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)
33
Q
Hormone basics
A
- Hormones enable communication between cells
- Hormones are secreted by specialised glands Endocrine Glands
- Hormones are carried in the bloodstream to specific target regions (e.g., other endocrine glands, organs, cells, the brain)
- Not to be confused with Exocrine Glands (secrete products to outside through ducts)
34
Q
Neural & Endocrine Communication
A
- SIMILARITIES:
∙ Production of chemicals stored for later release
∙ Stimulated to release chemicals
∙ Some chemicals act as hormones & neurotransmitters
∙ React with specific receptors - DIFFERENCES:
∙ Neural communication is fixed between channels to precise locations; hormonal signalling is more generalised
∙ Neural messages are very rapid; hormonal communication is slower and more prolonged
∙ Neural messages are digitised – they fire or not; hormonal signalling is analogue – the more hormone, the greater the effect
∙ Some neural communication is under voluntary control (e.g., muscle), hormone release is not
35
Q
Summary of Functions
A
- Hormone: derived from Greek – To excite / set in motion
- But hormones do not just excite they regulate
►Growth & development
►Reproduction
►Metabolism (intake, production and utilisation of energy)
►Maintenance of internal environment (e.g., homeostasis of bodily systems – temperature, sleep)
►Control of internal organs & systems (e.g., regulation of heart rate, blood pressure, immunity)
36
Q
Maintenance of Homeostasis
A
- Most hormonal release is regulated by process of Negative Feedback
- Output from a gland (hormones) responsible for preventing further release
37
Q
The Pineal Gland (not connecting body and soul)
A
- Produces Melatonin
- Entrainment: Matching of a physiological event to an environmental oscillation
38
Q
Control of Hormone Release
A
- Hormone release generally controlled by 2 key structures in the brain
1. Hypothalamus:
►Located at base of brain
►Hypothalamic Nuclei synthesise Hypothalamic Releasing Hormones that either stimulate or inhibit hormone release from pituitary gland
39
Q
The Pituitary Gland
A
- Releases Tropic Hormones: Hormones that influence release of hormones from other glands
- Anterior Pituitary: Controlled by Hypothalamic, Releasing Hormones
- Posterior Pituitary: Controlled by nerve stimulation from hypothalamus
40
Q
Posterior Pituitary Gland (1)
A
- In response to nerve impulse from hypothalamus releases…Anti-diuretic Hormone (ADH / Vasopressin):
►Stimulates the re-absorption of water by kidneys (conserves water as prevents it being lost in urine)
►Stimulates vasoconstriction (> BP in response to stress)
41
Q
Posterior Pituitary Gland (2)
A
- Oxytocin:
►Causes muscle contraction in uterus (quite handy in childbirth!)
►Stimulates ejection of breast milk (quite handy, but not always!) - Oxytocin – The Tend & Befriend Hormone:
►Elevated levels during sexual arousal & orgasm
►Levels respond to social stimulation - Causing anti-stress effects (inhibiting stress hormones)
42
Q
Anterior Pituitary Gland (1)
A
- In response to hypothalamic releasing hormones…
- Growth Hormone – does what it says
►Pre-pubertal deficits – Pituitary Dwarfism
►Pre-pubertal excess - Gigantism - Thyroid Stimulating Hormone: Stimulates release of Thyroxine by Thyroid Gland
✳︎ If thyroid gland is unable to produce enough thyroxine it swells up in attempt to meet deficit - This is called a Goiter
43
Q
Anterior Pituitary Gland (2)
A
- Gonadotrophins - Sex Hormone Release
►Luteinizing Hormone: Increases production: ∼Progesterone (ovaries)
∼Testosterone (testes & adrenal cortex)
►Follicle Stimulating Hormone:
Increases production:
∼Estrogen (ovaries)
∼Sperm (testes) - Adrenocorticotropic Hormone (ACTH) – Stress Hormone Release: Stimulates release of stress hormones from adrenal cortex
44
Q
Anterior Pituitary Gland (3)
A
- Prolactin:
►Promotes tissue development in breasts during pregnancy
►Stimulates milk production after birth
✳︎Prolactin – The Sexual Desire Hormone? Recent research shows that Prolactin also plays an important role in sexual desire
45
Q
Prolactin & Sexual Desire in Males
A
- Sustained elevation of prolactin post orgasm…
►Increases sexual satiety / reduces sexual desire
►Decreases likelihood of subsequent erections & orgasms - Evidence:
1. Multi-orgasmic men – produce significantly less prolactin at orgasm…So, no reduction in desire – ability for more orgasms
2. [some] Impotence treatments (e.g., Cabergoline)
►Decreases prolactin release (Prolactin Antagonist)
►INCREASE Sexual desire
►DECREASE Refractory period (time before able / want to have sex again)
46
Q
The Adrenal Gland
A
- The Adrenal Glands sit on top of the kidneys
- The Adrenal Glands made up of 2 areas:
1. Medulla (inside) - Responds to nerve impulses from hypothalamus
2. Cortex (outside) - Responds to ACTH (from Anterior Pituitary)
47
Q
The Adrenal Medulla
A
- Secretes Noradrenaline & Adrenaline
►Increase heart rate
►Constrict peripheral blood vessels
►Glucose release - Increased blood flow & energy supply to essential areas (e.g., muscles)
- Short-term preparation for stress - Flight Fight Hormones
48
Q
The Adrenal Cortex
A
- Secretes 3 types of hormones
1. Sex Hormones (Androgens & Estrogens) But mostly secreted by Testes & Ovaries
2. Mineralocorticoids - Aldosterone - Helps kidneys retain sodium & excrete potassium
✳︎ Maintains blood pressure
✳︎ Maintains balance of salt & water in the body
3. Corticosteroids (Stress hormones) - Principally Cortisol - Maintains essential responses during stressful events
49
Q
The Pancreas
A
- The pancreas secretes 2 main hormones: Insulin, Glucagon
50
Q
The Testes
A
- The testes secrete Male Sex Hormones (Androgens)
- Also secreted in small amounts from Adrenal Cortex (so also produced by women)
- The main Androgen is Testosterone
- Production begins during foetal development (organisational effect on sex)
- Testosterone burst at puberty stimulates male secondary characteristics
►Growth & development of male reproductive structures
►Increased skeletal & muscle growth
►Enlargement of larynx (& voice changes)
►Increased body hair
►Sexual drive
51
Q
The Ovaries
A
- Ovaries secrete Female Sex Hormones (Estrogens)
- Also secreted in small amounts from Adrenal Cortex
(so also produced by men) - At onset of puberty (female secondary characteristics)
- Estradiol:
►Breast development
►Distribution of fat (hips, legs, breasts)
►Maturation of uterus & vagina - Progesterone:
►Thickens lining of uterus in pregnancy - Progesterone & Estradiol:
►Stimulate changes in uterus during menstrual cycle
►Sexual behaviour
52
Q
Hormones & Behaviour
A
- Hormones do NOT cause a particular behaviour to change…They change the likelihood of behaviours occurring in appropriate contexts
- Certain behaviours / stimuli can also influence hormone levels e.g., Cortisol levels increase when you get stressed during exams - Testosterone levels increase when a contest has been won
✳︎ BUT - Which comes first – the behaviour or the hormonal change
53
Q
Ventral
A
Toward the front of the body or towards the bottom of the head
54
Q
Dorsal
A
Toward the back of the body, or towards the top of the head
55
Q
Anterior / Rostral
A
Nose end
56
Q
Posterior / Caudal
A
Tail end
57
Q
Lateral
A
Towards the sides
58
Q
Medial
A
Towards the middle
59
Q
Bilateral
A
On both sides of the body or head
60
Q
Ipsilateral
A
On the same side of the body or head
61
Q
Contralateral
A
On the opposite side of the body or head
62
Q
Anatomical Planes
A
- You create a horizontal section when you cut a bread roll for a burger
- You create a sagittal section when you cut a baguette in half (down the middle from the top)
- You create a coronal section when you slice bread
63
Q
Blood Supply to the CNS
A
- A vast circulatory system…to ensure constant supply of resources
64
Q
Fact Time
A
- The brain cannot store glucose…it relies on constant supply of blood for glucose & O2
- 1 sec interruption in supply uses ALL of the brain’s resources
- 6 sec interruption causes unconsciousness
- A few minutes interruption can cause brain damage
65
Q
Protecting the CNS (1): Skull & Spine
A
The Brain & Spinal Cord are delicate & require protection
66
Q
Protecting the CNS (2): Meninges
A
Between skull & brain / spinal cord & spinal column
67
Q
Meningitis
A
Infection / inflammation of the meninges
68
Q
Protecting the CNS (3): Blood-Brain Barrier (BBB)
A
- The CNS cannot kill viruses
- BBB keeps out harmful substances (viruses / bacteria / harmful chemical)
- Small / uncharged molecules (O2 / CO2) can pass through
- Active transport system pumps essentials into brain - glucose / amino acids / vitamins / hormones
69
Q
Protecting the CNS (4): The Ventricular System
A
- The brain floats in a bath of protective fluid (Cerebrospinal Fluid – CSF)
- CSF flows around:
- Subarachnoid space (meninges) - 4 ventricles (little bellies) in the brain
70
Q
The Central Nervous System
A
- Forebrain
- Midbrain
- Hindbrain
71
Q
Hindbrain: Myelencephalon; Medulla oblongata (Medulla)
A
- Control of vital functions:
- Cardiovascular system
- Respiration
- Muscle tone
….through receiving information on heart rate, blood pressure, O2 and CO2 levels
72
Q
Hindbrain: Metencephalon; The pons (bridge)
A
- Serves as link (bridge) between hindbrain & midbrain
- Also involved in:
- Respiration
- Eye movement
- Facial expressions
- Chewing
73
Q
Hindbrain: Metencephalon; Cerebellum (little brain)
A
- Communicates to motor cortex & sense organs:
- Voluntary muscle movement
- Maintenance of balance & equilibrium
- Muscle tone & posture
74
Q
Midbrain: Mesencephalon;
Tectum (roof) & Tegmentum (covering)
A
- Major pathway for sensory & motor impulses between forebrain & hindbrain
- Tectum: Auditory & visual communication
- Tegmentum: Sensory processes, movement, motor control (substantia nigra)
75
Q
Forebrain
A
- Telencephalon (the hemispheres)
- Diencephalon (interbrain)
76
Q
Forebrain: Diencephalon
A
- Thalamus (chamber): Receives sensory information & relays to sensory processing in cortex
- Hypothalamus - Connected to Pituitary gland: Regulation of ANS and Endocrine System
77
Q
Forebrain: Telencephalon (the hemispheres)
A
- Corpus callosum: Nerve fibres that connect he hemispheres
- White Matter: axons covered in myelin sheath
- Grey Matter: Cortex made up of cells
78
Q
Forebrain - Telencephalon
A
- The Limbic System: A group of structures involved in stress & emotion, memory storage & retrieval
- Cingulate Gyrus: Control of emotional behaviour
- Fornix: Links hippocampus to hypothalamus
- Amygdala: Emotional processing & motivation
- Hippocampus: Involved in learning & memory (detection of threat / emotionally charged memories
79
Q
Forebrain: Bumps & Grooves
A
- 3 major grooves divide the cortex: Longitudinal fissure, Central sulcus, Lateral fissure
80
Q
Forebrain: The grooves form 4 major divisions (lobes)
A
- Central sulcus divides the frontal lobe from the parietal lobe,
- Lateral fissure divides the temporal lobe from the frontal & parietal lobes
- Frontal lobe
- Parietal lobe
- Temporal lobe
- Occipital lobe
81
Q
Forebrain - Telencephalon; Cerebral Cortex
A
- These lobes form the structure of the cortex
- Frontal lobe
- Parietal lobe
- Temporal lobe
- Occipital lobe
