“…The prolonged depolarizations were absent in mitral cells lacking intact apical dendrites, suggesting a common glomerular origin with LLDs (Carlson et al, 2000 ). Candidate mechanisms that may generate these depolarization in synaptic blockers are: (1) an excitatory chemical transmitter released in the glomeruli, e.g., excitatory actions of glutamate acting at mGluR1 (Schoppa and Westbrook, 2001 ; Heinbockel et al, 2004 ; Yuan and Knopfel, 2006 ), cholecystokinin (Ma et al, 2013 ) or β adrenoreceptors (Nai et al, 2010 ; Zhou et al, 2016 ); and (2) an intrinsic membrane current such as a sustained sodium current; and/or depolarizations transmitted by electrical synapses between glutamatergic apical dendrites in the glomeruli (Schoppa and Westbrook, 2002 ; Christie et al, 2005 ; Hayar et al, 2005 ; Ma and Lowe, 2007 ; Pimentel and Margrie, 2008 ; De Saint Jan et al, 2009 ).…”