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Male reproduction depends on hormonally driven behaviors and numerous genes for testis development and spermatogenesis. Neuroplastin-deficient (<i>Nptn^−/−</i>) male mice cannot sire offspring. By immunohistochemistry, we characterized neuroplastin expression in the testis. Breeding, mating behavior, hormonal regulation, testicular development, and spermatogenesis were analyzed in cell-type specific neuroplastin mutant mice. Leydig, Sertoli, peritubular myoid, and germ cells express Np, but spermatogenesis and sperm number are not affected in <i>Nptn^−/−</i> males. Neuroplastin lack from CNS neurons or restricted to spermatogonia or Sertoli cells permitted reproduction. Normal luteinizing hormone (LH) and follicle-stimulating hormone (FSH) blood levels in <i>Nptn^−/−</i> males support undisturbed hormonal regulation in the brain. However, <i>Nptn^−/−</i> males lack mounting behavior accompanied by low testosterone blood levels. Testosterone rise from juvenile to adult blood levels is absent in <i>Nptn^−/−</i> males. LH-receptor stimulation raising intracellular Ca²⁺ in Leydig cells triggers testosterone production. Reduced Plasma Membrane Ca²⁺ ATPase 1 (PMCA1) in <i>Nptn^−/−</i> Leydig cells suggests that <i>Nptn^−/−</i> Leydig cells produce sufficient testosterone for testis and sperm development, but a lack of PMCA-Np complexes prevents the increase from reaching adult blood levels. Behavioral immaturity with low testosterone blood levels underlies infertility of <i>Nptn^−/−</i> males, revealing that Np is essential for reproduction.