Proceedings of The Physiological Society
Cardiff University (2009) Proc Physiol Soc 17, C07
Pharmacological modulation of oscillatory local field potentials in the accessory olfactory bulb of anaesthetised mice
E. Leszkowicz1, P. Brennan1
1. Department of Physiology and Pharmacology, University of Bristol, Bristol, United Kingdom.
Synaptic changes in the accessory olfactory bulb (AOB) have been proposed to underlie the ability of female mice to learn the chemosensory signature of their mate at mating. Mate recognition is vital for reproductive success and is thought to involve a learning-induced increase in feedback inhibition, which selectively gates the transmission of the learned signal at the level of the AOB1. The tight coupling between excitatory projection neurons and inhibitory interneurons, at dendrodendritic reciprocal synapses, produces synchronized neural activity that is evident in the oscillatory local field potential (LFP) recorded in the AOB. Our aim was to investigate whether changes in the balance of excitatory and inhibitory neurotransmission could affect the oscillatory dynamics of AOB activity, with the potential to affect functional coupling with other brain areas2. Mice were anaesthetised by intraperitoneal injection of urethane (1.6g/kg body weight, 22% urethane) and a bipolar recording electrode, with integral drug delivery cannula, was inserted in the mitral/tufted cell layer of the AOB. LFP power and dominant frequencies in different frequency bands were analysed pre-infusion and following a 1μl infusion of either drug or artificial cerebrospinal fluid (CSF) at intervals up to 1 hour post-infusion. Infusions of 100pmol of the type II metabotropic glutamatergic receptor agonist DCG-IV (n=4), or 1nmol of the GABAA receptor agonist isoguvacine (ISO, n=5) resulted in a significant and lasting reduction in power in bands between 4 and 90Hz, compared to CSF (n=4) (Tukey post-hoc multiple comparisons test: DCG-IV: p=0.002 (4-12Hz), p=0.001 (12-30, 60-90Hz); ISO: p<0.001 (4-12, 12-30Hz), p=0.003 (60-90Hz)). This effect is consistent with a direct inhibition of excitatory neurons by isoguvacine and a pre-synaptic inhibition of glutamate release by DCG-IV. Infusion of 0.5ng of the GABAA antagonist gabazine (n=5), which would be expected to disinhibit the excitatory neurons, failed to have a significant effect on the power of LFP oscillations. This might be explained by the dose of gabazine being too low, but increases in the dose to 2ng resulted in epileptiform-like activity that precluded analysis. Surprisingly, none of the drugs significantly affected the dominant frequency of oscillatory activity in any of the frequency bands. This suggests that the frequency of oscillatory neural activity in the AOB might be more dependent on aspects of neural connectivity rather than the balance between excitatory and inhibitory neurotransmission. This finding would support the hypothesis that the gating of learned vomeronasal information at the level of the AOB may occur through direct inhibition of mitral/tufted projection neuron activity rather than by a decoupling of neural oscillators in the AOB and central brain areas2.
Where applicable, experiments conform with Society ethical requirements