Biological Basis of Behavior

Increased reading comprehension abilities due better word recognition

Enhanced auditory perception leading improved listening skills

Improved writing proficiency due enhanced grammar usage

Difficulty speaking while understanding language remains intact

It enhances dopamine reuptake efficiency thereby reducing synaptic transmission intensity.

It mimics dopamine's effects by activating neurons more effectively than natural neurotransmitters can do so themselves.

It increases dopamine production leading to heightened activation of neural pathways associated with reward and pleasure.

It will block dopamine from activating neurons by occupying its receptors without triggering them.

Social interaction and cultural determinants

Unconscious conflicts arising from childhood

Brain chemistry imbalances

Evolutionary inherited traits

Pre-synaptic release

Threshold triggering

Repolarization

Hyperpolarization

Rapid succession of small excitatory signals from one presynaptic neuron triggers an action potential.

Multiple weak excitatory and inhibitory signals arrive at varying times without prompting any response.

Several different presynaptic neurons simultaneously send inhibitory signals to a postsynaptic neuron.

A single strong signal from one presynaptic neuron immediately results in maximum depolarization of a postsynaptic cell.

Serotonin deficits are commonly found across all cases of schizophrenia regardless of symptom type or severity.

Acetylcholine levels tend to show abnormalities that directly correlate with cognitive dysfunction in schizophrenia patients.

An excess of dopamine activity is often associated with schizophrenia symptoms.

Glutamate hypoactivity has been proposed as being responsible for all subtypes of schizophrenia uniformly across individuals afflicted by it.

The pathway for electrical signals in the neuron

The junction where two neurons meet

The gap between the axon of one neuron and the dendrites of another

The location where neurotransmitters are stored

The neurotransmitter molecules bind to receptor sites on the post-synaptic neuron’s membrane.

The pre-synaptic neuron reabsorbs excess neurotransmitters through reuptake.

Sodium-potassium pumps restore resting potential after an action potential.

Voltage-gated ion channels in the axon hillock open in response to stimulus.

Speeds up neural impulses

Stops neural impulses

Slows down neural impulses

Generates neural impulses

Maintenance of resting membrane potential

Formation of cytoskeletal transport structures

Regulation of neurotransmitter synthesis

Leading to saltatory conduction