β-Adrenoceptor blockade depresses molecular and functional plasticities in the rat neocortex

• Published in: Brain research bulletin 2010-07, Vol.82 (5), p.284-288
• Main Authors: Flores, Osvaldo, Núñez, Héctor, Pérez, Hernán, Morgan, Carlos, Soto-Moyano, Rubén, Valladares, Luis, Burgos, Héctor, Olivares, Ricardo, Hernández, Alejandro
• Format: Article
• Language: English
• Subjects: Adrenergic beta-Antagonists - pharmacology; Analysis of Variance; Animals; Brain-derived neurotrophic factor; Brain-Derived Neurotrophic Factor - administration & dosage; Brain-Derived Neurotrophic Factor - metabolism; Conditioning, Operant - physiology; Corpus Callosum - physiology; Dose-Response Relationship, Drug; Electric Stimulation - methods; Gene Expression Regulation - drug effects; Gene Expression Regulation - physiology; Long-term potentiation; Long-Term Potentiation - drug effects; Long-Term Potentiation - physiology; Male; Neocortex - drug effects; Neocortex - physiology; Neurology; Neuronal Plasticity - drug effects; Neuronal Plasticity - physiology; Occipital cortex; Operant conditioning; Propranolol; Propranolol - pharmacology; Rats; Rats, Sprague-Dawley; Receptors, Adrenergic, beta - metabolism; Time Factors; β-Adrenoceptor
• ISSN: 0361-9230; 1873-2747
• DOI: 10.1016/j.brainresbull.2010.05.010

Abstract β-Adrenergic receptor stimulation can significantly facilitate synaptic potentiation in the hippocampus and enhance memory processes, but its effect on neocortical plastic mechanisms is less conclusive. In the present study we determined the effect of propranolol, a β-adrenoceptor antagonist, on long-term potentiation (LTP) induced in vivo in rat occipital cortex by tetanizing stimulation of corpus callosum and observed a dose-dependent inhibition of LTP. We further administered propranolol through mini-osmotic pumps during 3 days, and observed the performance of rats in a complex operant conditioning learning paradigm and assessed the expression of brain-derived neurotrophic factor (BDNF) in the occipital cortex. Propranolol exposure depressed both the number of reinforced responses in the operant conditioning task and BDNF expression in occipital cortex. Taken together, our results suggest that propranolol impairs memory formation by inhibiting cortical LTP induction and associated BDNF expression.