Tunicamycin impairs olfactory learning and synaptic plasticity in the olfactory bulb.

Area of Science:

• Neuroscience
• Cell Biology
• Molecular Biology

Background:

• Endoplasmic reticulum (ER) stress, induced by tunicamycin (TM), is linked to neuronal death in neurodegenerative diseases.
• Impaired olfactory recognition is a common symptom in patients with Alzheimer's and Parkinson's disease.

Purpose of the Study:

• To investigate the impact of TM-induced ER stress on aversive olfactory learning.
• To explore the effects of TM on synaptic plasticity in the main olfactory bulb (MOB).

Main Methods:

• Intrabulbar infusion of TM in rodents.
• Behavioral analysis of aversive olfactory learning and memory.
• Histological examination for ER stress markers (CHOP).
• Electrophysiological recordings of long-term potentiation (LTP) at MOB synapses.

Main Results:

• TM infusion impaired aversive olfactory learning but not short-term memory.
• TM upregulated CHOP, an ER stress marker, in MOB.
• TM inhibited LTP at mitral-granule cell synapses, affecting early and/or late phases depending on dose.
• High-dose TM reduced paired-pulse facilitation, indicating presynaptic involvement.

Conclusions:

• TM-induced ER stress disrupts olfactory learning by inhibiting synaptic plasticity in the MOB.
• Both presynaptic and postsynaptic mechanisms contribute to TM's inhibitory effects on LTP.
• ER stress is a potential factor in olfactory deficits observed in neurodegenerative conditions.