in concentration) to inside the cell (where these ions are lower in
concentration). This produces a change in the membrane voltage such
that the inside of the cell becomes more positive, a depolarization. The
membrane potential moves away from its value at rest and closer to
the threshold for triggering the opening of voltage-gated Na* chan-
nels and the resulting generation of an action potential and neural
signal. This is excitation.
Billions of nerve cells in the brain use glutamate as their neuro-
transmitter. That is, billions of neurons store glutamate in the storage
vesicles in their axon terminals and release it into the synaptic cleft
as a result of a nerve impulse propagating along the axon—these are
called glutamatergic cells. These billions of neurons form trillions of
synaptic connections with other neurons. Most, if not all, neurons
have glutamate receptors on their cell surfaces, receiving excitatory
input from glutamatergic cells.
-ergic: from the Greek ergon = work, -ergic has come to be used as a
suffix for neurotransmitter names, turning them into adjectives.
Glutamatergic has a more poetic ring to it than glutamate-releas-
ing, glutamate-binding, or glutamate-using. Thus, we may speak of
glutamatergic neurons, glutamatergic receptors, glutamatergic
synapses, glutamatergic circuits, glutamatergic drugs, and so
forth.In addition to excitatory input, most if not all neurons will receive
inhibitory input. The major inhibitory neurotransmitter in the
human brain is the molecule gamma-amino-butyric acid, commonly
known as GABA. Large numbers of GABA receptors in the brain are
ionotropic receptors that are Cl channels. The binding of GABA to