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Sam P Javedan

Publications and source records attributed to Sam P Javedan.

4 recordsLinked to original sources

Role of alpha7-nicotinic acetylcholine receptors in tetanic stimulation-induced gamma oscillations in rat hippocampal slices.

Hippocampal gamma oscillations, as a form of neuronal network synchronization, are speculated to be associated with learning, memory and attention. Nicotinic acetylcholine receptor alpha7 subtypes (alpha7-nAChRs) are highly expressed in hippocampal neurons and play important roles in modulating neuronal function, synaptic plasticity, learning and memory. However, little is known about the role of alpha7-nAChRs in hippocampal gamma oscillations. Here, we examined the effects of selective alpha7- and non-alpha7-nAChR antagonists on tetanic gamma oscillations in rat hippocampal slices. We found that brief tetanic stimulation-induced gamma oscillations (30-80 Hz) and pharmacological blockade of alpha7-nAChRs using the relatively selective alpha7-nAChR antagonists, methyllycaconitine (10 or 100 nM) or alpha-bungarotoxin (10 nM), significantly reduced the frequency spectrum power, the number of spikes, and burst duration of evoked gamma oscillations. Neither mecamylamine nor dihydro-beta-erythroidine, which are selective antagonists of non-alpha7-nAChRs, demonstrated significant effects on tetanic gamma oscillations. Nicotine exposure promotes hippocampal gamma oscillations in a methyllycaconitine-sensitive manner. It is concluded that alpha7-nAChRs in hippocampal slices play important roles in regulation of gamma oscillations, thus potentially helping to explain roles of nAChRs in cognitive functions such as learning, memory and attention.

Aconitine↗

Cooling abolishes neuronal network synchronization in rat hippocampal slices.

PURPOSE: We sought to determine whether cooling brain tissue from 34 to 21 degrees C could abolish tetany-induced neuronal network synchronization (gamma oscillations) without blocking normal synaptic transmission. METHODS: Intracellular and extracellular electrodes recorded activity in transverse hippocampal slices (450-500 microm) from Sprague-Dawley male rats, maintained in an air-fluid interface chamber. Gamma oscillations were evoked by afferent stimulation at 100 Hz for 200 ms. Baseline temperature in the recording chamber was 34 degrees C, reduced to 21 degrees C within 20 min. RESULTS: Suprathreshold tetanic stimuli evoked membrane potential oscillations in the 40-Hz frequency range (n = 21). Gamma oscillations induced by tetanic stimulation were blocked by bicuculline, a gamma-aminobutyric acid (GABA)A-receptor antagonist. Cooling from 34 to 21 degrees C reversibly abolished gamma oscillations in all slices tested. Short, low-frequency discharges persisted after cooling in six of 14 slices. Single-pulse-evoked potentials, however, were preserved after cooling in all cases. Latency between stimulus and onset of gamma oscillation was increased with cooling. Frequency of oscillation was correlated with chamber cooling temperature (r = 0.77). Tetanic stimulation at high intensity elicited not only gamma oscillation, but also epileptiform bursts. Cooling dramatically attenuated gamma oscillation and abolished epileptiform bursts in a reversible manner. CONCLUSIONS: Tetany-induced neuronal network synchronization by GABAA-sensitive gamma oscillations is abolished reversibly by cooling to temperatures that do not block excitatory synaptic transmission. Cooling also suppresses transition from gamma oscillation to ictal bursting at higher stimulus intensities. These findings suggest that cooling may disrupt network synchrony necessary for epileptiform activity.

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