### A. Overview

Extracellular purines (adenosine, ADP, and ATP) and pyrimidines (UDP and UTP) are important signaling molecules that mediate diverse biological effects via cell-surface receptors termed purine receptors. In this review particular emphasis is placed on the discrepancy between the

/pdf/receptors-for-purines-and-pyrimidines-56f78tnpew.pdf

Receptors for Purines and Pyrimidines

The ionotropic glutamate receptors are ligand-gated ion channels that mediate the vast majority of excitatory neurotransmission in the brain. The cloning of cDNAs encoding glutamate receptor subunits, which occurred mainly between 1989 and 1992 ([Hollmann and Heinemann, 1994][1]), stimulated this

/pdf/the-glutamate-receptor-ion-channels-560mntczdb.pdf

The glutamate receptor ion channels

The Cationminus signpi Interaction.

A review of central 5-HT receptors and their function

http://www.back-in-business-physiotherapy.com/images/files/DescendingControl.pdf

Descending control of pain.

Nicotinic receptors in the brain: correlating physiology with function.

https://www.cell.com/trends/pharmacological-sciences/pdf/S0165-6147(14)00215-6.pdf

Nicotinic ACh receptors as therapeutic targets in CNS disorders

Desensitization of nicotinic ACh receptors: shaping cholinergic signaling

Timing-Dependent Septal Cholinergic Induction of Dynamic Hippocampal Synaptic Plasticity

1. Neuronal nicotinic ACh receptors (nAChRs) were studied in the rat hippocampal slice preparation using whole-cell patch-clamp recording techniques. 2. Responses to ACh (100 microM) were detected on inhibitory interneurones in the Ca1 field of the hippocampus proper and in the dentate gyrus, but not on principal excitatory neurones in either region. The different neuronal types were identified based on their morphology and location. 3. ACh excited interneurones in the hippocampus and dentate gyrus in current-clamp recordings. In voltage-clamp recordings, ACh-activated inward currents were recorded from interneurones in the presence of blockers of synaptic transmission and the muscarinic ACh receptor antagonist atropine. The zero current potential for this response to ACh was near 0 mV. 4. The effect of ACh was mimicked by the nAChR-selective agonists nicotine (100 microM) and 1,1-dimethyl-4-phenyl-piperazinium iodide (DMPP, 100 microM). The response to ACh was reversibly antagonized by the neuronal nAChR antagonist mecamylamine (10 microM). The nAChR alpha 7 subunit-selective antagonists alpha-bungarotoxin (100 nM) and methyllycaconitine (10 nM) also inhibited the response to ACh. 5. These observations demonstrate the presence of functional nAChRs on inhibitory interneurones in the rat hippocampus. Thus, a novel mechanism by which ACh can regulate neuronal activity in the hippocampus is revealed.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1469-7793.1997.603bd.x

Jerrel L. Yakel

Papers

Nicotinic receptors in the brain: correlating physiology with function.

Nicotinic ACh receptors as therapeutic targets in CNS disorders

Desensitization of nicotinic ACh receptors: shaping cholinergic signaling

Timing-Dependent Septal Cholinergic Induction of Dynamic Hippocampal Synaptic Plasticity

Functional nicotinic ACh receptors on interneurones in the rat hippocampus