Hungarian National Research Fund grants OTKA(K119443)
(PD121123)
(KKP126998) Támogató: NKFIH
(K137886)
Hungarian Brain Research Program(2017-1.2.1-NKP-2017-00002) Támogató: NKFIH
(KTIA-NAP17-3-2017-0001)
A neuroinflammáció vizsgálata a neurodegenerativ folyamatokban: a molekulától a betegágyig(EFOP-3.6.2-16-2017-00008)
Támogató: EFOP
Szakterületek:
Agykutatás
Idegtudományok (benne pszichofiziológia)
Neuroanatómia és neurofiziológia
Neurokémia és neurofarmakológia
Neurológiai betegségek (pl. Alzheimer-kór, Huntington-kór, Parkinson-kór)
Inhibitory neurons innervating the perisomatic region of cortical excitatory principal
cells are known to control the emergence of several physiological and pathological
synchronous events, including epileptic interictal spikes. In humans, little is known
about their role in synchrony generation, although their changes in epilepsy have
been thoroughly investigated. This paper demonstraits how parvalbumin (PV)- and type
1 cannabinoid receptor (CB1R)-positive perisomatic interneurons innervate pyramidal
cell bodies, and their role in synchronous population events spontaneously emerging
in the human epileptic and non-epileptic neocortex, in vitro. Quantitative electron
microscopy showed that the overall, PV+ and CB1R+ somatic inhibitory inputs remained
unchanged in focal cortical epilepsy. On the contrary, the size of PV-stained synapses
increased, and their number decreased in epileptic samples, in synchrony generating
regions. Pharmacology demonstrated-in conjunction with the electron microscopy-that
although both perisomatic cell types participate, PV+ cells have stronger influence
on the generation of population activity in epileptic samples. The somatic inhibitory
input of neocortical pyramidal cells remained almost intact in epilepsy, but the larger
and consequently more efficient somatic synapses might account for a higher synchrony
in this neuron population. This, together with epileptic hyperexcitability, might
make a cortical region predisposed to generate or participate in hypersynchronous
events.