Introduction to Biopsychology

Biopsychological Processes

Neuropsychology
Study of the function of the brain, by looking at the efects of brain damage on bodily functon

Concerned with integration of psychological observations of behaviour + mind with neurological
observations of brain + nervous system.i

Fairly new and rising feld of psychology.

Roles of neuropsychologists
 Diagnosis of neurological disease
 Organic vs non-organic disease
 Diferentaton of normal aging
 Hospital work and rehabilitaton
 Academic research
 Private practse and medico-legal work

Causes of brain damage
 Vascular strokes (brain + blood supply)
 Tumours (can impact functons or cause damage upon removal)
 Degeneratve diseases (eg: Alzheimerss)
 Infectous diseases (eg: HIV/AIDS)
 Trauma (brain injuries)
 Epilepsy (transient loss of consciousness)

Diagnosis
 Can infer behavioural changes from brain injuries (using scans)
 Can determine brain injuries from behavioural changes

If there are physical changes in the lef side of the body, it means the right hemisphere of the brain
has been efected.

Organic Disease
Observable causes in the brain of changed behaviour

 Traumatc brain injury (leads to bruising and swelling)
The frontal lobe of the brain is more vulnerable
Medulla oblongata: regulates heart rate and breathing
Brain stem: controls the bodyss vital functons
 Degenerate brain diseases
Eg: Parkinsonss, Dementa of Alzheimerss
 Chronic Traumatc Encephalopathy (repeated concussions sufered by football players and
boxers)

Non-organic Disease
 Pseudodementa: suddenly comes on due to an event. For example, depression caused by
bereavement and / or drugs.

,  Psychogenic non-epileptc seizures (not reflected in brain scans)
Can be caused by: Malingering (for insurance claims, for personal gain) ; Psychological
conversion disorder (traumatc mental event reflects outwardly but not in the brain)

Types of Dementia
 Dementa of Alzheimer
 Vascular dementa: sudden drop in functoning, followed by a recovery. Litle strokes over
tme that start to compound.
 Dementa with Lewy bodies
 Dementa of frontotemporal lobes

Phineas Gage: a classic case
US railway worker who made a mistake when plantng dynamite charge.

Blew a steel rod through his head. Showed quick recovery + no discernible cognitve damage.

BUT a complete personality change took place.

Normal  aggressive behaviour etc

The Nervous System
Divided into CNS + peripheral nervous system (PNS)

1. CNS = brain and spinal cord

2. PNS: Somatc (voluntary muscle actvaton) + Autonomic (automatc, cardiac, glands) system:


 Autonomic further divided into sympathetc and parasympathetc nervous systems
Controls glands, organs + involuntary muscles
- Sympatheti: actvaton or arousal functon. Gets the body ready to deal with stress.
- Parasympatheti: slows down the body, maintains homeostasis (delicately balanced
internal state) Is normally actve.
 Somatc further divided into aferent (sensory) and eferent (motor) pathways
Controls skeletal muscles / voluntary movement + senses


Communication in the nervous system
Hardware

Neurons – communicaton

- Dendrites: receive info from other neurons
- Soma: cell body
- Axon: transmit info away

Neurons arenst the only cells in the brain, there are also glial cells: serve as a structure on which
neurons can develop / hold neurons in place / get nutrients for neurons / insulaton. Produce myelin
(faty substance).

, - Myelin sheath: speeds up transmission of electrical transmissions and insulates axon (prevents
dissipaton of electrical signal). Demyelinaton disrupts transmission of neural impulse.
- (axon) Terminal buton: end of axon. Secretes neurotransmiters.
- Neurotransmiters: chemical messengers (serotonin, dopamine etc)
- Synapse: point at which neurons connect



Neural Impulses

 Fluids both inside and outside the neuron (carry electrically charged partcles / ions)
 Neuron at rest: negatie iharge on insid e compared to outside
 Negatve protein ions are too big to ft through ion channels in neural cell membrane.
 Restng potental = -70 millivolts
 Neural cell membrane is semi-permeable.
 Outside neuron: positvely charged.
 Positvely charged sodium ions outside neuron cluster around the membrane.
 Diference in charges creates an electrical potental.
 Neuron dendrites becomes stmulated. Membranes open.
 Influx of positvely charged sodium ions into the neuron.
 Outside of neuron thus becomes more negatvely charged, and the inside positve.
 Shif in electrical charge travels along the axon.
 Reversal of electrical charge is known as the Aiton Potentaa.
 Sodium ion channels close as soon as the acton potental has passed.
 Cell membrane pumps the positve sodium ions out of the cell again.
 Small positvely charged potassium ions also move from inside the neuron to the outside to help
return the neuron to a negatve electrical charge.
 Neuron is now capable of ‘fring ofs again (dependent on sum of excitatory + inhibitory
messages received by the cell)


Acton Potental follows the ‘aaa-or-non aaw’: either fres at full strength or not at all.

Absoaute refraitory period : the tme during which another stmulus given to the neuron (no mater
how strong) will not lead to a second acton potental.

Neurons receive some neurotransmiters that are aimed at causing it to fre, and others that are
aimed at preventng it from fring. The neuron adds together the efects of these messages.

A strong stmulaton: will cause the neuron to fre repeatedly and causes more neurons to fre.

What happens at the synapse:

 Presynaptc neuron: has synaptc vesicles containing neurotransmiters.
 Postsynaptc neuron: ion channels that have receptor sites (proteins that allow only
partcular molecules of a certain shape to ft into it).
 Charge travels along axon to buton.
 Release of neurotransmiters into the synaptc clef when electrical charge reaches the
synaptc vesicles.
 Receptor sites on postsynaptc neurons only bind with corresponding neurotransmiters
(lock and key system).