Research summary
Gaseous neurotransmitters and receptor-based pharmacology define Solomon H. Snyder's contributions to neuroscience and pharmacology. Tritiated naloxone, a potent opiate antagonist, was shown to bind specifically to an opiate receptor in mammalian brain and guinea-pig intestine, with competition for the receptor by various opiates and antagonists closely paralleling their pharmacological potencies; the opiate receptor was found to be confined to nervous tissue, providing the molecular basis for opioid pharmacology and analgesic drug screening [2]. Tritiated haloperidol and tritiated dopamine were used to label postsynaptic dopamine receptors in mammalian brain, with clinical potencies of butyrophenones, phenothiazines, and related antipsychotics correlating closely with their ability to inhibit haloperidol binding, providing a simple in vitro means for evaluating new antischizophrenic candidates [4]. Nitric-oxide synthase was purified 6000-fold to homogeneity from rat cerebellum using a 2',5'-ADP affinity column eluted with NADPH, migrating as a single 150 kDa band on SDS/PAGE with the native enzyme apparently monomeric and requiring calmodulin in addition to NADPH and Ca2+; the work established the enzymatic basis for NO production from arginine with stoichiometric citrulline release [1]. NADPH-diaphorase-staining neurons, uniquely resistant to toxic insults and neurodegenerative disorders, were colocalised with NO-synthase-containing neurons in brain and peripheral tissues, with both markers identifying medium-to-large aspiny neurons in striatum and cortex, often co-expressing somatostatin and neuropeptide Y, and overlapping with choline acetyltransferase in the pedunculopontine nucleus [5]. Carbon monoxide produced by heme oxygenase was proposed as a neuronal messenger acting on guanylyl cyclase; in situ hybridization revealed neuronal expression of constitutive heme-oxygenase messenger RNA matching the localisation of soluble guanylyl cyclase, and zinc protoporphyrin-9 depleted endogenous cGMP in olfactory primary cultures, providing the first evidence that CO functions as a physiologic cGMP regulator analogous to NO [6]. Hydrogen sulfide was identified as a physiologic vasorelaxant: mice with genetic deletion of cystathionine gamma-lyase (CSE) showed markedly reduced H2S levels in serum, heart, aorta, and other tissues, displaying pronounced hypertension and diminished endothelium-dependent vasorelaxation, with calcium-calmodulin shown to activate CSE physiologically [3].
Recent publications
- Isolation of nitric oxide synthetase, a calmodulin-requiring enzyme.DOI
- Handbook of PsychopharmacologyDOI
- Opiate Receptor: Demonstration in Nervous TissueDOI
- Cloned and expressed nitric oxide synthase structurally resembles cytochrome P-450 reductaseDOI
- H 2 S as a Physiologic Vasorelaxant: Hypertension in Mice with Deletion of Cystathionine 纬-LyaseDOI
- Dopamine Receptor Binding Predicts Clinical and Pharmacological Potencies of Antischizophrenic DrugsDOI
- Nitric oxide synthase and neuronal NADPH diaphorase are identical in brain and peripheral tissues.DOI
- Carbon Monoxide: a Putative Neural MessengerDOI
- RAFT1: A mammalian protein that binds to FKBP12 in a rapamycin-dependent fashion and is homologous to yeast TORsDOI
- Protein S-nitrosylation: a physiological signal for neuronal nitric oxideDOI
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Email Solomon H. Snyder 6-12 months before your application deadline. Read several recent papers and reference specific work in your message. Use our how to email a Japanese professor guide for the proven email structure.
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External profiles
- ORCID: https://orcid.org/0000-0002-6818-7022
- OpenAlex: openalex.org
Profile compiled from public sources (Researchmap, OpenAlex, Keio University faculty directory). Last refreshed 2026-05. Report incorrect information.