thought to underlie learning and memory

Long-term potentiation (LTP)

Researchers who first showed LTP, in the hippocampus of an anaesthetised rabbit

Bliss and Lomo (1973); Collingridge et al. (1983) showed NMDA dependence

Drug that blocks LTP in brain slices, showing it needs NMDA receptors

AP5 (NMDA antagonist)

Limits of recording LTP in brain slices

Inputs cut, no behaviour, viable for hours only, a cellular mechanism not memory itself

Why a tone alone can come to trigger fear

The weak tone synapse in the lateral amygdala is strengthened by LTP

The three parts of an emotional response

Behavioural, autonomic, hormonal

Amygdala region that receives input from neocortex, thalamus and hippocampus, where learning changes happen

Lateral nucleus

Amygdala region that sends output to hypothalamus, midbrain, pons and medulla

Central nucleus

Animals show no fear to stimuli paired with aversive events, act tamer, and have lower stress hormones; where is the damage?

Central nucleus (stimulating it causes fear; long-term stimulation causes ulcers)

In fear conditioning: the shock

Unconditioned stimulus (US); the UR is jumping and a racing heart

In fear conditioning: the tone that comes to trigger fear

Conditioned stimulus (CS); the CR is freezing to the CS alone

Tone repeatedly presented without the shock until the fear fades

Extinction: new learning, not forgetting; the memory remains; context-dependent

Area that inhibits the conditioned fear response during extinction

vmPFC

Area at the bottom front of the brain made up of orbitofrontal cortex and subgenual anterior cingulate

vmPFC

Area that receives from the mediodorsal thalamus, temporal lobes, VTA, olfactory system and amygdala, and sends to cingulate, hippocampal formation, basal ganglia, lateral hypothalamus and amygdala

vmPFC

Study: square paired with wrist shock then shown alone; vmPFC activity changed with success

Phelps et al. (2004)

Study with three patient groups: one loses the conditioned emotional response but keeps the facts about it

Bechara et al. (1995): amygdala damage impairs the response, facts spared (hippocampal damage shows the reverse)

Study of 9 patients with amygdala stimulation: most had a body response without a felt emotion

Inman et al. (2020)

Patient with vmPFC damage who reasoned well on hypotheticals but ruined his real life

E.R.

Study finding emotional dysfunction (not IQ) correlated with poor real-world competence after vmPFC damage

Anderson et al. (2006)

Why younger people have more emotional outbursts

Amygdala matures early; prefrontal cortex matures late

Theory that body reactions come first and the feeling follows; criticised for ignoring context

James-Lange theory

Who argued facial expressions are innate and universal; caveat that not all emotions were tested

Darwin

The muscle around the eyes that marks a genuine smile

Duchenne's muscle (orbicularis oculi)

Idea that making an expression changes your body state, so emotions are contagious; involves mirror neurons

Ekman's facial feedback hypothesis

Frontal area that executes movement and gives rise to the corticospinal tract

Primary motor cortex (M1)

Area that orders internally generated, memorised sequences of movement

Supplementary motor area (SMA)

Area that plans movements using visual cues; holds mirror neurons

Premotor cortex

Parietal area that works out where the target is and sends it to frontal motor areas

Parietal reach region (inferior parietal lobule); intraparietal sulcus shapes the hand

Giant layer V neurons that start the corticospinal tract

Betz cells

Tract of about 1 million glutamate axons, vital for fine finger movements

Corticospinal tract

After damage to that tract, the one ability that does not return

Independent finger control (precision grip); power grip and arm reach return

Tract controlling face, neck, tongue and eye muscles

Corticobulbar

Tract from the red nucleus to forearms and hands

Rubrospinal

Neurons that fire when you do an action and when you watch it; found in premotor, primary motor and parietal areas

Mirror neurons (Rizzolatti)

Study: neurons fired for memorised button sequences but little when visually cued

Mushiake et al. (1991): SMA; recording, so correlational

Study: magnetic pulses over left SMA before each response; learned with right hand, poor transfer to left

Perez et al. (2008): causal

Study: fMRI region active just before reaching or pointing

Connolly et al. (2003): parietal reach region

Study: patients with limb apraxia and damage to this frontal gyrus couldn't recognise gestures

Pazzaglia et al. (2008): inferior frontal gyrus

Ignoring the left side of space or body after damage here

Right parietal lobe (neglect)

Can't copy gestures or use tools though muscles and sensation work

Limb apraxia (left frontal or parietal damage)

Invasive method using a microwire; current acts like action potentials; mapped the motor homunculus

Microstimulation (Penfield)

Non-invasive coil method that can excite or inhibit depending on pulse pattern

TMS

The three parts of the basal ganglia

Caudate nucleus, putamen, globus pallidus

Cause of tremor, rigidity and trouble starting movement

Death of dopamine neurons in the substantia nigra, so the striatum is starved of dopamine (treat with L-DOPA)

Memory for facts and objects depends on these areas

Cortical areas of the medial temporal lobe (semantic memory)

Memory for events depends on these structures

Hippocampal formation and subcortical structures (episodic memory)

Medial temporal area carrying object ("what") information; its neurons respond to familiar but not novel objects

Perirhinal cortex

Medial temporal area carrying spatial ("where") information, working with the parietal lobes

Parahippocampal cortex

The main cortical gateway into the hippocampus

Entorhinal cortex

Where hippocampal output mainly leaves, then goes back to association cortex and the PFC

CA1 and the subiculum

Tract linking the hippocampus to the mammillary bodies

Fornix

Tract carrying signals from the mammillary bodies to the anterior thalamus

Mammillothalamic tract

Difficulty learning new information after brain damage

Anterograde amnesia (retrograde = can't recall before the damage; pure anterograde is rare)

Chronic alcohol misuse plus thiamine deficiency damaging the anterior and midline thalamus and mammillary bodies

Korsakoff's syndrome