Striatum: Anatomy, Function & Role in Basal Ganglia | 2-Min Neuroscience

Neurons communicate at specialized junctions called synapses. An action potential in a presynaptic neuron travels down the axon to release neurotransmitters that bind to postsynaptic receptors, changing membrane potential. Glutamate is the main excitatory neurotransmitter, increasing firing probability, while GABA is the primary inhibitory neurotransmitter, decreasing firing. Acetylcholine was the first identified neurotransmitter, functioning at neuromuscular junctions. Dopamine is involved in reward-based learning and linked to Parkinson's disease and schizophrenia. Beyond small molecules, neuropeptides like met-enkephalin and oxytocin serve as neurotransmitters, with new ones continually being discovered.

Acetylcholine was the first neurotransmitter discovered, identified in the 1920s through studies of the neuromuscular junction. It plays a crucial role in muscle contraction and in the brain regulates arousal, attention, and learning. Curare blocks acetylcholine receptors at neuromuscular junctions, causing paralysis, while nicotine acts as an agonist at acetylcholine receptors in the brain. Glutamate and GABA are the two most important neurotransmitters in the brain, accounting for approximately 80% of all synaptic transmission. Glutamate is the primary excitatory neurotransmitter, while GABA is the primary inhibitory neurotransmitter. The balance between them is crucial for normal brain function—imbalance can cause seizures (too much glutamate) or excessive sedation (too much GABA). Benzodiazepines enhance GABA effects and are used to treat anxiety, seizures, and insomnia. Dopamine is associated with reward, motivation, and movement, with dysfunction implicated in Parkinson's disease (dopamine loss) and schizophrenia (dopamine excess).

Neurotransmitters are chemical messengers that transmit signals between neurons or from neurons to other cells. Receptors are protein structures on the cell surface that bind to specific neurotransmitters and trigger cellular responses. There are two main types of receptors: ionotropic receptors directly open ion channels when neurotransmitters bind, resulting in fast synaptic transmission. Metabotropic receptors activate G-proteins and second messenger systems, which then open ion channels, resulting in slower but more complex responses. G-proteins include Gs (stimulatory), Gi (inhibitory), and Gq types. Neurotransmitters can be classified into six main categories: amino acids (glutamate, aspartate, glycine, GABA), amines (dopamine, serotonin, norepinephrine), acetylcholine, purines, peptides, and gases. Glutamate is the major excitatory neurotransmitter, while GABA is the major inhibitory neurotransmitter. During synaptic transmission, an action potential arrives at the presynaptic neuron and opens voltage-gated calcium channels, triggering neurotransmitter release. Excitatory neurotransmitters depolarize the postsynaptic membrane by opening sodium channels, while inhibitory neurotransmitters hyperpolarize the membrane by opening potassium or chloride channels. Glutamate receptors include ionotropic receptors (NMDA, AMPA, and kainate) and metabotropic receptors (mGluRs). NMDA receptors require both glutamate binding and membrane depolarization to open, allowing calcium influx that triggers signaling cascades for synaptic plasticity. After neurotransmitter release, glutamate is rapidly removed from the synaptic cleft by astrocytes through sodium-dependent glutamate transporters. Glutamate is converted to glutamine by glutamine synthetase in astrocytes, and glutamine is transported back to neurons and converted back to glutamate by glutaminase, completing the glutamate-glutamine cycle. GABA is synthesized from glutamate by glutamate decarboxylase, requiring pyridoxal phosphate (vitamin B6) and zinc as cofactors. GABA receptors include ionotropic receptors (GABA-A and GABA-B) and metabotropic receptors. GABA-A receptors are ligand-gated chloride channels that mediate fast inhibitory transmission. GABA-B receptors are G-protein coupled receptors that mediate slower inhibitory effects. Benzodiazepines bind to GABA-A receptors at a site distinct from the GABA binding site, enhancing the effect of GABA by increasing the frequency of chloride channel opening. Barbiturates bind to GABA-A receptors at a different site, enhancing the effect of GABA by increasing the duration of channel opening. Barbiturates can activate GABA-A receptors in the absence of GABA, which can lead to respiratory depression and death.

Dopamine, a key catecholamine, mediates reward and motivation through D1 (excitatory) and D2 (inhibitory) receptors in the basal ganglia. Dopamine deficiency causes Parkinson's disease, impairing movement initiation and coordination. Serotonin regulates sleep and mood through multiple receptor subtypes (inhibitory 5-HT1/5-HT5 and excitatory 2/3/4/6/7). GABA serves as the primary inhibitory neurotransmitter, preventing excessive neuronal firing through chloride influx causing hyperpolarization; GABA enhancement treats epilepsy. Glutamate, the most abundant excitatory neurotransmitter, activates NMDA and AMPA receptors but excessive release causes neurotoxicity linked to dementia and Alzheimer's disease. These neurotransmitters collectively govern complex CNS functions from cognition to neurodegeneration.

Neurons communicate through electrical and chemical signals. Action potentials are rapid membrane potential changes generated by sodium and potassium ion movements. Neurotransmitters (dopamine, serotonin, glutamate, GABA) transmit signals across synapses. Dopamine is involved in reward and motor control; serotonin regulates mood; glutamate is the primary excitatory neurotransmitter; GABA is the primary inhibitory neurotransmitter. Synaptic plasticity underlies learning and memory.

Voluntary movement is a conscious, purposeful action performed with awareness and intention to meet body needs, controlled by the motor cortex (specifically the precentral gyrus) which generates motor nerve impulses that travel through motor nerves to effector organs (muscles or glands); the motor cortex exhibits contralateral control where the right hemisphere controls left body movements and vice versa, with different body parts represented in specific regions of the motor homunculus, and motor impulses follow two pathways: direct pathways for head/neck muscles and pathways through the spinal cord for limb muscles.

The motor cortex, located in the frontal lobe, consists of three interconnected areas—the primary motor cortex (area 4), premotor cortex, and supplementary motor area (area 6)—that work hierarchically to produce voluntary movement: the parietal and prefrontal areas first decide what action to take, the supplementary motor area and premotor cortex plan the movement strategy, and the primary motor cortex initiates the actual movement by sending signals to motor neurons; these areas exhibit somatotopic organization, meaning different cortical regions correspond to different body parts, and the supplementary motor area is particularly important for coordinating bilateral movements and planning complex movement sequences.

The motor cortex, located in the frontal lobe, plays a crucial role in planning and initiating voluntary movements. Research using brain-computer interfaces has demonstrated that imagining a movement (without physically executing it) activates the same neural patterns as actually performing the movement. This finding has enabled paralyzed patients to control external devices by simply thinking about desired movements, as the motor cortex generates the neural signals necessary for movement regardless of whether the body can execute them.

Voluntary movements are intentional actions initiated by internal decisions, originating from neurons in the motor cortex. The motor cortex comprises three main areas: primary motor cortex (execution), premotor cortex (planning), and supplementary motor cortex (planning). The prefrontal cortex aids decision-making about which movement to perform. Motor commands follow a pathway: decision-making in prefrontal cortex, planning in premotor and supplementary motor cortices, then execution in primary motor cortex. Motor neurons are organized somatotopically in the primary motor cortex, forming a motor homunculus where larger body part representations correlate with greater movement precision. Commands reach spinal motor neurons via the corticospinal tract, with 90% crossing to the contralateral side in the medulla to innervate distal muscles, while anterior fibers innervate proximal muscles for posture.

Operant conditioning involves learning from consequences: behaviors producing favorable outcomes are strengthened, while those producing unfavorable outcomes are weakened. The brain contains specialized reward circuits that mediate reinforcement. Self-stimulation experiments show organisms will work to produce stimulation in reward circuits, even overriding other drives. The reward system involves two components: 'liking' (pleasure, mediated by opioids) and 'wanting' (motivation, mediated by dopamine). This distinction is important for understanding addiction and motivation.

All animals, including humans, are sensitive to reward, which generates operant conditioning. When the brain encounters an unexpected reward, dopamine is released. Over time, the environment associated with the reward becomes sufficient to trigger reward signals. The brain eventually anticipates the reward and produces reward signals during anticipation, even if the actual reward disappears. This mechanism explains how behaviors can become self-sustaining without the original reward.

Operant conditioning is an organism's adjustment of behavior based on responses to stimuli. Unlike classical conditioning (involuntary, species-specific behaviors), operant conditioning involves conscious responses. B.F. Skinner discovered this through experiments with rats and pigeons. Reinforcement (positive or negative) increases behavior frequency: positive reinforcement adds pleasant stimuli, negative reinforcement removes unpleasant stimuli. Punishment (Type 1 adds unpleasant stimuli, Type 2 removes pleasant stimuli) is less effective. The brain's reward system, particularly the mesolimbic pathway and dopamine, underlies this learning mechanism.

Reinforcement strengthens behavior through two mechanisms: positive reinforcement (acquisition of pleasurable responses) and negative reinforcement (removal of aversive conditions). Both increase behavior repetition. Punishment, involving aversive consequences, decreases behavior. Operant conditioning, developed by Thorndike and expanded by Skinner, demonstrated that behaviors with satisfactory outcomes are repeated. Animals learn to associate specific actions (like lever-pressing) with rewarding outcomes, enabling efficient goal-directed behavior.

The brain has a powerful reward system that operates through two main pathways: positive reinforcement and negative reinforcement (punishment). When a behavior receives a reward, it is likely to repeat and increase in frequency. Conversely, when a behavior receives punishment or criticism, it tends to decrease in frequency. This fundamental mechanism explains how behaviors are shaped and maintained in our daily lives.