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Published on: February 2, 2024
[Neonatal treatment effect with selective inhibitor of 5-HT recapture on [corrected] the cranium-encephalic anatomic
Carolina Peixoto Magalhães1, Luciene Oliveira de Lima, Matilde Cesiana da Silva
1Universidade Federal de Pernambuco, Recife, PE, Brasil.
Insights
Chronic treatment with selective serotonin reuptake inhibitors (SSRIs) in neonatal rats caused significant deficits in somatic growth, brain, and skull size. This highlights the critical role of serotonin in early development.
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Context:
- Selective serotonin reuptake inhibitors (SSRIs) are widely prescribed antidepressants.
- Neonatal exposure to SSRIs may impact neurodevelopment and growth.
- The precise effects of chronic SSRI treatment on early somatic and cranial development require further investigation.
Purpose:
- To investigate the effects of chronic neonatal SSRI (citalopram) treatment on somatic growth, brain development, and skull morphology in male rats.
Summary:
- Neonatal male rats treated with citalopram exhibited reduced body weight, skull size, and brain measurements compared to controls.
- Measurements included body weight, axial length, and skull circumference at 21 days post-birth.
- Brain evaluations were conducted at 8, 15, and 22 days post-birth.
Impact:
- Results suggest SSRIs can impair somatic and craniofacial development, potentially via altered serotonin signaling.
- This underscores the serotonergic system's crucial role in somatic and ontogenic growth.
- Potential hypophagic effects of SSRIs warrant consideration in future studies.
Abstract:
Neonatal repercussion researched of the serotonin selective recapture inibitor (SSRI) chronic treatment about the somatic growth, of the encephalon and skull. Male rats were divided into groups: control (NaCl) and Cit (10 microL/Kg citalopram 10 mg). In 21 post birth days were measured body weight, side axle , front and rear and skull circle. At 8, 15, 22 days after birth, animals were sacrified for the encephalon withdrawal to evaluate the measurements mentioned above. SSRI use caused body growth deficit, skull and encephalon reduction. The retard is possibly caused by the magnitude change of the trophic serotonin action over the skull-facial morphogenesis, reinforcing the serotoninergic system participation over the somatic and ontogenic growth. The SSRI possible hypophagic effects are not discarded.
