RESUMEN
Temporal lobe epilepsy (TLE) is the most prevalent form of epilepsy, through the neuronal mechanisms of this syndrome remain elusive. In addition to the temporal lobe structures, it was found that the basal forebrain cholinergic cells are also involved in epileptogenesis. However, little is known about the involvement of the basal forebrain GABAergic neurons in epilepsy; despite this, they largely project to the temporal lobe and are crucial for the regulation of the hippocampal circuitry. In this study, we assessed epilepsy-induced changes in parvalbumin (PARV) immunoreactive neurons of the medial septum (MS) and of the magnocellular preoptic nucleus (MCPO) using the kainic acid (KA) model in rats. In addition, we estimated the respective changes in the cholinergic varicosities in the MS, where we observed a significant reduction in the PARV cell number (12849 ± 2715 vs. 9372 ± 1336, p = .029) and density (16.2 ± 2.62 vs. 10.5 ± 1.00 per .001 mm3, p =.001), and an increase in the density of cholinergic varicosities (47.9 ± 11.1 vs. 69.4 ± 17.8 per 30,000 µm2, p =.036) in KA-treated animals. In the MCPO, these animals showed a significant increase in somatic volume (827.9 ± 235.2 µm3 vs. 469.9 ± 79.6 µm3, p = .012) and total cell number (2268.6 ± 707.1 vs. 1362.4 ± 262.0, p =.028). These results show that the basal forebrain GABAergic cell populations undergo numerical and morphological changes in epileptic animals, which may contribute to an increased vulnerability of brain circuits to epilepsy and epilepsy-related functional impairments.
RESUMEN
Nociceptive trigeminal afferents innervating craniofacial area, eg, facial skin and cranial meninges, project to a broad region in the medullary and upper cervical dorsal horn designated as the trigeminocervical complex. Lamina I neurons in the trigeminocervical complex integrate and relay peripheral inputs, thus playing a key role in both cranial nociception and primary headache syndromes. Because of the technically challenging nature of recording, the long-range trigeminal afferent inputs to the medullary and cervical lamina I neurons were not intensively studied so far. Therefore, we have developed an ex vivo brainstem-cervical cord preparation with attached trigeminal nerve for the visually guided whole-cell recordings from the medullary and cervical lamina I neurons. Two-thirds of recorded neurons generated intrinsic rhythmic discharges. The stimulation of the trigeminal nerve produced a complex effect; it interrupted the rhythmic discharge for hundreds of milliseconds but, if the neuron was silenced by a hyperpolarizing current injection, could elicit a discharge. The monosynaptic inputs from the trigeminal Aδ, high-threshold Aδ, low-threshold C, and C afferents were recorded in the medullary neurons, as well as in the cervical neurons located in the segments C1 to C2 and, to a lesser degree, in C3 to C4. This pattern of supply was consistent with our labelling experiments showing extensive cervical projections of trigeminal afferents. Excitatory inputs were mediated, although not exclusively, through AMPA/kainate and NMDA receptors, whereas inhibitory inputs through both GABA and glycine receptors. In conclusion, the trigeminocervical lamina I neurons receive a complex pattern of long-range monosynaptic and polysynaptic inputs from a variety of the trigeminal nociceptive afferents.
