Neuronal system

Basic spinal reflex

1. Receptors

2. Afferent signal

3. Integration centre

4. Efferent signal

5. Effectors

Central nervous system

Brain, spinal cord

Peripheral nervous system

Cranial (12), Spinal nerves (31)

Afferent devision

Somatic, visceral, special sensory

Efferent devision

Somatic, automatic (SNS, PNS, Enteric) motors

Soma

Big nucleus, same organelles

Dendrite

Main site for synaptic output

Axon

Send electrical impulses to distant sites in the nervous system

Action potential

1. Resting potential (-70)

2. Threshold reached

3. Na⁺ in → depolarisation

4. K⁺ out → repolarisation

5. Hyperpolarisation

6. Return to resting state

Glia

No electron impulses, support cells

Myelin sheets

Glia membrane wraps around zonal membrane, increase signal speed

Oligodendrocytes - CNS

Schwann - PNS

Astrocytes

CNS start like glia cells, supply metabolites to neurons

Microglia

Innate immune cells of the brain

Ependymal cells

Generate cerebrospinal fluid

Grey/White matter

Grey matter - collection of neuronal cell bodies (outside the brain)

White matter - collection of axons

Cerebrum

Frontal - motor

Parietal - somatosensory

Temporal - auditory

Occipital - visual

Brainstem

Original of cranial nerves, motor function

Cerebellum

Regulation of movement (balance, coordination, posture)

Parkinson’s disease

Familial/sporadic: Mostly sporadic (~90%); some familial (LRRK2, PARK genes)

Cause: Loss of dopamine neurons in substantia nigra; Lewy bodies (α-synuclein)

Symptoms: Resting tremor, bradykinesia, rigidity, postural instability

Treatment: Levodopa/carbidopa, dopamine agonists, deep brain stimulation

Huntington’s disease

Familial/sporadic: Autosomal dominant familial (HTT gene, CAG repeats)

Cause: Degeneration of caudate + putamen due to mutant huntingtin protein

Symptoms: Chorea, psychiatric changes, dementia, personality change

Treatment: Symptomatic only — tetrabenazine, antipsychotics, supportive care

Alzheimer’s disease

Familial/sporadic: Mostly sporadic; some familial (APP, presenilin)

Cause: β-amyloid plaques + tau tangles

Symptoms: Memory loss → cognitive decline

Treatment: Donepezil, rivastigmine, memantine

Multiple sclerosis

Familial/sporadic: Mostly sporadic; genetic predisposition

Cause: Autoimmune CNS demyelination

Symptoms: Optic neuritis, weakness, sensory loss, diplopia, relapsing-remitting

Treatment: Steroids for relapses; interferon-β, ocrelizumab, fingolimod for disease control