Neurophysiology Flashcards
What electrical values describe:
- Resting potential
- Threshold value for Na+ channels to open (Na+ influx) to initiate action potential
- Threshold value for K+ channels to open (K+ outflow) to signal end of action potential
- resting potential -70mV
- when the synaptic signals received by the dendrites and soma of the axon hillock reach -55mV Na+ channels open and Na+ ions enter the axon - “depolarisation”
- When the membrane potential is reversed to +40mV the Na+ channels close and the voltage gated ion channels open causing K+ to move out - “repolarisation”
Describe three types of synapses
a) Chemical - neurotransmitters/chemical molecules released from presynaptic neuron induces changes on the post synaptic neuron
b) Electrical - there is purely electrical communication between the presynaptic and post-synaptic neuron
c) Conjoint - mixture of both electrical and chemical stimulation
What is meant by the following terms in the context of communication between synapses:
a) Facilitation
b) Spatial summation
c) Temporal stimulation
a) Facilitation refers to a presynaptic neuron inducing changes in the post-synaptic neuron which means an action potential is more likely. While some pre-synaptic neurons may directly induce an action potential in the post-synaptic neuron others will cause either slight depolarisation (excitatory neurotransmitters) or hyperpolarisation (inhibitory neurotransmitters) which serve to make an action potential respectively more or less likely
b) Spatial summation indicates that a post-synaptic neuron may be connected to several nearby pre-synaptic neurons. These pre-synaptic neurons may work together to increase/decrease the likelihood of an action potential
c) Temporal summation refers to when one post-synaptic neuron is stimulated several times by the same pre-synaptic neuron the summation of these effects increases/decreases the likelihoog of an action potential.
What are the satiety and feeding centres
- Ventromedial hypothalamus is the feeding centre
- Lateral hypothalamus is the satiety centre
Describe mediators of appetite (oxigenic) and satiety (anorexigenic)
Oxigenic:
-Ghrelin (only oxigenic mediator produced in the CNS)
- Neuropeptide Y
Anorexigenic:
- Leptin (produced by adipose tissue)
- Cholecystokinin
- Serotonin
Food and food cues increase dopaminergic activity in nucleus accumbens - destruction of dopamine pathways reduces eating behaviour
In obesity D2 receptors are reduced in the striatum
What are the hypothermia and hyperthermia centres
- Preoptic anterior hypothalamus - hypothermia centre. Stimulation here causes sweating and vasodilation from parasympathetic drive
- Posterior hypothalamus - hyperthermia centre. Stimulation here causes shivering and vasoconstriction leading to hyperthermia.
A lesion in BLANK would affect diurnal body temperature
Median eminence
How does malignant hyperthermia arise?
Through abnormal excitation-contraction coupling in skeletal muscles
Can levodopa withdrawal cause NMS
Yes - NMS causes hyperthermia
What fibres carry pain sensation to the dorsal horn of the spinal cord?
- C fibres (unmyelinated)
- A-delta fibres (sparsely myelinated)
Which routes are responsible for fast and slow transmission of pain
Fast transmission of pain occurs through lateral spinothalamic tract - this aids localisation of pain
Slow transmission of pain occurs through recticulothalamic tract (this aids subjective sensation)
Name some neurochemical inputs that can modulate pain perception
- Opiod receptors in the dorsal horn and periaquetal grey matter (brain stem) modulate pain intensity
- Serotonergic raphne nuclei provide descending fibres that may affect how pain is perceived - explains the role of TCAs in pain
What is thalamic pain syndrome?
Stroke affecting thalamoperforating branches of posterior cerebral artery - here light cutaneous stimulation may cause contralateral loss of sensation with burning or aching pain
What areas of the brain play a role in the regulation of thirst
Subfornical organ
Organum vasculosum
Lamina terminalis
Name some inputs that may increase thirst
- Angiotensin II –> neurotransmitter that increases thirst
- Baroreceptors in aorta and carotid
How does ADH maintain a normal body fluid balance
Increases water reabsorption at renal tubules and maintains normal body fluid balance
Syndrome of inappropriate ADH secretion:
- Damage to paraventricular and supraoptic hypothalamic nuclei
- Carbamazepine or chlorpromazine
- Neoplastic syndromes
–> findings are low sodium, reduced osmolarity, normal renal excretion of sodium and high urine osmolality
How do the following disorders have abnormalities of physiological drives?
a) Kluver Bucy Syndrome
b) Laurence Moon-Biedl Syndrome
c) Prader-Wili Syndrome
d) Kleine-Levin Syndrome
e) Psychogenic polydipsia
a) Bilateral lesions of amygdala and hypothalamus. Reduced aggressive behaviour, examine objects with mouth, hypermetamorphosis, prominent oral exploratory behaviour and hypersexuality
b) Autosomal recessive genetic locus 11q13. Hypogonadism, obesity, low IQ, retinitis pigmentosa (no hypothalamic lesion)
c) Paternal deletion 15q11-q13. Reduced oxytocin neurons and satiety neurons. Poor control of body temperature and daytime hypersomnolence - related to hypothalamic disturbance. Obesity, short stature, hyperphagia, hypogenitalism, impaired glucose tolerance, hypotonia.
d) Kleine-Levin Syndrome - viral illness, resolves by 3rd decade of life. Compulsive eating, hyperphagia, hypersomnolence, hyperactivity, hypersexuality, exhibitionism - hypothalamic abnormality
e) Increase water intake not related to hypovolaemia or hypernatraemia
In fetal life where does neurogenesis occur?
Subventricular zone (surrounds the ventricles of the neural tube)
After neurons are produced in the subventricular zone they migrate outwards towards the cortical plate.
Thalamic axons that project to the cortical plate first synapse onto a transient layer of neurons called subplate neurons.
In normal development these axons detach from the subplate neurons and proceed to synapse to true cortical cells. This may not occur as readily in Schizophrenia
What is heterotopia?
Abnormalities of neural migration and neurons staying in ectopic positions
When does neuronal migration take place?
First 6 months of gestation
What is radial migration?
The process that excitatory neurons reach the cortex. Here radial glial cells form scaffolding that helps guide migrating neuronal cells - the cells accumulate in an inside out pattern (newest on outside) to form Rakic’s cortical columns
How does neuronal migration differ for inhibitory interneurons?
In external and internal granular layers - these cells tangentially migrate
Describe the time points that myelination occurs?
Starts around 4th gestational month
Largely completed by year 2
In association cortix may reach full extent by third decade of life
Which disease are associated with excessive vs. reduced synaptic pruning?
Schizophrenia - excessive
ASD - reduced
Synaptogenesis occurs between 2nd trimester - 10 years (peaks period < 2 years). By mid-childhood more neurons and cellular processes are established than needed for adult brain therefore pruning occurs into teenage years
What does cerebral plasticity refer to?
Ability of the capability of the brain to be moulded throughout life.
Cortical sensory maps can be reorganised - i.e. with practice for jugglers, musicians etc.
Phantom limb pain - amputated limb may show reorganisation so that area is on cortical face area
What hormones are released from the following areas?
a) Anterior pituitary
b) Posterior pituitary
c) Hypothalamus
Anterior pituitary:
- Growth Hormone
- Luetenizing hormone (gonadotrophin)
- Follicular stimulating hormone (gonadotrophin)
- Adrenocorticotrophic hormone (corticotrophin)
- Thyroid stimulating hormone (thyrotropin)
- Prolactin
Posterior pituitary:
- Vasopressin (ADH - antidiuretic hormone)
- Oxytocin
Hypothalamus:
- Corticotrophin releasing hormone
- Growth hormone releasing hormone
- Gonadotrophin releasing hormone
- Thyrotrophin releasing hormone (increases prolactin release)
- Somatostatin (inhibits GH)
- Prolactin inhibitory factor (dopamine)
Name some factors that affect the release of vasopressin?
Pain, stress , exercise, morphine, nicotine and barbituates increase release
Alcohol decreases release
Vasopressin is structurally very similar to Oxyctocin.
Vasopressin is involved in attention, memory and learning
What behaviours is Oxytocin involved in?
Bonding - initiation and maintenance of maternal behaviour, social bonding and sexual receptivity
Describe the pathway of thryoid hormone release?
TRH from hypothalamus –> TSH from anterior pituitary –> Thyroxine (T4) and Triidothyronine (T3, more potent. T4 is converted to T3 at target organs)
Patients with depression, mania, alcohol withdrawal and anorexia may show a blunted TSH response to exogenous administration of TRH
T3 activates nerve growth factor genes in early development but not in the adults brain
Hypothyroidism implicated in change to rapid cycling bipolar from previously stable. GAD associated with hyperthyroidism
Lithium may predisopose to hypothroidism in middle aged women who carry antithyroid autoantibodies
What is the pathway for cortisol release?
CRH (hypothalamus) –> ACTH (anterior pituitary) –> cortisol (adrenal glands)
How does chronic stress cause atrophy in the hippocampus
- Decreased neurogenesis in the hippocampus and atrophy of dendrites
- Atrophy of the hippocampus can cause impaired memory performance - additional as they may be aborisation of the dendrites in the basolateral amygdala there can be a memory bias towards negative events
When do cortisol levels peak?
6-7am and there is diurnal variation
Outline how cortisol levels have been found to vary in
a) Depression, Mania, (psychotic), OCD and Schizoaffective Disorder
b) PTSD
a) Hypercortisolemia - there may be loss of diurnal variation –> seen especially in melancholic depression
b) PTSD - due to increased glucocorticoid receptors in the pituitary there may be hypocortisolemia (? genetic vulnerability causing)
Outline how failure to suppress ACTH/CRH and cortisol production is shown with the dexamethasone suppression test:
At 11pm 1mg dexamethasone is administered with baseline cortisol measurement
The next day at 8am, 4pm and 11pm - serum cortisol is measured again
If any samples have > 5mcg/L this indicates non-suppression
DST non suppression is shown in….
DST suppression is shown in…
Non-suppression:
- Depression (especially if psychotic features/melancholic -sensitivity increases from 50% to 60-70%), mania, schizoaffective disorder
- Cushing’s, alcohol use disorder, extreme weight loss pregnany
- Use of other drugs that reduces dexamethasone availability - barbituates, anticonvulsants
Suppression:
- Hypopituitarism
- Steroids
- High-dose benzodiazepine
- Addisons
How does DST affect prognosis in depression:
- If non-suppression despite recovery from symptoms evidence suggests may be more likely to relapse, poor prognosis and possible later suicidality
Where are pinealocytes found and what do they secrete?
Pinealocytes are found in the pineal gland (epiphysis) and secrete serotonin and melatonin
What is corpora arenacea or brain sand?
Corpora Arenacea/Brain sand are calcium deposits that are found in the pineal gland that become more prominent with age
How is melatonin synthesised in the pineal gland?
Through the action of 2 enzymes:
- Serotonin-N-acetlyase
- 5-hydroxyindole-O-methylytansferase
