Chronic BDNF deficiency permanently modifies excitatory synapses in the piriform cortex

Area of Science:

• Neuroscience
• Synaptic Plasticity
• Molecular Biology

Background:

• Brain-derived neurotrophic factor (BDNF) is crucial for neuronal development, survival, and synaptic plasticity.
• BDNF signaling modulates central nervous system synaptic function.
• Gene deletion of BDNF (BDNF+/-) in mice reveals deficits in synaptic transmission.

Purpose of the Study:

• To investigate the role of BDNF in synaptic transmission at lateral olfactory tract (LOT) synapses.
• To differentiate between acute and developmental effects of BDNF deficiency on synaptic function.
• To explore the impact of BDNF deficiency on excitatory and inhibitory synaptic transmission in the piriform cortex.

Main Methods:

• Electrophysiological recordings of field excitatory postsynaptic potentials (fEPSPs) and excitatory postsynaptic currents (EPSCs) in mouse brain slices.
• Utilized BDNF gene-deficient (BDNF+/-) mice and wild-type littermates.
• Employing pharmacological blockade of BDNF signaling using TrkB-IgG and MK-801.

Main Results:

• BDNF+/- mice exhibited decreased glutamate release probability at LOT synapses, evidenced by increased paired-pulse facilitation (PPF).
• Slower blocking rates of NMDA receptor-mediated EPSCs by MK-801 were observed in BDNF+/- mice.
• Altered inhibitory drive onto mitral cells and decreased renewal rates in associated neurons were found in BDNF+/- mice.

Conclusions:

• Developmental BDNF deficiency leads to chronic alterations in excitatory transmission at LOT synapses.
• BDNF deficiency can exert both acute and long-term effects on synaptic function.
• Compromised BDNF signaling during early development may result in secondary complex changes, impacting neuronal survival and proliferation.