Biomedical subjects

E J Ramcharan

Publications and source records attributed to E J Ramcharan.

6 recordsLinked to original sources

PubMed2005

Higher-order thalamic relays burst more than first-order relays.

There is a strong correlation between the behavior of an animal and the firing mode (burst or tonic) of thalamic relay neurons. Certain differences between first- and higher-order thalamic relays (which relay peripheral information to the cortex versus information from one cortical area to another, respectively) suggest that more bursting might occur in the higher-order relays. Accordingly, we recorded bursting behavior in single cells from awake, behaving rhesus monkeys in first-order (the lateral geniculate nucleus, the ventral posterior nucleus, and the ventral portion of the medial geniculate nucleus) and higher-order (pulvinar and the medial dorsal nucleus) thalamic relays. We found that the extent of bursting was dramatically greater in the higher-order than in the first-order relays, and this increased bursting correlated with lower spontaneous activity in the higher-order relays. If bursting effectively signals the introduction of new information to a cortical area, as suggested, this increased bursting may be more important in corticocortical transmission than in transmission of primary information to cortex.

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PubMed2000

Cellular mechanisms underlying activity patterns in the monkey thalamus during visual behavior.

We show for the first time with in vitro recording that burst firing in thalamic relay cells of the monkey is evoked by activation of voltage-dependent, low threshold Ca(2+) spikes (LTSs), as has been described in other mammals. Due to variations in LTS amplitude, the number of action potentials evoked by an LTS could vary between 1 and 8. These data confirm the presence of two modes of firing in the monkey for thalamic relay cells, tonic and burst, the latter related to the activation of LTSs. With these details of the cellular processes underlying burst firing, we could account for many of the firing patterns we recorded from the lateral geniculate nucleus of the thalamus in behaving monkeys. In particular, we found clear evidence of burst firing during alert wakefulness, which had been thought to occur only during sleep or certain pathological states. This makes it likely that the burst firing seen in awake humans has the same cellular basis of LTSs, and this supports previous suggestions that burst firing represents an important relay mode for visual processing.

Action Potentials↗

PubMed1997

Membrane specializations in the developmentally transient perireticular nucleus of the rat.

The perireticular nucleus lies among the fibres of the internal capsule and in the rat is relatively large at birth. Like the subplate of the neocortex, it is dramatically reduced in the adult (Mitrofanis, 1992). On embryonic day 17 (E17), cells of the perireticular nucleus project to the cortex (Adams and Baker, 1995); at birth there is also a projection to the thalamus (Mitrofanis and Baker, 1993). When corticofugal axons reach the perireticular nucleus, they separate into the descending tracts and the corticothalamic pathway. The axons then enter the internal capsule on their way to the thalamus, defasciculate and contribute to a complex zone of interweaving fibres seen in this region (Adams and Guillery, 1994). We have found that the cells of the perireticular nucleus are immunopositive for an antibody (3A10) to a phosphorylated neurofilament protein (Yamada et al., 1991), and we have shown that these 3A10-positive perireticular cells extend their dendrites across the path of cortical fibres at the earliest age studied (E17). We have confirmed this dendritic orientation by Golgi staining at a later stage (P3). Electron micrographs show that axo-somatic and axo-dendritic synapses first appear in the perireticular nucleus at about the day of birth. Prenatally, between E14 and E19, the major specialized membrane interrelationships seen are omega formations between adjacent profiles that often contain vesicles. Omega formations are rarely seen at later stages. Puncta adhaerentia typified by opposing membrane densities with no associated vesicles were seen at all ages studied. We suggest that early membrane contacts (omega formations) may represent transient organisational or guidance influences since they occur during a period when axonal pathways are being defined.

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PubMed1996

Autoradiographic localization of functional muscarinic receptors in the rat superior cervical sympathetic ganglion reveals an extensive distribution over non-synaptic surfaces of neuronal somata, dendrites and nerve endings.

Fast synaptic transmission in sympathetic ganglia is mediated by acetylcholine, acting on nicotinic receptors, yet muscarinic receptors are also present and are involved in the production of slow postsynaptic potentials. In order further to elucidate the role of muscarinic receptors in ganglionic transmission their distribution in the rat superior cervical sympathetic ganglion was investigated autoradiographically by use of the tritiated irreversible muscarinic ligand propylbenzilylcholine mustard. It was observed that this agent blocked the carbachol-evoked hydrolysis of inositol phospholipids in the ganglion and that this response to carbachol is itself inhibitable by selective muscarinic antagonists with a potency sequence which indicates involvement primarily of M1 receptors. Light microscope autoradiography showed that labelling inhibitable by atropine and by the M1-selective muscarinic antagonist pirenzepine was essentially confined to the margins of neuronal somata and regions of dendritic arborization, which include synaptic contacts. Quantitative electron microscope autoradiography showed that binding of the radioligand, of which approximately 70% was inhibitable by atropine and 68% by pirenzepine, was associated predominantly with surface membranes of neuronal somata, dendrites, other neurites (including axons and uncharacterized dendrites) and nerve terminal profiles, in the approximate ratios 95:85:52:45. Of the inhibitable binding over neuronal membranes in the ganglion little more than 3% was found to be synaptically located, and this involved para- or peri-synaptic regions of nerve terminal contacts rather than the specialized synaptic zone. About 5% of the inhibitable binding over neuronal membranes involved non-synaptic surfaces of nerve terminals and preterminal axon segments; almost 70% was distributed over non-synaptic surfaces of neuronal somata and dendrites, and about 21% upon other neurites. Binding sites were found not to be more highly concentrated at or adjacent to synapses than over other regions of neuronal surface membranes. About 50%, possibly more, of the binding on non-synaptic surfaces of nerve endings, and about 7% of binding upon dendritic membranes, was of non-M1, possibly M2 type, inhibitable by atropine but not by pirenzepine. Non-synaptic neuro-neuronal appositions, which involve dendrites and somata and often lie adjacent to synapses, showed rather more than twice the binding expected for each membrane individually; and neuronal membrane exposed to basal lamina lining ganglionic tissue spaces showed high levels of binding. Little inhibitable binding was seen over membranes of satellite and Schwann cells, or over cytoplasmic territories or ganglionic interstitial tissue. A model was constructed of the distribution of label, which showed that the observed results for total binding could be approximately matched by assuming the following relative densities of ligand binding sites: interstitial tissue space and supporting cells 1, soma cytoplasm 3, cytoplasm of dendrites, neurites and nerve terminals 4.5, surfaces of mesodermal elements 15, surfaces of neurites and nerve endings including sites of synapse 45, surfaces of dendrites 90, surfaces of neuronal somata 120, non-synaptic neuro-neuronal appositions 180. It is concluded that functional muscarinic receptors in this sympathetic ganglion, predominantly of the M1 type linked with slow depolarizations, but including some non-M1 receptors, are widely distributed over non-synaptic surfaces of the neuronal somata and dendrites and are not concentrated at synapses. Presynaptic autoreceptors are also present, of which half or more are of non-M1, possibly M2, type which might be inhibitory. The presence of M4 receptors is not excluded...

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PubMedDate not supplied

Burst and tonic firing in thalamic cells of unanesthetized, behaving monkeys.

Thalamic relay cells fire in two distinct modes, burst or tonic, and the operative mode is dictated by the inactivation state of low-threshold, voltage-gated, transient (or T-type) Ca2+ channels. Tonic firing is seen when the T channels are inactivated via membrane depolarization, and burst firing is seen when the T channels are activated from a hyperpolarized state. These response modes have very different effects on the relay of information to the cortex. It had been thought that only tonic firing is seen in the awake, alert animal, but recent evidence from several species suggests that bursting may also occur. We have begun to explore this issue in macaque monkeys by recording from thalamic relay cells of unanesthetized, behaving animals. In the lateral geniculate nucleus, the thalamic relay for retinal information, we found that tonic mode dominated responses both during alert behavior as well as during sleep. We nonetheless found burst firing present during the vigilant, waking state. There was, however, considerably more burst mode firing during sleep than wakefulness. Surprisingly, we did not find the bursting during sleep to be rhythmic. We also recorded from relay cells of the somatosensory thalamus. Interestingly, not only did these somatosensory neurons exhibit much more burst mode activity than did geniculate cells, but bursting during sleep was highly rhythmic. It thus appears that the level and nature of relay cell bursting may not be constant across all thalamic nuclei.

Action Potentials↗

PubMedDate not supplied

The effects of saccadic eye movements on the activity of geniculate relay neurons in the monkey.

Saccadic suppression is the reduced visibility that occurs during saccadic eye movements. Recent psychophysical studies have suggested that this is due to a reduction in responsiveness of magnocellular (M), but not parvocellular (P), cells of the lateral geniculate nucleus. To address this and other phenomena of responsiveness during saccades, we recorded from geniculate neurons in the behaving monkey before, during, and after saccades. Specifically, we measured neuronal responses to a flashing, whole-field illumination. Contrary to the prediction, most M neurons showed pronounced enhancement of visual activity during saccades, whereas such responsiveness of parvocellular (P) neurons was not significantly affected by saccades. We also analyzed the extent to which saccades affected burst firing, which results from activation of a voltage-dependent Ca2+ conductance. We found that both M and P cells displayed a significant suppression of burst firing during saccades. These results do not support the idea that saccadic suppression has an obvious substrate in reduced responsiveness of geniculate cells, but this suppression may be related to an increased visual threshold for detection associated with reduced burst firing.

Action Potentials↗