Neuronal cell death results from various circumstances such as hypoxia, ischemic and neurodegenerative diseases (NDs). In these events, the resulting modification of neurotransmitters, either excitatory or inhibitory, mediate much of the neuronal damage. However, this consequence depends upon their pre and post synaptic receptor activities which are the key mechanism for signal regulation. Among these, acetylcholine (ACh) is a well known neurotransmitter which is predominantly involved in neuroprotection as well as cognitive functions through its receptors activity, particularly the nicotinic subtypes. Several lines of evidence suggest that among these subtypes, a7 nicotinic acetylcholine receptor (a7nAChR) offers much promise for neuroprotective role in relation to the central nervous system (CNS) disorders like schizophrenia and Alzheimer's disease (AD). Several lines of evidence exist to show the potential mechanisms in which this nAChR subtype and its agonists such as nicotine, that trigger the a7nAChR-mediated suppression of neuronal cell death. This review focuses on the potential role of a7nAChR in neuroprotection by examining recent experimental data, both in vitro and in vivo, that argue for the neuroprotective role of a7nAChR in the CNS.
Glutamate is the principal excitatory neurotransmitter in the central nervous system, and plays important roles in both physiological and pathological neuronal processes. Current understanding of the exact mechanisms involved in glutamate-induced neuronal excitotoxicity, in which excessive glutamate causes neuronal dysfunction and degeneration, whether acute or chronic, remain elusive. Conditions, due to acute insults such as ischaemia and traumatic brain injury, and chronic neurodegenerative disorders such as multiple sclerosis and motor neuron disease, suffer from the lack of translational neuroprotection in clinical setting to tackle glutamate excitotoxicity despite steady growth of animal studies that revealed complex cell death pathway interactions. In addition, glutamates are also released by non-neuronal cells including astrocytes and oligodendroglia. Thus, attempts to elucidate this complexity are closely related to our understanding of the glutamatergic circuitry in the brain. Neuronal cells develop a glutamatergic system at glutamatergic synapses that utilise glutamate as an intercellular signaling molecule to characterise the output, input, and termination of this signaling. As to signal input, various kinds of glutamate receptors have been identified and characterized. Na+-dependent glutamate transporters at the plasma membrane are responsible for the signal termination through sequestration of glutamate from the synaptic cleft. The signal output systems comprise vesicular storage and subsequent exocytosis of glutamate by using vesicular glutamate transporters. Similar to the mammalian brain, the regional differences of glutamatergic neurons and glutamate receptor neurons suggest many glutamatergic projections in the avian brain, as supported by recent evidence of glutamate-related genes distribution. Glutamatergic target areas are expected to show high activity of glutamate transporters that remove released glutamate from the synaptic clefts. This review summarises and compares glutamatergic circuits in the avian and mammalian brain, particularly in the olfactory pathway, the paffial organization of glutamatergic neurons and connection with the striatum, hippocampal-septal pathway, visual and auditory pathways, and granule cell-Purkinje cell pathway in the cerebellum. Comparative appreciation of these glutamatergic circuits, particularly with the localisation and/or expression of specific subtypes of glutamate transporters, would provide the morphological basis for physiological and pharmacological designs that supplement existing animal studies of the current proposed mechanisms that underlie glutamate-induced neuronal excitotoxicity.
Reflex epilepsy is usually induced by external stimulation, photosensitive epilepsy being the most common. Epilepsy induced by auditory stimulation is rarely studied. There are no currently published magnetoencephalographic (MEG) studies demonstrating the initiation of epileptic neuronal discharges by repeated auditory stimulations in temporal lobe epilepsy (TLE) patients. We retrospectively studied one TLE patient who underwent a MEG study to localize her epileptic focus. Auditory, somatosensory, visual and motor evoked potential studies were performed during the MEG recording. A single dipole method calculated equivalent current dipoles to localize the epileptic source. The least-squares minimization method was used to obtain the optimal solution with goodness-of-fit of greater than 80%. Periodic lateralized epileptiform discharges (PLEDs) were recorded in the temporal region when repeated auditory stimulations were done. We postulated that neuronal cortical suppression occurred during repeated stimulations which provoked epileptiform discharges (PLEDs) without any physical symptoms or aura. It was concluded that repeated stimulations could facilitate epileptiform discharges in focal area/areas in certain subjects.
The human brain generates different oscillations at different frequencies during various consciousness levels. When these brain waves synchronize with exogenous rhythmic stimulation, the brain experiences strong, yet relaxing emotion that could be involved in the formation of memory. We investigated the character of rhythmic oscillatory dynamics by electroencephalography (EEG) of subjects listening to a short verse of the Holy Quran compared to resting and Arabic news listening. The mean power amplitudes of each frequency band for wavelet-based time-frequency analysis were obtained from 5000 ms of segmented EEG recordings during rest, news and Quran listening conditions. The time series analysis of power from each of three conditions in each frequency band from the grand averaged data was then subjected to autocorrelation study. The results showed significant cyclic overall trends of increasing and decreasing patterns of power in the low frequency brain wave oscillation of different head regions especially global, frontal and temporal sites. These results provided a basis for prediction of the periodicity of the power of the oscillatory brain dynamics of delta and robustly in theta regions which occurred during Quran listening. Despite several limitations, our data offered a plausible scientific basis to the emotional induction during Quran listening that mimics recognized as data from music listening studies. This offered a promising perspective for future studies in translational neurophysiological, cognitive and biofeedback on Quran listening to modify brain behaviour in health and disease.
Epilepsy is a neurological disorder characterized by recurrent seizures resulting from excessive abnormal electrical discharges in the brain. Medicinal plants may play an invaluable role to discover the new antiepileptic drugs. The aim of the present study was to investigate the anticonvulsant activity of α-terpineol isolated from Myristica fragrans Hountt. The α-terpineol showed a significant inhibition of the seizure episodes and spikes in absence seizures model of Genetic Absence Epilepsy Rats from Strasbourg (GAERS) rats by using electroencephalography records. It showed dose-dependent anticonvulsant activity that was comparable to the known antiepileptic drug of diazepam. It showed a rapid onset and relatively short duration of anticonvulsant effects. The present findings suggest that α-terpineol might possess antiepileptic activities against the partial seizures of human because it prevented seizures in well-established genetic absence seizure animal model of GAERS rats.