Biomedical subjects

M Deschênes

Publications and source records attributed to M Deschênes.

At least 55 records · Page 3Linked to original sources

PubMed1994

Corticothalamic projections from layer V cells in rat are collaterals of long-range corticofugal axons.

The vast majority of corticothalamic (CT) axons projecting to sensory-specific thalamic nuclei arise from layer VI cells but intralaminar and associative thalamic nuclei also receive, to various degrees, a cortical input from layer V pyramidal cells. It is also well established that all long-range corticofugal projections reaching the brainstem and spinal cord arise exclusively from layer V neurons. These observations raise the possibility that the CT input from layer V cells may be collaterals of those long-range axons projecting below thalamic level. The thalamic projections of layer V cells were mapped at a single cell level following small microiontophoretic injections of biocytin performed in the motor, somatosensory and visual cortices in rats. Camera lucida reconstruction of these CT axons revealed that they are all collaterals of long-range corticofugal axons. These collaterals do not give off axonal branches within the thalamic reticular nucleus and they arborize exclusively within intralaminar and associative thalamic nuclei where they from small clusters of varicose endings. As layer V cells are involved in motor commands everywhere in the neocortex, these CT projections and their thalamic targets should be directly involved in the central organization of motor programs.

Animals↗

PubMed1993

The behavior of mossy cells of the rat dentate gyrus during theta oscillations in vivo.

Intracellular current clamp recordings were obtained from mossy cells (n = 6, identified by intracellular injection of biocytin) of the dorsal dentate gyrus from rats under ketamine-xylazine anesthesia. During electroencephalographic theta rhythm (4-6 Hz), recorded with a macroelectrode placed in the contralateral dorsal hippocampus near the fissure, mossy cells displayed intracellular membrane potential oscillations at low frequencies (4-6 Hz) which appeared to be phase locked to the electroencephalographic theta rhythm. The frequency of the intracellular theta rhythm was independent of the membrane potential. However, the phase difference between the intracellular and the electroencephalographic theta rhythms as well as the amplitude of the intracellular theta oscillations were voltage-dependent. These findings are consistent with the hypothesis that rhythmic GABAA receptor-mediated inhibitory postsynaptic potentials contribute to the genesis of the intracellular theta rhythm. Indeed, mossy cells displayed an early, fast inhibitory postsynaptic potential in response to electrical stimulation of the entorhinal cortex, which most likely represents a GABAA receptor-mediated event, indicating that mossy cells possess functional GABAA receptors. At the resting membrane potential, mossy cells did not fire at each cycle of the electroencephalographic theta rhythm but fired only rarely (< 1 Hz). However, when they did fire they did so preferentially in phase with the peak positivity of the electroencephalographic theta rhythm. Reconstruction of two mossy cells with axonal projections to the inner molecular layer showed that the spatial extent of the influence such weakly discharging mossy cells may have on other dentate gyrus neurons during theta oscillations can be several millimeters in the septotemporal direction. In conclusion, these findings show that mossy cells of the rat hilus during ketamine-xylazine anesthesia participate in theta oscillations of the hippocampal formation, during which their low-frequency firing may contribute to the phase-locking of a large number of spatially distributed postsynaptic neurons with postsynaptic sites in the inner molecular layer of the dentate gyrus.

Animals↗

PubMed1993

Low- and high-frequency membrane potential oscillations during theta activity in CA1 and CA3 pyramidal neurons of the rat hippocampus under ketamine-xylazine anesthesia.

1. Intracellularly recorded low- and high-frequency (4-6 and 25-50 Hz, respectively), rhythmic, spontaneous membrane potential oscillations were investigated in pyramidal neurons of the rat hippocampus in vivo, during theta (theta, 4-6 Hz) electroencephalographic (EEG) activity, under ketamine-xylazine anesthesia. 2. The EEG activity showed two spectral peaks, one in the theta range, the other at higher frequencies (25-50 Hz). On the basis of their electrophysiological and pharmacological properties, it was concluded that the EEG theta-waves, and the fast EEG rhythm, recorded during ketamine-xylazine anesthesia, share the basic properties of those theta and fast rhythms that are recorded under the effects of other types of anesthetics. 3. When intracellular recordings (n = 32) were made with electrodes filled with potassium-acetate (K-acetate), the only CA1 and CA3 pyramidal cells (PCs) considered for further analysis were those that did not fire rhythmically at most or each cycle of the theta rhythm at the resting membrane potential. During EEG-theta, the membrane potential (Vm) of these cells showed a prominent oscillation (3-15 mV) with frequencies similar to those of the EEG-theta (the intracellular theta rhythm, intra-theta). 4. The frequency of the intra-theta was independent of the Vm. However, the phase difference between the intra-theta and the EEG-theta was voltage dependent in both types of cells. CA1 PCs showed a large (120-180 degrees, where 360 degrees is the full cycle), gradual shift in the phase difference between the intra-theta and the EEG-theta, when the membrane was hyperpolarized to -85 from -65 mV. Although CA3 PCs displayed a larger variability in their phase-voltage relations, a voltage-dependent phase shift (90-180 degrees) could be observed in CA3 PCs as well. 5. Although the amplitude of the intra-theta in both CA1 and CA3 PCs could display large, sudden, spontaneous changes at a given Vm, the amplitude-Vm plots tended to show a minimum between -70 and -80 mV. Spontaneous changes in the amplitude of the intra-theta did not affect the phase difference between the intra- and the EEG-theta rhythms. 6. Intracellular injection of QX-314 (50-100 mM) did not change the phase-Vm or the amplitude-Vm relationships of CA1 PCs. 7. Intracellular injection of chloride (Cl-) ions greatly reduced the voltage dependency of the phase difference and revealed fast (duration: 20-25 ms), depolarizing potentials (5-20 mV), which appeared at high frequencies (25-50 Hz), amplitude modulated at theta-frequencies.(ABSTRACT TRUNCATED AT 400 WORDS)

Anesthesia, General↗

PubMed1992

The origin of rhythmic fast subthreshold depolarizations in thalamic relay cells of rats under urethane anaesthesia.

Intracellular recordings were performed in relay neurons of the dorsal thalamus in rats under urethane anaesthesia. In 77 out of 127 neurons of the ventro-posterolateral and ventral lateral nuclei, but not in neurons of the ventro-posteromedial and posterior nuclei, a highly rhythmic pattern of subthreshold depolarizations was present at rest. The average frequency of these rhythmic depolarizations in ventro-posterolateral cells was 23.36 +/- 11.48 Hz (range: 6-60 Hz); in ventral lateral relay cells higher frequencies were observed (65.86 +/- 17.42 Hz; range: 17-95 Hz). The rhythmic subthreshold events were identified as excitatory postsynaptic potentials generated by the regular firing of prethalamic afferents located in dorsal column and deep cerebellar nuclei. Indeed, in cells of the ventro-posterolateral nucleus these spontaneous potentials had a waveform similar to that of synaptic potentials triggered by somatosensory stimulation. They increased in amplitude with membrane hyperpolarization and their rhythmic occurrence was not affected by the injection of large inward currents. Moreover, they persisted after capsular transection, but they could no more be recorded in ventro-posterolateral cells after lesion of dorsal column nuclei. Finally, it was found that prethalamic afferents within the deep cerebellar nuclei discharged spontaneously in a rhythmic manner within the same frequency band as that of the rhythmic synaptic potentials recorded in ventral lateral cells. On the basis of these results, it is concluded that the rhythmic subthreshold depolarizations observed in thalamic neurons of animals under urethane anaesthesia are not generated intrinsically but that they represent excitatory postsynaptic potentials of prethalamic origin.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗

PubMed1992

Voltage-dependent 40-Hz oscillations in rat reticular thalamic neurons in vivo.

Extra- and intracellular recordings of thalamic reticular and relay neurons were performed in rats under urethane anaesthesia. Under this type of anaesthesia it was found that, throughout the whole reticular thalamic nucleus, a large proportion of cells (approximately 34%) discharged like clocks within a 25-60 Hz frequency band width (i.e. 40 Hz). Simultaneous recordings of pairs of reticular cells showed that the regular discharges of nearby units were not synchronous. Thus, the asynchronous 40-Hz firing of reticular thalamic cells was not correlated with any 40-Hz extracellular activity as revealed by the spectral analysis of the electroencephalogram and by recordings performed in various thalamic nuclei. In relay cells of the ventrobasal, ventral lateral and posterior thalamic nuclei, the regular firing of reticular thalamic neurons induced a rhythmic inhibitory modulation that was detected by the time-series analysis of the inhibitory postsynaptic potentials. In many relay cells, however, the disclosure of this inhibitory modulation required cellular depolarization since the resting potential in these cells was maintained at the reversal potential of the inhibitory events. Intracellular recordings of reticular thalamic cells showed that their regular firing was not driven in an all-or-nothing manner by 40-Hz synaptic inputs but rather that it depended upon the activation of a voltage-dependent pacemaker mechanism; this pacemaker activity was manifested by the presence of subthreshold oscillations that drove spike discharges and whose frequency was voltage dependent. In the context of data already published on the genesis of 40-Hz oscillations in the brain, and given the key position of reticular thalamic neurons in thalamocortical networks, the present results indicate that the reticular thalamic nucleus might play a pacemaker function in the genesis of 40-Hz oscillations in the thalamus and cortex during states of focused arousal.

Animals↗

PubMed1992

Control of 40-Hz firing of reticular thalamic cells by neurotransmitters.

This study bears on the control exerted by neurotransmitters on the expression of a 40-Hz pacemaker activity observed in reticular thalamic cells. Experiments were conducted in urethane-anaesthetized rats using extracellular recordings and local applications of antagonists against the neurotransmitters involved in the modulation of reticular thalamic cells. All drugs were dissolved in a Ringer's solution (pH 7.4) and were applied in small quantities (25-150 nl) by pressure through one barrel of a micropipette assembly. Forty-Hertz firing was abolished by local application of the alpha 1 antagonist prazosin and by bilateral lesion of the locus coeruleus. Local applications of glutamate antagonists reduced the rate of discharges by 30-50% as did cortical cooling or complete transection of the internal capsule. Conversely, scopolamine exerted a permissive action on the expression of 40-Hz activities; many spontaneously bursting units started firing at 40 Hz under the influence of this muscarinic antagonist. Since reticular thalamic cells are GABAergic and synaptically coupled via axonal collaterals, we investigated how GABAergic drugs affected the regular firing of these cells. Local applications of bicuculline produced a transient increase of the firing rates while the application of GABA induced intermittent pauses on a background of regular discharges. The application of piperidine-4-sulphonic acid, a GABAA receptor agonist, produced a similar effect. The length of pauses generated by piperidine was statistically analysed. It was found that the duration of short pauses was a multiple integer of the mean interspike interval of surrounding discharges. The preservation of the period and phase of the rhythm across the pauses implies that a subthreshold oscillation was presented into the cells during the arrests of discharges. Given the mode of action of noradrenaline and acetylcholine on reticular thalamic neurons, and considering a possible metabotropic action of glutamate, the above results suggest that deactivation of a leaky K conductance is critically involved in the regular firing of these cells in urethane-anaesthetized rats. Alternatively, because reticular cells are coupled via inhibitory synapses, it is proposed that the 40-Hz firing frequency reflects, in the frequency domain, a point of equilibrium in the reticular thalamic network when the leaky K conductance is fully deactivated by the metabotropic effects of monoamines and/or excitatory amino acids.

2-Amino-5-phosphonovalerate↗

PubMed1992

Muscarinic inhibition of reticular thalamic cells by basal forebrain neurones.

Pressure injections of a Ringer's solution containing glutamate (10 or 20 mM) into the nucleus basalis of Meynert inhibited the tonic firing of reticular thalamic (RT) neurones which were recorded in rats under deep urethane anaesthesia. When the inhibition was strong enough to stop the discharges, a burst firing mode was induced in RT cells before the recovery of tonic discharges. This glutamate-induced inhibition of RT cells was completely abolished following the systemic administration of the muscarinic antagonist, scopolamine (150 micrograms kg-1, i.v.). These results indicate that the cholinergic cells of the nucleus basalis of Meynert can control the mode of discharges of RT neurones through the activation of muscarinic receptors.

Animals↗

PubMed1990

Membrane resistance increase induced in thalamic neurons by stimulation of brainstem cholinergic afferents.

The synaptic response induced in thalamic relay cells by stimulation of peribrachial cholinergic afferents was studied in cats maintained under urethane anesthesia. Recordings were performed in the ventral lateral nucleus after destruction of the reticular thalamic complex and cortical lesion. Some animals were also pretreated with reserpine (1.2 mg/kg) 24 h before recording sessions. Repetitive stimulation (25-60 Hz for 200-600 ms) of the peribrachial area produced a slow depolarization and tonic firing in thalamic cells. The depolarization was associated with an increase in membrane resistance and its amplitude decreased during membrane hyperpolarization. The reactivity of thalamic relay cells to a corticothalamic volley was also increased during the slow depolarization. Similar results were obtained in reserpinized animals. On the basis of previous data obtained in vitro, it is concluded that the slow depolarization resulted from the activation of muscarinic receptors by brainstem cholinergic afferents.

Animals↗

PubMed1990

Prolonged enhancement of anterior thalamic synaptic responsiveness by stimulation of a brain-stem cholinergic group.

This study describes the effects of brain-stem cholinergic laterodorsal tegmental (LDT) stimulation on the synaptic responsiveness of anterior thalamic (AT) neurons. A sample of AT cells, physiologically identified by their short-latency (less than 6.5 msec) response to mammillary body (MB) stimulation, was recorded in unanesthetized, chronically implanted cats and in urethane-anesthetized cats. In chronic experiments, LDT stimulation evoked a short-latency (10-20 msec) excitation in most AT cells. Moreover, brief LDT trains (3 shocks at 300 Hz, every 3 sec) enhanced the responsiveness of AT cells to both MB (orthodromic) and cortical (ortho- and antidromic) stimuli. This effect did not vary as a function of the interval between LDT conditioning and MB or cortical testing shocks, but as a function of the number of trials. The effects of LDT stimuli resisted reserpine treatment (0.75 mg/kg), suggesting that they were not dependent on the coactivation of monoaminergic fibers. Finally, LDT trains did not suppress inhibitory processes in AT neurons when conditioning-testing intervals were longer than 60 msec. Intracellular recordings performed in urethane-anesthetized cats revealed that LDT stimulation induced a short-latency depolarization which increased with membrane hyperpolarization and was associated with an increase in apparent membrane conductance. Usually, isolated LDT trains did not evoke lasting changes in membrane potential or conductance. However, when LDT trains were applied every 3 sec, they gradually decreased the apparent membrane conductance without altering the membrane potential. This conductance change had a time course similar to the LDT-induced potentiation of responsiveness observed in the chronic experiments. In some neurons, LDT conditioning trains also induced a marked increase in the probability of fast prepotentials being triggered by subthreshold MB or cortical orthodromic volleys. In order to distinguish the cumulative effects of repeated LDT trains from the possibly slow time course of LDT influences, we studied the effects of a unique 1 sec LDT train (at 30 Hz) on the synaptic responsiveness of AT cells recorded extracellularly in reserpine-treated, urethane-anesthetized animals. Such LDT trains induced a 2.9-fold increase in synaptic responsiveness, reaching its peak 40-50 sec after the LDT train and lasting up to 4 min. Iontophoretic application of the muscarinic blocker scopolamine blocked these long-lasting potentiating effects of LDT stimuli. Removal of cortical and basal forebrain inputs to the AT nuclear complex by appropriate transections did not abolish the potentiating effects of LDT trains.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1989

The effects of brainstem peribrachial stimulation on perigeniculate neurons: the blockage of spindle waves.

The mode of action of afferents arising from the brainstem peribrachial region at the midbrain-pontine junction on neurons recorded from the reticular thalamic sector adjacent to the lateral geniculate nucleus (perigeniculate cells) was investigated at the intracellular level in the cat. Experiments were performed in cats under barbiturate or urethane anaesthesia and in non-anaesthetized deafferented animals. Most cats were pretreated with reserpine (1-2 mg/kg) and were also acutely deprived of their retinal and cortical visual inputs. It was found that peribrachial stimulation produced a short train of fast-rising depolarizations followed by a long-lasting period of hyperpolarization in all perigeniculate neurons. Although the latest part of the early depolarizations preceding the hyperpolarization resulted from a parallel activation of lateral geniculate relay neurons by peribrachial afferents, those occurring at shortest latencies appear to result from a direct excitation produced by peribrachial afferents. Furthermore, these early excitatory postsynaptic potentials persisted under deep barbiturate anaesthesia, a condition that prevents activation of thalamic relay neurons by peribrachial stimulation. The evoked hyperpolarization decreased with membrane hyperpolarization, was associated with a 40-50% increase in membrane conductance and was insensitive to Cl injections. It was no longer observed within one hour after i.v. injection of scopolamine. However, the depolarizing responses were not depressed by this muscarinic antagonist. Iontophoretic applications of scopolamine also removed peribrachial-evoked inhibition of synaptic responses triggered by optic chiasma stimulation. The peribrachial input exerted a powerful control on the oscillatory behavior of perigeniculate neurons. Spindle oscillations which are generated within the reticular thalamic complex were readily blocked by peribrachial stimulation. It is then concluded that the transition from an oscillatory to a relay mode of operation in the thalamus is controlled at least in part by a muscarinic inhibition of reticular thalamic neurons. The synaptic mechanism responsible for the early depolarization remains to be elucidated.

Action Potentials↗

PubMed1989

The effects of brainstem peribrachial stimulation on neurons of the lateral geniculate nucleus.

The intracellular effects of brainstem peribrachial stimulation on lateral geniculate neurons were investigated in the cat. Experiments were performed in cats under barbiturate or urethane anaesthesia and in non-anaesthetized deafferented animals. Most animals were pretreated with reserpine and were acutely deprived of their retinal and visual cortical inputs. Short trains of stimuli triggered a transient depolarization in most relay neurons (latency: 20-30 ms; duration: 200-300 ms). This depolarization could be interrupted by a short-duration unitary inhibitory postsynaptic potential. The depolarization increased with membrane hyperpolarization and was associated with an increase in membrane conductance. The inhibitory postsynaptic potential had an intrathalamic origin and likely resulted from parallel activation of intrageniculate interneurons. The above responses were largely enhanced in reserpinized cats and were completely abolished by small doses of barbiturates. Iontophoretic applications of the nicotinic blocker, hexamethonium, eliminated peribrachial-evoked discharges in these cells, while similar applications of the muscarinic antagonist, scopolamine, were devoid of any effect. The conclusion is reached that the depolarization of lateral geniculate relay neurons by peribrachial afferents represents a direct postsynaptic effect and does not result from a global disinhibitory mechanism involving inhibition of perigeniculate cells and intrageniculate interneurons. This peribrachial-evoked transient excitation of relay neurons results from a nicotinic mechanism.

Action Potentials↗

PubMed1989

The cellular mechanism of thalamic ponto-geniculo-occipital waves.

The cellular mechanisms underlying the genesis of thalamic ponto-geniculo-occipital waves were studied in reserpinized cats under urethane anaesthesia. Simultaneous field potential and intracellular recordings were performed in the lateral geniculate nucleus after acute lesions of retinal and visual cortical inputs. In most relay cells, reserpine-induced ponto-geniculo-occipital waves were associated with a transient depolarization that was often interrupted by a unitary inhibitory postsynaptic potential. The depolarization grew in size with membrane hyperpolarization and was accompanied by an increase in membrane conductance. The inhibitory postsynaptic potential is likely to have resulted from the activation of intrageniculate interneurons since perigeniculate cells were always inhibited during the occurrence of ponto-geniculo-occipital waves. Under reserpine, thalamic ponto-geniculo-occipital waves could also be triggered by peribrachial or auditory stimulation. These evoked ponto-geniculo-occipital waves were associated with intracellular events identical to those occurring spontaneously after reserpine administration. In addition, thalamic spindle oscillations were readily blocked by the occurrence of spontaneous or evoked ponto-geniculo-occipital waves. On the basis of the present results and those already published in the literature, the conclusion is reached that lateral geniculate ponto-geniculo-occipital waves result from a nicotinic activation of relay cells and from a parallel muscarinic inhibition of perigeniculate cells by peribrachial afferents. The functional significance of the ponto-geniculo-occipital activity is discussed on the basis of the antagonistic action of these signals on thalamic oscillations. It is proposed that these signals are the central correlates of orienting reactions elicited by sensory stimuli during waking (the so-called eye movement potentials) and by internally generated drives during paradoxical sleep.

Action Potentials↗

PubMed1989

Suppression of primary antibody response in genetically susceptible mice infected with Salmonella typhimurium: restoration by catalase.

Susceptible C57BL/6 mice infected with a temperature-sensitive mutant of Salmonella typhimurium exhibited a marked depression of in vivo and in vitro primary antibody response to sheep erythrocytes which persisted for several weeks. The antibody response to a T-independent antigen (TNP-polyacrylamide) was also depressed. Cell-mixing experiments indicated that spleen cells from infected animals contained adherent suppressor cells and that the functional activity of T and B cells was unaffected. The antibody response of spleen cells from infected mice was restored by the addition of catalase, suggesting that hydrogen peroxide is involved in the mechanism of suppression.

Animals↗

PubMed1989

Phasic activation of lateral geniculate and perigeniculate thalamic neurons during sleep with ponto-geniculo-occipital waves.

Ponto-geniculo-occipital (PGO) waves are spiky field potentials generated in cholinergic nuclei of the dorsolateral mesopontine tegmentum just prior to and during rapid-eye-movement (REM) sleep and transferred toward thalamic nuclei. These events are commonly regarded as physiological correlates of oneiric behavior. We have examined the PGO-related discharges of physiologically identified neurons located in the dorsal lateral geniculate (LG) nucleus and perigeniculate (PG) sector of the reticular thalamic complex in chronically implanted, naturally sleeping cats. PGO focal waves and associated unit discharges were simultaneously recorded by the same microelectrode. PGO waves herald the other signs of REM sleep (EEG desynchronization and muscular atonia), appearing 30-90 sec before REM sleep over the EEG-synchronized activity of slow-wave sleep (pre-REM epoch). (1) Most PG neurons discharged bursts of action potentials in relation to PGO waves during both pre-REM and REM sleep. (2) The PGO-related activity of LG neurons was quite different. During the pre-REM stage, PGO waves correlated with a short (7-15 msec), high-frequency (300-500 Hz) spike burst of LG neurons, followed by a long (0.2-0.4 sec) train of single spikes, whereas during REM sleep, the PGO-related activity lacked the initial burst and consisted of a spike train that only slightly exceeded the tonically increased background firing of LG cells. The stereotyped characteristics of the PGO-related spike bursts during the pre-REM epoch suggest that they are the extracellular reflection of a low-threshold spike deinactivated by the tonic membrane hyperpolarization of LG cells associated with the EEG-synchronized sleep state. Such bursts are inactivated during the tonic depolarization of LG cells that occurs in REM sleep. The synchronous spike bursts discharged by LG cells in relation with the PGO waves of the pre-REM epoch probably underlie the much larger amplitude of the PGO waves of the pre-REM epoch as compared with those of the REM-sleep state. Since LG neurons have relatively low spontaneous firing rates during the EEG-synchronized pre-REM epoch, the PGO-related activity of this transitional stage leads to a higher signal-to-noise ratio in the visual thalamocortical channel than during REM sleep. We suggest that the PGO-related activity during the pre-REM epoch is related to vivid imagery during this stage of sleep.

Animals↗

PubMed1988

The blockage of ponto-geniculo-occipital waves in the cat lateral geniculate nucleus by nicotinic antagonists.

The cholinergic mechanism underlying the genesis of ponto-geniculo-occipital (PGO) waves recorded from the lateral geniculate (LG) nucleus was studied in reserpinized cats under urethane anesthesia. PGO field potentials and their related unit activities occurred spontaneously or were triggered by stimulation of the brainstem peribrachial (PB) area. It was found that PGO-related unit activities were strongly depressed by systemic or iontophoretic applications of nicotinic antagonists such as mecamylamine or hexamethonium but remained intact after similar applications of scopolamine. These results suggest that the genesis of thalamic PGO waves involves a nicotinic activation of relay neurons by PB cholinergic afferents.

Action Potentials↗

PubMed1988

Cholinergic and non-cholinergic projections from the upper brainstem core to the visual thalamus in the cat.

The projections of cholinergic and non-cholinergic neurons of the rostral brainstem reticular formation to the visual thalamic nuclei (dorsal lateral geniculate - LG, lateral posterior - LP, and perigeniculate - PG) were studied in cat by using the retrograde transport of horseradish peroxidase conjugated with wheat germ agglutinin (WGA-HRP) combined with choline acetyltransferase (ChAT) immunohistochemistry. After thalamic injections, less than 10% of all retrogradely labeled neurons in the upper brainstem reticular core were located at most rostral (perirubral) levels where there are virtually no cholinergic elements. Approximately 75-80% of all HRP-positive neurons in the reticular formation were found between stereotaxic planes anterior 1 and posterior 2, in the peribrachial (PB) area of the pedunculopontine nucleus and in the laterodorsal tegmental (LDT) nucleus. The brainstem afferents to LG and PG thalamic nuclei essentially derive from PB neurons, with a small contribution from LDT cells, whereas the LP thalamic nucleus receives massive inputs from both PB and LDT brainstem nuclei. Of all HRP-positive elements visualized in the PB nucleus after an LG or a PG injection, 87% and 73%, respectively, were also ChAT-positive. Of all HRP-positive elements in the PB and LDT nuclei after an LP injection, 82% and 92%, respectively, were also ChAT-positive. The numbers of labeled neurons in the contralateral brainstem reticular nuclei reach 30% to 50% of the numbers found in the ipsilateral reticular formation. These findings reveal the existence of a prominent cholinergic projection from the brainstem reticular formation to the visual thalamic nuclei. Such a chemospecific projection is probably involved in phasic and tonic events of activated behavioral states.

Animals↗

PubMed1987

Thalamic and cortical spindles during early ontogenesis in kittens.

On birth, focal thalamic recordings show sporadic sequences of spindle waves whereas EEG cortical recordings show no trace of spindles. Thalamic spindles are occasionally transferred to the cortex beginning with the 3rd-4th day. On the 8th-9th day, clear-out spindle sequences, with the same patterns as in the adult animal, appear simultaneously in the thalamus and cortex.

Animals↗

PubMed1987

The deafferented reticular thalamic nucleus generates spindle rhythmicity.

The hypothesis that nucleus reticularis thalami (RE) is the generator of spindle rhythmicity during electroencephalogram (EEG) synchronization was tested in acutely prepared cats. Unit discharges and focal waves were extracellularly recorded in the rostral pole of RE nucleus, which was completely disconnected by transections from all other thalamic nuclei. In some experiments, additional transections through corona radiata created a triangular island in which the rostral RE pole survived with the caudate nucleus, putamen, basal forebrain nuclei, prepyriform area, and the adjacent cortex. Similar results were obtained in two types of experiments: brain stem-transected preparations that exhibited spontaneous spindle sequences, and animals under ketamine anesthesia in which transient spindling was repeatedly precipitated during recording by very low doses of a short-acting barbiturate. Both spindle-related rhythms (7- to 16-Hz waves grouped in sequences that recur with a rhythm of 0.1-0.3 Hz) are seen in focal recordings of the deafferented RE nucleus. The presence of spindling rhythmicity in the disconnected RE nucleus contrasts with total absence of spindles in cortical EEG leads and in thalamic recordings behind the transection. Oscillations within the same frequency range as that of spontaneous spindles can be evoked in the deafferented RE nucleus by subcortical white matter stimulation. In deafferented RE cells, the burst structure consists of an initially biphasic acceleration-deceleration pattern, eventually leading to a long-lasting tonic tail. Quantitative group data show that the burst parameters of disconnected RE cells are very similar to those of RE neurons with intact connections. In the deafferented RE nucleus, spike bursts of RE neurons recur periodically (0.1-0.3 Hz) in close time-relation with simultaneously recorded focal spindle sequences. The burst occurrence of deafferented RE cells is greatly reduced after systemic administration of bicuculline. The preservation of both spindle-related rhythms in the disconnected RE nucleus, together with our recent experiments showing abolition of spindle oscillations in thalamic nuclei after lesions of RE nucleus (24), demonstrate that RE nucleus is the generator of spindle rhythms.

Afferent Pathways↗