Abstract 907, Date 1:00 pm, Monday, February 16, 2009 (24 hours)|
Session K9: Poster
|Inputs to Neurons Expressing HCN Channels in the Auditory Brainstem|
|*David Perez-Gonzalez, Adrian Rees|
Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels have been associated with the generation of pacemaker-like firing, regulation of the resting potential and the integration of dendritic inputs. HCN channels are fully activated at potentials greater than -100 mV and this raises questions about the origins of such hyperpolarization, and the role of inhibitory inputs in the activation of these channels.
The aim of this study was to map the distribution of neurons that express HCN1 in the inferior colliculus (IC) and lateral lemniscus (LL) of the guinea pig, and discover the types of projections these cells receive, using VGLUT and VGAT as markers of glutamatergic and inhibitory terminals, respectively.
Fresh-frozen brain sections were collected from adult guinea pigs, and were fixed by immersion in paraformaldehyde. HCN1, VGLUT-1 and -2 and VGAT were detected using monoclonal and polyclonal antibodies, and were visualized by means of fluorescent secondary antibodies.
HCN1 is present in the somatic and dendritic membranes of neurons in the IC and LL. Within the IC, it is most significantly expressed in the ventral part of the central nucleus, whereas in the other subdivisions the level of expression is considerably lower. HCN1 is not expressed in the dorsal nucleus of the LL, only in the ventral nucleus (VNLL), mainly its dorsal part.
In all the studied nuclei, the main type of projection to HCN1+ cells is axo-dendritic, being denser in the VNLL than in the IC. Axo-somatic contacts are less frequent, being only significant in the IC and only for VGAT+ terminals.
The relatively limited inhibitory projection to HCN1+ somata may indicate that inhibition is not a major contributor to the activation of HCN1 channels in these nuclei, where perhaps the intrinsic process of repolarization is sufficient. On the other hand, since most of the contacts are axo-dendritic, HCN1 may play a role in the integration of dendritic inputs.
Supported by the EPSRC.