Essential Biopsychology

Most notes and the great diagrams below came from the brilliant Biopsychology by John Pinel (click image), which I recommend.



Drugs that reduce or increase neurotransmitter (NT) will tell us what the NT does

Drugs tell us about receptors: if drugs have an effect >> search for receptor & natural NT



– Neurons are cells that receive, conduct and transmit electrochemical signals

– Human brain has around 100 billion neurons

– Each makes on average 7000 connections with other neurons



– Neurons send messages via electrical action potentials

– these happen when the soma is sufficiently stimulated: excitation threshold

– this process is an ‘all-or-nothing’ stimulation

– propagation is the movement of the signal (the AP) along the axon

– movement is caused by influx & efflux of charged ions (Na++ and K+) along the axon

– These cause the release of chemical neurotransmitters into synapses

– Synapses are the small gaps between axon terminal buttons and dendrites/ soma of receiving neuron

– These neurotransmitters are received by receptors in the receiving cell

– Stimulation of receptors may cause an AP in the receiving neuron

– This happens via e.g. the opening/closing of an ion channel allowing ions in/out of the neuron

  1. dendrites/soma stimulated by incoming signals
  2. sufficient stimulation above threshold triggers AP/firing
  3. impulse propagates down axon to terminals
  4. axon terminals impact on dendrites of next cells (and so on to next…)


Axon Action Potential Dendrites Soma Synapse

Soma: metabolic centre of the neuron; cell body containing nucleus

Myelin: fatty insulation around many Axons

Cell membrane: semi-permeable membrane enclosing neuron

Dendrites: projections from the cell body receiving synaptic contacts from other neurons

Axon: long narrow projection from the cell body carrying signal from neuron to neuron

Buttons: the endings of Axon branches that release chemicals into synapses

Synapses: gaps between adjacent neurons where chemicals are released across

Synaptic vesicles: ball membrane packages storing neurotransmitter molecules ready for release near synapses

Neurotransmitters: molecules in vesicles released from neurons

Reuptake: drawing back of neurotransmitters into buttons by transporters

Enzymatic degradation: breaking up of neurotransmitters by enzymes

Autoreceptor: monitors neurotransmitters in synapse to regulate future exocytosis

Axon Terminal Button Vesicles Enzymes Autoreceptor Postsynaptic Cleft




Glial cells: other cells (apart from neurons) found in NS. Several found in NS:

Oligodendrocytes: glial cells with extensions forming many myelin sheaths wrapping around axons of some neurons in the CNS



– Glial support cells called oligodendrocytes have extensions forming myelin sheaths

– These wrap around the axons of some neurons in the CNS

– There are breaks between the myelin sheaths called Nodes of Ranvier

– APs jump from node to node (gap to gap) – called saltatory conduction

– The electrical signal is therefore conducted faster down the myelinated axon than without

– also protects signal from dissipation & interference (my usu. on longer axons)

Myelination Oligodendrocyte Glial Cells



  • an autoimmune disorder where immune system attacks myelin of axons in ANS & CNS as if a foreign substance
  • axons become dysfunctional and degenerate: impairs signal propagation
  • hard scar tissue develops in the CNS white matter
  • causes muscular weakness, numbness, tremor, pain
  • sometimes cognitive decline (65% people) and emotional/ mood issues
  • decline not just demy but L-T tissue destruction, repair & func reorganisation
  • has different levels of severity e.g. steady progressive disability no attacks; or progressive disability with attacks


Other Disease States Involving Myelin Damage:

Guillain-Barre syndrome (corrects itself)

IDP: inflammatory demyelinating polyneuropathies




ARTICLE: Fox et al (2006) –  ‘MS: advances in understanding, diagnosing and treating the underlying disease’

– affects brain, spinal cord & optic nerve

– 2m sufferers worldwide; women:men 2:1; typically 30s/40s

– symptoms vary: numbness or pain, weakness, tiredness, coordination

concentration, exec function, visuo-spatial, processing speed

– tissue injury can involve cerebral grey as well as white matter

– oligodendrocyte progenitor cells can migrate to areas of tissue injury & sometimes replace myelin sheath and sometimes not


ARTICLE: Calabrese (2006) – ‘Neurophysiology of MS’

– in a review of research found conflicting conclusions > more research

– no uniform pattern of cognitive impairments

unaffected: primary language functions, immediate & implicit memory, verbal intellectual skills

usually impaired: information processing, complex visuo-spatial tasks, conceptual reasoning, sustained attention

greatest deficits: working memory, retrieval functions in LT & ST memory


McIntosh-Michaelis (1991) – study of 200 UK sufferers: cognitive impairment e.g. memory and executive problems

Rao (1995) – cognitive dysfunction is highly connected with the amount & location of white matter disease in cerebral hemispheres


Scelerotic plaques indicate secondary inflamation which is more harmful than demyelination alone



ARTICLE: Chiaravalloti & DeLuca (2008) – ‘cognitive impairment in MS’

– review confirms memory issues but also highlights processing speed

– scans show diffs in brain regions used for tests between MS patients & controls

– poss due to: cerebral reorganisation to compensate for damage

pulling in extra resources when difficulty reaches certain level

neuronal damage itself would cause different paths of activation



ARTICLE: Muhlert et al (2014) – ‘the grey matter correlates of impaired decision making in MS’

– speed of decision making impaired esp. in more advanced MS

– in particular gauging risk & adapting (risk adjustment) & slow deliberation

– slower decision making even where MS patient didn’t have other cognitive deficits

– relate findings to grey matter abnormalities (as well as white)

– so cognitive issues not just demyelination per se, because MS impacts grey and not just white matter  




ARTICLE: Chiaravalloti & DeLuca (2008) – ‘cognitive impairment in MS’

– review confirms memory issues but also highlights processing speed

– studies show connection between demyelination & depression 


Siegert & Abernethy (2005)

– in  a review of studies suggest a higher incidence of depression, anxiety and suicide amongst MS sufferers compared to controls

– may be proportionately related to neuropathology in the left anterior temporal/ parietal regions


Is depression caused by organic injury or simply having a life-limiting illness & diagnosis?

Could depression itself have an impact on cognitive health?