The human brain contains billions of specialized cells called neurons that transmit information. Among these, spiny neurons are characterized by small protrusions called dendritic spines along their dendrites—the branch-like extensions that receive signals. These spines function as the primary postsynaptic sites, receiving the vast majority of excitatory inputs.
These neurons are the most abundant type in specific brain regions. Their spiny structure greatly increases the surface area for forming synapses, allowing a single spiny neuron to integrate information from thousands of other cells. This makes them integral to complex neural circuits.
Anatomy and Location of Spiny Neurons
Spiny neurons are categorized into two main types. The first is the pyramidal neuron, named for its pyramid-shaped cell body. These are the most numerous excitatory neurons in forebrain structures like the cerebral cortex and hippocampus, featuring multiple dendrites covered in spines.
The second class is the medium spiny neuron (MSN), which constitutes about 90-95% of the neurons in the striatum. Unlike pyramidal cells, MSNs are inhibitory, meaning they decrease the likelihood that connected neurons will fire. MSNs have a more rounded cell body and project a dense network of dendrites.
The placement of these neurons relates to their roles. Pyramidal neurons in the cortex and hippocampus are involved in higher cognitive processes like thought and memory. In contrast, MSNs are in the basal ganglia, a group of structures for controlling movement, processing rewards, and forming habits.
Function in Learning and Memory
Learning and memory are linked to the brain’s ability to adapt, a property known as synaptic plasticity. Dendritic spines are the physical sites where this plasticity occurs. Each spine forms a synapse with another neuron, and the ability of these synapses to strengthen or weaken over time is the cellular basis of information storage.
This process is clearly demonstrated in pyramidal neurons of the hippocampus and cerebral cortex. When a synapse is repeatedly stimulated, it can undergo long-term potentiation (LTP), which strengthens the connection. LTP involves a cascade of biochemical events, often initiated by calcium ions entering the spine, that increases the number and sensitivity of neurotransmitter receptors on its surface. This makes the neuron more responsive to future signals from the same source.
The physical structure of the spines can also change. In response to new experiences, new dendritic spines can grow, while existing ones can alter their size and shape. Larger, mushroom-shaped spines are associated with stronger, more stable synapses, representing well-established memories. This dynamic process provides a mechanism for encoding and retaining new information.
Role in Motor Control and Motivation
Medium spiny neurons (MSNs) in the striatum regulate movement and motivation. The striatum acts as a gatekeeper, receiving information from the cortex about potential actions and using MSNs to select which action to perform while suppressing others. This process is managed by two circuits: the “Direct Pathway” and the “Indirect Pathway.”
The Direct Pathway is often called the “Go” pathway because its activation facilitates movement. It is composed of MSNs that express D1-type dopamine receptors. When these neurons are activated, they send inhibitory signals directly to the output nuclei of the basal ganglia, which in turn reduces the inhibition these nuclei exert on the thalamus. This disinhibition allows the thalamus to excite motor areas in the cortex, promoting the initiation of voluntary movement.
Conversely, the Indirect Pathway acts as a “No-Go” or braking system and involves MSNs that express D2-type dopamine receptors. When activated, these neurons set off a process that increases the inhibitory output from the basal ganglia. This heightened inhibition suppresses thalamic activity, making it more difficult to initiate movements.
The balance between the “Go” and “No-Go” pathways allows for smooth, controlled motion. This balance is modulated by dopamine, which energizes the “Go” pathway and dampens the “No-Go” pathway, linking motor control to motivation and reward.
Involvement in Neurological Conditions
Dysfunction of medium spiny neurons (MSNs) in the striatum is a feature of several neurological disorders. When the balance between the direct (“Go”) and indirect (“No-Go”) pathways is disrupted, movement problems can arise.
Huntington’s disease is a neurodegenerative disorder characterized by uncontrolled, jerky movements called chorea. This condition is caused by the degeneration of MSNs in the indirect pathway. The loss of these “No-Go” neurons removes the brake on the motor system, leading to a state where involuntary movements cannot be suppressed.
In contrast, Parkinson’s disease presents with symptoms like difficulty initiating movement (akinesia) and slowness of movement (bradykinesia). This is due to the loss of dopamine-producing neurons that project to the striatum. Dopamine depletion impairs the “Go” pathway while leaving the “No-Go” pathway overactive, which makes it difficult to execute voluntary actions.
The plasticity of dendritic spines on MSNs also makes them vulnerable to changes from addiction. Chronic drug exposure can alter the structure and density of spines on these neurons, especially in the brain’s reward circuits. These changes are thought to strengthen pathways that drive compulsive drug-seeking while weakening impulse control.