Gap junctions between neurons have been particularly well studied for inhibitory interneurons. For example, the diagram here (to the right) shows gap junctions between cells in a population of inhibitory neurons (FSI) in the striatum (1).
There is evidence that gap junctions between neurons can contribute to synchronized neuronal activity. For example, using knockout mice engineered to lack connexin-36, it was found that the mice had reduced gamma frequency (30-60 Hz) oscillations (2).
There is interest in the idea that widely synchronized neuronal activity is important for brain function. In particular, a popular hypothesis is that regions of synchronized neuronal activity are involved in making the distinction between conscious and unconscious brain activity (3). It is also hypothesized that abnormal patterns of synchronized neuronal activity might be involved in medical conditions such as schizophrenia (4).
Parkinson disease has been associated with abnormal synchronization of neuronal activity (5). It has been hypothesized that regulated gap junctions might provide a convenient mechanism for modulating the activity of neuronal circuits (6). There is evidence that dopamine regulates the extent of gap junction coupling between striatal neurons (7, 8, 9, 10). In addition to the FSI cells (in the figure, above) there are also cholinergic interneurons and low-threshold spike (LTS) interneurons (11). It was reported that a population of non-FSI cells develops an altered oscillatory pattern of activity upon dopamine deprivation (12). It would be interesting if the dopamine-regulated gap junction coupling of interneurons played an important role in both Parkinson disease and schizophrenia.
Image credits. The circuit diagram is modified from “Reconstructing the Three-Dimensional GABAergic Microcircuit of the Striatum” © 2010 Humphries et al. distributed under the terms of the Creative Commons Attribution License.
Related hypothesis – do gap junctions function to regulate conscious experience?