PubMed · 15490696
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Jane Bates. Magic touch.. https://doi.org/10.7748/ns.19.2.27.s38
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State-dependent EEG in the hippocampus (HPC) has traditionally been divided into two activity patterns: theta, a large-amplitude, regular oscillation with a bandwidth of 3-12 Hz, and large-amplitude irregular activity (LIA), a less regular signal with broadband characteristics. Both of these activity patterns have been linked to the memory functions subserved by the HPC. Here we describe, using extracellular field recording techniques in naturally sleeping and urethane-anesthetized rats, a novel state present during deactivated stages of sleep and anesthesia that is characterized by a prominent large-amplitude and slow frequency (< or =1 Hz) rhythm. We have called this activity the hippocampal slow oscillation (SO) because of its similarity and correspondence with the previously described neocortical SO. Almost all hippocampal units recorded exhibited differential spiking behavior during the SO as compared with other states. Although the hippocampal SO occurred in situations similar to the neocortical SO, it demonstrated some independence in its initiation, coordination, and coherence. The SO was abolished by sensory stimulation or cholinergic agonism and was enhanced by increasing anesthetic depth or muscarinic receptor antagonism. Laminar profile analyses of the SO showed a phase shift and prominent current sink-source alternations in stratum lacunosum-moleculare of CA1. This, along with correlated slow oscillatory field and multiunit activity in superficial entorhinal cortex suggests that the hippocampal SO may be coordinated with slow neocortical activity through input arriving via the temporo-ammonic pathway. This novel state may present a favorable milieu for synchronization-dependent synaptic plasticity within and between hippocampal and neocortical ensembles.
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Stimulation of nucleus of the solitary tract (NTS) A(2a)-adenosine receptors elicits cardiovascular responses quite similar to those observed with rapid, severe hemorrhage, including bradycardia, hypotension, and inhibition of renal but activation of preganglionic adrenal sympathetic nerve activity (RSNA and pre-ASNA, respectively). Because adenosine levels in the central nervous system increase during severe hemorrhage, we investigated to what extent these responses to hemorrhage may be due to activation of NTS adenosine receptors. In urethane- and alpha-chloralose-anesthetized male Sprague-Dawley rats, rapid hemorrhage was performed before and after bilateral nonselective or selective blockade of NTS adenosine-receptor subtypes [A(1)- and A(2a)-adenosine-receptor antagonist 8-(p-sulfophenyl)theophylline (1 nmol/100 nl) and A(2a)-receptor antagonist ZM-241385 (40 pmol/100 nl)]. The nonselective blockade reversed the response in RSNA (-21.0 +/- 9.6 Delta% vs. +7.3 +/- 5.7 Delta%) (where Delta% is averaged percent change from baseline) and attenuated the average heart rate response (change of -14.8 +/- 4.8 vs. -4.4 +/- 3.4 beats/min). The selective blockade attenuated the RSNA response (-30.4 +/- 5.2 Delta% vs. -11.1 +/- 7.7 Delta%) and tended to attenuate heart rate response (change of -27.5 +/- 5.3 vs. -15.8 +/- 8.2 beats/min). Microinjection of vehicle (100 nl) had no significant effect on the responses. The hemorrhage-induced increases in pre-ASNA remained unchanged with either adenosine-receptor antagonist. We conclude that adenosine operating in the NTS via A(2a) and possibly A(1) receptors may contribute to posthemorrhagic sympathoinhibition of RSNA but not to the sympathoactivation of pre-ASNA. The differential effects of NTS adenosine receptors on RSNA vs. pre-ASNA responses to hemorrhage supports the hypothesis that these receptors are differentially located/expressed on NTS neurons/synaptic terminals controlling different sympathetic outputs.