Acetylcholinesterase (ACHE; EC 3.1.1.7) is a cholinergic enzyme mainly found in neuromuscular junctions and cholinergic type chemical synapses, and is often used in biochemical research. Acetylcholinesterase catalyzes the breakdown or hydrolysis of acetylcholine and some other choline esters that act as neurotransmitters into acetate and choline. Acetylcholinesterase's main role is to terminate neuronal transmission and signaling between synapses to prevent ACh spread and activation of nearby receptors [1] .

D-Amphetamine sulfate, a central nervous system (CNS) stimulant, acts on monoamine transporters to increase noradrenaline, dopamine, and serotonin levels in synapses. Additionally, it serves as an antagonist to the α7 nicotinic acetylcholine receptor (nAChR).

VU10010 (VU 10010) is allosteric potentiator of M4 acetylcholine receptors.

Acetylcholine perchlorate is the perchlorate salt of acetylcholine. Acetylcholine, an endogenous neurotransmitter at cholinergic synapses, could amplify the action potential of the sarcolemma following by inducing muscle contractions.

Leptin (116-130), a bioactive fragment of leptin, enhances synaptic plasticity in the hippocampus by promoting AMPA receptor trafficking to synapses. It preserves hippocampal synapse integrity and prevents neuronal cell death in amyloid toxicity models, showing promise for Alzheimer's disease (AD) research [1].

S-8510 is a GABA-A receptor inverse agonist. S-8510 selectively potentiated pentylenetetrazol-induced convulsion without affecting minimal electroconvulsive shock- or strychnine-induced convulsion in ddY mice. S-8510 ameliorated memory impairment induced

Phenytoin (5,5-Diphenylhydantoin) is a hydantoin derivative and a non-sedative antiepileptic agent with anticonvulsant activity. Phenytoin potentially acts by promoting sodium efflux from neurons located in the motor cortex reducing post-tetanic potentiation at synapses. The reduction of potentiation prevents cortical seizure foci spreading to adjacent areas, stabilizing the threshold against hyperexcitability. In addition, this agent appears to reduce sensitivity of muscle spindles to stretch causing muscle relaxation.

Aniracetam (Ro 13-5057)(Ro 13-5057), a nootropic and neuroprotective drug, selectively modulates the AMPA receptor and nAChR.

Rp-cAMPS sodium salt, a cAMP analog, is a potent, competitive cAMP-induced activation of cAMP-dependent PKA I and II (Kis of 12.5 μM and 4.5 μM, respectively) antagonist. Rp-cAMPS sodium salt is resistant to hydrolysis by phosphodiesterases[1][2][3][4][5][6]. A membrane-permeable competitive cAMP antagonist (Rp-cAMPS) that blocks PKA activation by binding to the regulatory subunits without dissociating the kinase holoenzyme also inhibits synaptic plasticity but has no effect on normal synaptic transmission[2]. Rp-cAMPS (10 μM, 15 min) decreases the monosynaptic EPSCs evoked at the PB-CeLC and BLA-CeLC synapses in slices from arthritic rats but not in control neurons from normal animals. The inhibitory effect of Rp-cAMPS is significant compared to predrug (ACSF) control values obtained in the same neurons[2]. [1]. R J de Wit, et al. Inhibitory action of certain cyclophosphate derivatives of cAMP on cAMP-dependent protein kinases. Eur J Biochem. 1984 Jul 16;142(2):255-60. [2]. Rothermel JD, et al. A mechanistic and kinetic analysis of the interactions of the diastereoisomers of adenosine 3’,5’-(cyclic)phosphorothioate with purified cyclic AMP-dependent protein kinase. Biochem J. 1988 May 1;251(3):757-62.[3]. Fu Y, et al. PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior. Mol Pain. 2008 Jul 16;4:26.[4]. Kuriyama S, et al. Isoproterenol inhibits rod outer segment phagocytosis by both cAMP-dependent and independent pathways. Invest Ophthalmol Vis Sci. 1995 Mar;36(3):730-6.[5]. Dostmann WR, et al. Probing the cyclic nucleotide binding sites of cAMP-dependent protein kinases I and II with analogs of adenosine 3’,5’-cyclic phosphorothioates. J Biol Chem. 1990 Jun 25;265(18):10484-91.[6]. Van Haastert PJ, et al. Competitive cAMP antagonists for cAMP-receptor proteins. J Biol Chem. 1984 Aug 25;259(16):10020-4.

Dehydroepiandrosterone sulfate (PB-005) influences the migration of neurons, arborization of dendrites, and formation of new synapses.

In the central nervous system, 2-Arachidonoylglycerol is a second endogenous cannabinoid ligand