PMC

Steroid hormones such as glucocorticoids bind to proteins within the cytoplasm of the cell. Upon steroid binding the protein moves to the nucleus where it can affect protein synthesis at the transcription step.
GR = Glucocorticoid receptor; GRE = glucocorticoid response element, a stretch of DNA that binds the GR and activates gene transcription.

Neurotransmitters with discrete localization within the brain. A) The chemical structure of the monoamine neurotransmitter dopamine and a schematic drawing of the localization of dopamine-containing neurons in the human and rat brain and the sites where dopamine-containing axons are found. B) The chemical structure of the monoamine neurotransmitter serotonin and similar brain map showing locations of serotonin-containing cells and their axons.

Schematic drawing of a neuron showing dendrites, where neurons receive chemical input from other neurons; soma (cell body); and axon terminal, where neurons communicate information to other cells. Voltage-gated sodium channels in the membrane of the soma, axon, and axon terminal allow positively charged sodium ions to enter the neuron and produce rapid (in milliseconds) conduction of the excitatory action potential to the terminal. This signal stimulates neurotransmitter release at the axon terminal.

Schematic drawing of a synapse between two neurons. Synaptic vesicles contain a neurotransmitter (NT) and release it when their membranes fuse with the outer cell membrane. Neurotransmitter molecules cross the synaptic cleft and bind to receptors known as ligand-gated ion channels (LGICs) and G-protein–coupled receptors (GPCRs) on the postsynaptic neuron. GPCRs on the presynaptic neuron’s axon terminal alter the function of voltage-gated ion channels and modulate neurotransmitter release. Neurotransmitter transporters remove neurotransmitter molecules from the synaptic cleft so that they can be repackaged into vesicles.

Neurotrophin binding to TRK receptors attracts a variety of intracellular signaling proteins to the intracellular portion of the TrK protein. Activation of these signaling proteins in turn activates transcription factor proteins that act on the nucleus to alter gene expression, as well as other intracellular signaling pathways that promote the growth and differentiation of neurons. Activation of neurotrophin–TrK–intracellular signaling pathways also promotes long-lasting plasticity of synaptic transmission.
BDNF = brain-derived neurotrophic factor.

Schematic drawing of a ligand-gated ion channel (left) showing the confluence of individual subunit proteins that define a pore where the ions flow across the cell membrane. A neurotransmitter binds to part of the protein located outside of the cell. Schematic drawing of a G-protein– coupled receptor (right). Neurotransmitter binds either to sites outside the cell or in a “pocket” formed by protein domains that span the membrane. The G-protein that consists of three separate protein subunits (α, β and γ, light blue) is associated with part of the protein inside the cell.

Schematic drawing of the γ-aminobutyric acid receptor (GABA_A) ligand-gated ion channel complex. The receptor molecule is formed by the confluence of five subunit proteins. In this case, two of the subunits are of the α type, two β and one γ, although many combinations of the 20 known subunits are possible. Globular regions of the protein stick out from the membrane on the extracellular side, and the interfaces between these regions are targets for GABA and for the benzodiazepines and related drugs. The protein domains that span the outer cell membrane are depicted as cylinders. These regions are thought to be targets for general anesthetics (e.g., propofol) neurosteroids, and alcohol. A hole in the middle of the five subunits is the ion conduction pathway, or channel pore.