Mortality and ventilatory effects of central serotonin deficiency during postnatal development depend on age but not sex.

Serotonin (5-HT) influences brain development and has predominantly excitatory neuromodulatory effects on the neural respiratory control circuitry. Infants that succumb to sudden infant death syndrome (SIDS) have reduced brainstem 5-HT levels and Tryptophan hydroxylase 2 (Tph2). Furthermore, there are age- and sex-dependent risk factors associated with SIDS.

Rare anoxic brain injury sequela of delayed posthypoxic leukoencephalopathy due to recreational drug overdose with benzodiazepines.

A growth in recreational drug use will lead to a rise in delayed posthypoxic leukoencephalopathy cases. Physicians may inadvertently misdiagnose this rare condition as a primary psychiatric disorder by not maintaining a broad differential diagnosis.

Chronic central serotonin depletion attenuates ventilation and body temperature in young but not adult Tph2 knockout rats.

Genetic deletion of brain serotonin (5-HT) neurons in mice leads to ventilatory deficits and increased neonatal mortality during development. However, it is unclear if the loss of the 5-HT neurons or the loss of the neurochemical 5-HT led to the observed physiologic deficits. Herein, we generated a mutant rat model with constitutive central nervous system (CNS) 5-HT depletion by mutation of the tryptophan hydroxylase 2 (Tph2) gene in dark agouti (DA(Tph2-/-)) rats.