Abstract

This study investigated effects of post-training treatment with phaclofen, GABAB receptor antagonist, on the memory of food location and on the expression of Synapsin I in the hippocampus of pigeons. Pigeons were trained in food location (7 sessions) and underwent post-training treatment with phaclofen (0.3 mg/kg, i.p.; PHAC), saline (SAL) or non-treated (NTR). Testing for memory persistence occurred 7 days after the last training session (PHACR, SALR and NTRR Groups). Pigeons treated with phaclofen had lower latency and higher correct choice values than saline and non-treated controls (p p B receptors.

Highlights

  • Spatial memory involves brain functions responsible for recognizing, codifying, storing and recovering informa-How to cite this paper: Canova, F., Faria, R.S. and Ferrari, E.A.M. (2014) Effects of Post-Training Blockade of GABAB Receptor on Memory of Food Location and Expression of Synapsin I in the Hippocampus of Pigeons (Columba livia)

  • This study indicated that the post-training administration of the GABAB receptor blocker, phaclofen, resulted in significant decrease in the latency of choice response and in a significant increase in the rate of correct choice responses across the sessions of training in a task of food location by pigeons

  • The performance of PHAC pigeons support the consideration of facilitation of food location memory by the blockade of GABAB receptor, training has been efficient for learning and memory of the spatial task by the three groups of pigeons, independently of treatment condition

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Summary

Introduction

Spatial memory involves brain functions responsible for recognizing, codifying, storing and recovering informa-How to cite this paper: Canova, F., Faria, R.S. and Ferrari, E.A.M. (2014) Effects of Post-Training Blockade of GABAB Receptor on Memory of Food Location and Expression of Synapsin I in the Hippocampus of Pigeons (Columba livia). Most of the knowledge about synaptic mechanisms underlying spatial learning and memory has been essentially related with glutamatergic neurotransmission in the hippocampus [4]. It is worth considering the regulatory role played by other neurotransmitters in these mechanisms, the gamma-amino butyric acid (GABA)—a major inhibitory neurotransmitter in the brain. GABA prevents neuronal hyperexcitation, playing a complementary function in the control of signal transduction in the hippocampus [3] [5], the structure essentially involved with the organization of place learning and spatial mapping [1] [2] [6]. The GABAergic neurotransmission, provides a balance between neurotransmitters, which is basic for the regulation of essential mechanisms underlying memory [7]

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