Direct ligand-gated ion channels

Receptors Direct ligand-gated ion channel l-Aminobutyrlc-add (GABA)- Barbiturates (allosteric agonists)... 

VI. Direct Ligand-gated Ion Channels (Receptors with Intrinsic Ion Channel)... 

VI. DIRECT LIGAND-GATED ION CHANNELS (RECEPTORS WITH INTRINSIC ION CHANNEL)... 

Neurotransmitter transport can be electrogenic if it results in the net translocation of electrical charge (e.g. if more cations than anions are transferred into the cell interior). Moreover, some transporters may direction-ally conduct ions in a manner akin to ligand-gated ion channels this ion flux is not coupled to substrate transport and requires a separate permeation pathway associated with the transporter molecule. In the case of the monoamine transporters (DAT, NET, SERT) the sodium current triggered by amphetamine, a monoamine and psychostimulant (see Fig. 4) is considered responsible for a high internal sodium concentration... 

The addition of CaBPs can directly activate the IP3-R in a Ca2+-dependent manner, via interaction with the N-terminus region of the receptor. This raises the possibility that CaBPs can act on IP3-Rs to potentiate the Ca2+ signals that arise from other sources, e.g. ligand-gated ion channels. 

Both the inhaled and the intravenous anesthetics can depress spontaneous and evoked activity of neurons in many regions of the brain. Older concepts of the mechanism of anesthesia evoked nonspecific interactions of these agents with the lipid matrix of the nerve membrane (the so-called Meyer-Overton principle)—interactions that were thought to lead to secondary changes in ion flux. More recently, evidence has accumulated suggesting that the modification of ion currents by anesthetics results from more direct interactions with specific nerve membrane components. The ionic mechanisms involved for different anesthetics may vary, but at clinically relevant concentrations they appear to involve interactions with members of the ligand-gated ion channel family. 

---