Biological Psychology Flashcards
1
Q
From Axon to Synapse: 1) Synthesis & Storage
A
- Neurotransmitters (chemical messengers) are synthesised by Golgi Apparatus
- Neurotransmitters are stored in spherical packets called Synaptic Vesicles
- Synaptic Vesicles are passed down microtubules to the Pre-Synaptic Button
2
Q
From Axon to Synapse: 2) Receiving the Action Potential
A
- Synaptic vesicles float around waiting for an action potential to arrive
- The Action Potential (electrical) is received by the pre-synaptic membrane causing depolarisation (membrane becomes more positive)
3
Q
From Axon to Synapse: 3) The Effects of Depolarisation
A
- Depolarisation causes vesicles to dock on pre-synaptic membrane
- Depolarisation causes Calcium channels to open and calcium floods into pre-synaptic button
4
Q
From Terminal to Synaptic Cleft: 4) Release of Neurotransmitters into Cleft
A
- Some calcium ions attach to the dock causing the vesicle to fuse with the membrane
- This creates fusion pores
- The vesicles releases the neurotransmitters into the synaptic cleft through the fusion pores
- The process of neurotransmitter release is called Exocytosis
- The process of exocytosis lasts around 1-2 milliseconds
5
Q
From Synaptic Cleft to Post-Synaptic Membrane: 5) Attachment & Activation
A
- When the neurotransmitter attaches to the post-synaptic membrane it changes its membrane potential (to allow the signal to continue to the next axon….or not)
- Neurotransmitters only attach to specific binding sites / receptors
- Neurotransmitter that attach to specific binding sites are called Ligands
6
Q
Stopping the Information Flow: 6) Deactivation
A
- Activation does not continue for ever (Axons & synapses would become over-stimulated)
- So once the message is received Synaptic transmission is terminated in 2 ways:
1. Reuptake
2. Enzymatic Breakdown
7
Q
Stopping the Information Flow: 1) Reuptake
A
- Neurotransmitters detach from receptors and are taken back into the pre-synaptic membrane
(The neurotransmitters can then be re-used)
8
Q
Stopping the Information Flow: 2) Enzymatic Breakdown
A
- Specific enzymes destroy the neurotransmitters preventing further activation
9
Q
Neurotransmitters
A
- Neurotransmitters – chemicals that communicate between neurons
- Some neurotransmitters cause Depolarisation at post-synaptic membrane - EPSP
- Some neurotransmitters cause Hyperpolarisation at post-synaptic membrane - IPSP
- Some neurotransmitters are inhibitory, some are excitatory and some are both (depending on their receptors)
10
Q
Neuropeptides
A
- The most common neuropeptides are Endogenous Opioids
- (enkephalins / endorphins) → Slows firing rate of neurons carrying pain signals → Natural pain relief & pleasure
11
Q
Glutamate & GABA
A
- Most communication in brain is carried out by Glutamate & GABA
- Glutamate is Excitatory
(it turns things up) - producing EPSPs - it increases/speeds up - GABA is Inhibitory
(it turns things down) - producing IPSPs - it decreases/slows - Both are abundant in CNS (& also in simple organisms)
12
Q
Glutamate
A
- Synapses that use Glutamate are Glutamatergic Synapses
- Glutamate increases activation by:
1. Causing depolarisation = Excitatory Post Synaptic Potentials (EPSPs)
2. Lowering the threshold required for excitation = Increasing firing rate in neurons
13
Q
GABA
A
- Synapses that use GABA are GABAergic Synapses
- GABA prevents the brain from becoming excessively aroused by:
1. Causing hyperpolarisation = Inhibitory Post Synaptic Potentials (IPSPs)
2. Increasing the threshold required for excitation = Decreasing firing rate in neurons
14
Q
Monoamines
A
- Monoamines are synthesised from a single Amino Acid
- They are most abundant in neurons with cell bodies in the brain stem (lots of dendritic spines to allow increased communication)
- 2 types of Monoamines (classified by structure):
1. Catecholamines - adrenaline, noradrenaline, dopamine
2. Indolamines - serotonin
✳︎ Catechol group - (benzene ring & 2 hydroxyl groups)
15
Q
Catecholamine synthesis
A
- Phenylalanines - e.g. cow, eggs, milk, chicken, fish
- Tyrosine (Amino Acid) - (Tyrosine hydroxyls) → L-Dopa - (Dopa decarboxylase) → Dopamine (Dopamine β-hydroxylase) → Noradrenaline (PNMT) → Adrenaline
✳︎ Each step is pre-cursor to next
16
Q
Dopamine
A
- Synapses that use dopamine are Dopaminergic Synapses
- 3 main dopaminergic systems in the mid-brain:
1. Nigrostriatal System: substantia nigra – neostriatum (part of basal ganglia) - Sensory stimuli, Movement, Balance
2. Mesolimbic System
ventral tegmental area – parts of limbic system - (amygdala, nucleus accumbens) - Reinforcement / Reward & Emotion
3. Mesocortical System
(ventral tegmental area – pre-frontal cortex) - Cognition (ST memory, planning, strategy)
17
Q
Excess dopamine levels
A
- Schizophrenia is associated with excessive dopaminergic activity
- (SOME) schizophrenia treatments reduce symptoms by blocking dopamine action
- Side effects of these treatments include the development of Parkinson’s like symptoms - Tardive Dyskinesia: Involuntary movements of face and/or body
- BUT - dopamine not the only chemical implicated in schizophrenia (other treatments also act on serotonergic systems)
18
Q
Noradrenaline & Adrenaline
A
- Noradrenaline & Adrenaline are neurotransmitters in the brain [Also released as hormones from the Adrenal Medulla]
- Noradrenaline (& Adrenaline) synapses are… Noradrenergic (or Adrenergic) Synapses
- The axons of adrenergic neurons project to most areas of the brain and have effect on wide variety of functions mostly to do with arousal & alertness
✳︎ Cognition
✳︎ Motivation
✳︎ Attention & vigilance
✳︎ (also reward pathways)
19
Q
Indolamines [Serotonin]
A
- Tryptophan (Amino Acid) - (Tryptophan hydroxylase) → 5-hydroxytryptophan (5-HTP) - (5-HTP decarboxylase) → 5-hydroxytryptamine - Serotonin
- Synapses that use serotonin are called Serotonergic Receptors
20
Q
Serotonergic pathways
A
- Serotonergic neurons project to most brain areas notably: ∙ Limbic system ∙ Basal ganglia ∙ Cerebral cortex ∙ (and descend along spinal cord)
21
Q
Serotonin - (some) of the roles of Serotonin
A
- Most serotonergic synapses cause IPSPs
- So, most behavioural effects are inhibitory
- Serotonin important for Sleep regulation
∙ Serotonin depletion decreases sleep duration
∙ Ingesting tryptophan may make you sleepy - Serotonin important for Mood regulation
∙ Serotonin depletion related to depression
∙ Drugs that prevent serotonin re-uptake increase activation on serotonin at the synapse e.g., Selective Serotonin Reuptake Inhibitors (SSRIs)
22
Q
Breakdown & Reuptake of Monoamines
A
- Monoamines are broken down by an enzyme called Monoamine Oxidase (MAO)
- MAO converts excess monoamines into inactive substances
- Drugs that prevent the action of MAO are called Monoamine Oxidase Inhibitors
- These drugs increase levels of monoamines
23
Q
Acetylcholine
A
- Acetylcholine (ACh) is synthesised from Choline & Acetate
- Synapses that use acetylcholine are called Cholinergic Synapses - They are generally excitatory
- The are 2 types of cholinergic receptors:
1. Muscarinic (slower, prolonged reactions)
2. Nicotinic (fast acting responses)
24
Q
Breakdown & Reuptake of Acetylcholine
A
- Choline is transported back into pre-synaptic terminal for future use
- Acetylcholine is broken down by the enzyme acetylcholinesterase (AchE)
- Acetylcholinesterase is abundant in the synaptic cleft to prevent over stimulation → muscle spasm - paralysis
25
Q
Pharmacology and the Synapse
A
- Many drugs can alter the action of neurotransmitters
- Agonists: Drugs that increase the action of the neurotransmitter
- Antagonists: Drugs that decrease the action of a neurotransmitter
26
Q
Effects on production of neurotransmitters
A
- L-Dopa is given to Parkinson’s patients to increase release of Dopamine
- α-methyl-ρ-tyrosine (AMPT) inactivates tyrosine hydoxylase preventing synthesis of tyrosine into L-Dopa
∙ Tyrosine (amino acid) - (AMPT - Tyronsine hydroxylase) → L-Dopa - (Dopa decarboxylase) → Dopamine - (Dopamine β-hydroxylase)
27
Q
Effects on storage and release
A
- Reserpine (traditional use as calming agent & snake-bite anti-venom): Makes vesicles leaky, monoamines leak out of vesicles and are broken down by enzymes
- Black widow spider venom: Stimulates the release of acetylcholine
- Botulinum toxin – Botox: Prevents the release of acetylcholine
28
Q
Effects on receptors
A
- Nicotine: Mimics acetylcholine at nicotinic receptors
- Atropine: Blocks muscarinic receptors preventing autonomic functions
29
Q
Effects on degradation and reuptake
A
- Sarin (nerve agent): Prevents acetylcholine breakdown by destroying acetylcholinesterase (action continues)
- Clozapine (Atypical antipsychotic): Blocks serotonergic & dopaminergic receptors preventing serotonin & dopamine binding with receptors
30
Q
Reward pathways
A
- The brain-reward pathway is mostly dopaminergic - (ventral tegmental area – limbic system – frontal cortex)
- It makes us feel good when we engage in behaviour necessary for survival: eating, drinking, having sex
- Not surprisingly most drugs (of use & abuse) also work along this pathway
31
Q
Individual differences
A
- There are large individual differences in drug responsiveness
- Different people have different numbers of receptors which vary in sensitivity depending on genetic & environmental factors
32
Q
some Drugs of Use & Abuse
A
- Cocaine: Triple Reuptake Inhibitor, Blocks reuptake of catecholamines
- Amphetamines: Increases release of dopamine & noradrenaline (& serotonin in higher doses)
- Heroin: Mimics endogenous opioids stimulating dopamine release
- MDMA (Ecstasy): Low doses – dopamine release, Higher doses – stimulate serotonergic synapses
- Marijuana: Mimics endogenous cannabinoids turning off inhibition of dopamine
- Alcohol: Blocks glutamate activity, Stimulates GABAA receptors
- Methamphetamine (crystal meth): Blocks catecholamine reuptake, Hyperstimulation in CNS (longer duration than cocaine)
