Nervous System and Neuronal Communication
Glial Cells and Neurons
The nervous system is composed of two basic cell types: glial cells (glia) and neurons.
Glial cells:
Provide support physically and metabolically.
Play roles in scaffolding for brain structure, aligning neurons for communication, insulating neurons, transporting nutrients and waste, and mediating immune responses.
Historical view vs. new evidence:
Long-held belief: glial cells outnumber neurons.
Suzanna Herculano-Houzel’s work suggests there may be a near 1:1 ratio of glia to neurons, which implies human brains are more similar to other primate brains than previously thought (Azevedo et al, 2009; Herculano-Houzel, 2012; Herculano-Houzel, 2009).
Neurons:
Interconnected information processors essential for all nervous system tasks.
Neuron structure overview (Figure 3.8):
Neurons have an outer semipermeable membrane that allows smaller or uncharged molecules to pass and restricts larger/charged molecules.
A neuron’s central building blocks include the soma (cell body), dendrites (input sites), axon (major output pathway), and terminal buttons (end of axon).
Neuron Structure and Function
Soma (cell body): contains nucleus.
Dendrites: branching extensions that receive signals from other neurons.
Axon: long projection that conducts electrical signals to terminal buttons.
Terminal buttons: contain synaptic vesicles housing neurotransmitters (chemical messengers).
Axon length: ranges from a fraction of an inch to several feet.
Myelin sheath:
Fatty insulation around some axons, formed by glial cells, which speeds signal transmission.
Not continuous; contains gaps called Nodes of Ranvier.
Importance of myelin:
Essential for normal neuron function; loss of insulation impairs signal transmission.
Examples of demyelinating conditions:
Phenylketonuria (PKU): reduces myelin and leads to white matter abnormalities with cognitive deficits, exaggerated reflexes, and seizures (Anderson & Leuzzi, 2010; Huttenlocher, 2000).
Multiple sclerosis (MS): autoimmune disorder with widespread myelin loss; causes dizziness, fatigue, loss of motor control, and sexual dysfunction; no known cure, though treatments may modify disease or manage symptoms.
Synaptic transmission precursor:
In healthy neurons, signal travels quickly along the axon to terminal buttons.
Terminal buttons release neurotransmitters into the synaptic cleft (the gap between neurons).
Neurotransmitters cross the synaptic cleft and bind to receptors on the postsynaptic neuron's dendrites.
Receptors are proteins with shapes that vary; neurotransmitters bind in a lock-and-key fashion.
Neurotransmitters fit receptors that match their shape, enabling signal transmission to the next neuron.
Figure 3.9 notes:
Each synaptic vesicle contains about 10,000 neurotransmitter molecules.
The synaptic cleft is a very small space essential for neuron-to-neuron communication.
Neuronal Communication: From Signal to Signal
Neuronal environment:
Extracellular fluid surrounds the neuron; intracellular fluid (cytoplasm) is inside the neuron.
The neuronal membrane keeps these fluids separate, creating a membrane potential that provides energy for signaling.
Membrane potential:
Electrical differences across the membrane arise from ion concentrations.
The semipermeable membrane restricts ion movement, causing uneven distribution of ions across the membrane.
Resting Potential and the Action Potential
Resting potential:
The neuron is in a ready state with ions arranged on either side of the membrane.
Na^+ (sodium) ions are more concentrated outside the cell and tend to move into the cell when gates open.
K^+ (potassium) ions are more concentrated inside the cell and tend to move out of the cell when gates open.
Inside of the cell is slightly more negative than outside, due in part to the Na^+/K^+ pump.
Sodium-Potassium Pump:
Actively transports 3 Na^+ ions out of the cell for every 2 K^+ ions in, creating a net negative charge inside and contributing to resting potential.
Representation:
Other ions:
Chloride ions (Cl^−) and negatively charged proteins contribute to the extracellular positive and intracellular negative charges, respectively.
Activation and threshold:
Incoming signals at dendrites cause gates to open, allowing Na^+ influx due to both charge and concentration differences.
If the membrane potential reaches the threshold of excitation, an action potential is triggered.
The Action Potential and Propagation
Action potential dynamics:
A huge influx of Na^+ ions causes a rapid positive spike in membrane potential (the action potential).
At the peak, Na^+ gates close and K^+ gates open.
K^+ efflux leads to repolarization, followed by hyperpolarization, and eventual return to resting potential.
All-or-none principle:
An incoming signal either reaches threshold and triggers a full-action potential, or it does not.
There is no partial action potential; once triggered, the action potential is regenerated at full strength along the axon (no attenuation).
Saltatory conduction:
The action potential moves down the axon in a leapfrogging fashion between Nodes of Ranvier (gaps in the myelin sheath).
At each node, the signal is refreshed, allowing rapid transmission over long distances.
Transmission to the next neuron:
When the action potential arrives at the terminal button, synaptic vesicles release neurotransmitters into the synaptic cleft.
Neurotransmitters bind to receptors on the postsynaptic neuron, propagating the signal.
Synaptic clearing and regulation:
Excess neurotransmitters are cleared from the synaptic cleft by degradation, diffusion, or reuptake into the presynaptic neuron.
Reuptake pumps neurotransmitters back into the originating neuron, helping to end signaling and regulate neurotransmitter production.
Figure 3.12 shows reuptake as moving a neurotransmitter from the synapse back into the axon terminal.
Neurotransmission speed and mode:
Neuronal communication is often described as an electrochemical event: electrical signal (action potential) along the axon; chemical signal (neurotransmitter) across the synapse.
There are also electrical synapses in which neurons connect via gap junctions, allowing current to pass directly; these are faster but less common in the brain (Connors & Long, 2004).
Neurotransmitters and Their Effects on Behavior (Table 3.1)
Neurotransmitter types and general roles:
Acetylcholine (ACh): involved in muscle action and memory; associated with increased arousal and enhanced cognition.
Beta-endorphin: involved in pain and pleasure; associated with decreased anxiety and tension.
Dopamine: involved in mood, sleep, and learning; associated with increased pleasure and suppressed appetite.
Gamma-aminobutyric acid (GABA): involved in brain function and sleep; associated with decreased anxiety and tension.
Glutamate: involved in memory and learning; associated with increased learning and enhanced memory.
Norepinephrine: involved in heart and intestines, and alertness; associated with increased arousal and suppressed appetite.
Serotonin: involved in mood and sleep; associated with modulated mood and suppressed appetite.
Psychopharmacology from a biological perspective:
Psychotropic medications aim to restore neurotransmitter balance to alleviate psychiatric symptoms.
Major concepts: agonists, antagonists, and reuptake inhibitors.
Agonists, Antagonists, and Reuptake Inhibitors
Agonists:
Chemicals that mimic a neurotransmitter at the receptor site.
Antagonists:
Chemicals that block or impede the normal activity of a neurotransmitter at the receptor.
Reuptake inhibitors:
Block the reuptake of neurotransmitters, keeping them in the synaptic cleft longer to increase their effectiveness.
Examples and applications:
Parkinson's disease involves low dopamine levels; treatment often uses dopamine agonists that mimic dopamine by binding to dopamine receptors.
Some schizophrenia symptoms are associated with overactive dopamine neurotransmission; antipsychotics act as dopamine antagonists by binding to dopamine receptors without activating them.
SSRIs (selective serotonin reuptake inhibitors) prevent reuptake of serotonin, enhancing serotonin signaling; common SSRIs include Prozac, Paxil, and Zoloft.
LSD is structurally similar to serotonin and affects serotonin pathways/receptors.
Practical considerations:
Psychotropic drugs are not instant solutions; improvements may take several weeks.
Many drugs have significant side effects and considerable individual variability in response.
It is common to combine pharmacotherapy with psychological and/or behavioral therapies, which may yield better outcomes than either approach alone (e.g., March et al., 2007).