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M H Lewandowski

Publications and source records attributed to M H Lewandowski.

13 recordsLinked to original sources

The serotonergic inhibition of slowly bursting cells in the intergeniculate leaflet of the rat.

Electrophysiological studies combined with local neurotoxic lesions were conducted on anaesthetized rats in order to determine whether the dorsal raphe nucleus (DRN) inhibits the intergeniculate leaflet (IGL) of the lateral geniculate nucleus by means of innervation by serotonin-containing fibres. In the control animals, electrical stimulation of the DRN induced the long-latency and long-lasting inhibition of the neuronal firing of the IGL cells that are characterized by rhythmic, slow-bursting activity in light conditions. The electrical destruction of the DRN resulted in an increase in the firing rate of the recorded IGL cells, whilst at the same time not affecting the rhythmic, bursting pattern of the activity. In the second group of animals, local neurotoxic lesion of serotonergic fibres was performed by injection of the toxin 5,7-dihydroxytryptamine into the IGL. After 10 days of postoperative recovery, electrophysiological experiments were performed on the toxin-treated rats. In these animals, electrical stimulation as well as electrical lesion of the DRN did not induce any change in the firing of the slowly bursting cells in the 5,7-dihydroxytryptamine-injected IGL. The results obtained provide evidence that inhibition of the IGL slowly bursting cells, by innervation from the dorsal raphe, is mediated by the release of serotonin. Furthermore, the observed serotonergic inhibition of the light-dependent activity of slowly bursting cells can contribute to the neuronal mechanism gating the information that flows through this nucleus to the vestibular, visuomotor, circadian and sleep/arousal systems, with which the IGL is strongly interconnected.

5,7-Dihydroxytryptamine↗

Blockade of GABAA receptors disrupts isoperiodic neuronal oscillations in the intergeniculate leaflet of the rat.

The intergeniculate leaflet of the thalamus is, besides the suprachiasmatic nucleus of the hypothalamus, the other important neuronal element of the mammalian biological clock. The extracellularly recorded activity of neurons constituting the intergeniculate leaflet, recorded in vivo, is characterized by distinct, very regular ultradian oscillations. The majority of neurons in the circadian timing system are GABAergic. Many, if not all, neurons of the suprachiasmatic nucleus and intergeniculate leaflet contain GABA. In the present study we examined the effects of the GABA(A) receptor antagonist bicuculline and the chloride channel blocker picrotoxin on isoperiodic neuronal oscillations in the intergeniculate leaflet of rats. We recorded extracellular multiple-unit neuronal activity from the intergeniculate leaflet of anesthetized rats. During the recording of isoperiodic oscillations, bicuculline or picrotoxin were stereotaxically injected at different concentrations into the lateral ventricle of rat brain. In all the experiments, injection of GABA(A) receptor antagonists transiently disrupted the isoperiodic phasic discharge recorded from the intergeniculate leaflet. These data suggest that GABA(A) receptors are involved in the generation of ultradian rhythmical neuronal oscillations in rat intergeniculate leaflet.

Action Potentials↗

Ultradian rhythmic neuronal oscillation in the intergeniculate leaflet.

Our paper is the first to describe ultradian rhythmic neuronal oscillation in the intergeniculate leaflet (IGL) of the rat. We recorded a multiple-unit neuronal activity (MUA) from dorsal to ventral parts of the lateral geniculate nucleus (LGN) in anaesthetized rats. In all the subdivisions of the lateral geniculate complex we observed spontaneous irregular firing rates of cells. However only at the anatomical localisation of the IGL, after the light was on, those responses exhibited burst firing with a constant interburst interval, which lasted several hours until the light was off. The duration of that rhythmic oscillation obtained by means of Fourier's analysis was approximately 124 s. To date we have not had sufficient data to discuss possible mechanisms of this neuronal rhythmicity. We can only conclude that light is the most important stimulus not only for suprachiasmatic nuclei (SCN), but also for the IGL. On the other hand, we can neither exclude nor confirm that in order to evoke ultradian rhythmical oscillation in the IGL, in addition to light also non-photic information is necessary.

Activity Cycles↗

[Application of electrophysiological methods in vivo to study circadian clock mechanisms in mammals].

The suprachiasmatic nuclei (SCN) of the hypothalamus and the intergeniculate leaflet (IGL) of the thalamic lateral geniculate complex are two main oscillators for circadian timing system. A lot of anatomical evidences indicated a strong neuronal connections between SCN and IGL. Relatively less, however, is know about the electrophysiology and functional interactions between SCN and IGL. The spontaneous firing rate of SCN neurons exhibits a remarkable circadian rhythm with a higher activity in the day and a lower at the night both in vivo and in vitro preparations. However, these rhythms my represent only clock output rather then the intrinsic clock mechanism. Last data described for the first time ultradian rhythmic neuronal oscillation recorded in vivo in the rat SCN and IGL. These isoperiodic phasic discharge probably constitute a basis necessary to generate circadian rhythms in mammals.

Animals↗

The effect of brainstem stimulation on the evoked potentials in the intergeniculate leaflet.

We have investigated the effect of the laterodorsal tegmental (LDTg) stimulation on evoked potentials in the intergeniculate leaflet (IGL) of the rat, in order to characterize how non-specific systems of the brain, whose activity indicates the influence of non-photic information, impact the activity of the IGL. IGL responses were evoked by electrical stimulation of contralateral suprachiasmatic nuclei (SCN). The amplitude of the evoked potentials was, in all experiments, significantly reduced after the LDTg stimulation. This effect indicated strong neuronal integration between the brainstem reticular formation and the IGL. These results are discussed in relation to the putative role of GABAergic projection.

Animals↗

[The biological clock in mammals: structure and function].

The mammalian circadian timing system has three principal components: entrainment pathways, pacemakers and efferent pathways that couple the pacemaker to effector systems which exhibit temporal organization for physiological processes and behaviour. Light is the primary circadian Zeitgeber and the suprachiasmatic nuclei (SCN) functions as the major pacemaker in the mammalian circadian timing system. A number of investigators have focused attention on the intergeniculate leaflet (IGL) and the geniculohypothalamic tract (GHT) that mediate the effects of nonphotic stimuli on SCN activity and how these pathways interact with photic information being transmitted to the SCN.

Animals↗

Effect of the cholinesterase-inhibiting substance galanthamine on evoked visual potentials in rats.

We studied the effect of intravenous injection of the cholinesterase inhibitor galanthamine (GAL) in doses from 0.025 to 5.0 mg/kg on electrically evoked field potentials in rat visual cortex. In all the experiments the amplitude of late components of evoked potentials was significantly reduced, while early components remained unaffected. These findings indicate that cortical cells are inhibited by acetylcholine (ACh). Furthermore, combined application of a muscarinic receptor blocker (atropine) and GAL reliably suppressed the effects of galanthamine. These observations suggest that ACh-induced inhibition may be mediated by activation of GABAergic interneurones that possess muscarinic receptors.

Animals↗

Reticular facilitation of cat visual cortical responses is mediated by nicotinic and muscarinic cholinergic mechanisms.

Stimulation of the mesencephalic reticular formation facilitates responses in the visual cortex elicited from the optic radiation. Using intravenous administration of cholinergic antagonists we investigated in adult cats and two kittens whether this effect is mediated by cholinergic mechanisms. When administered alone the muscarinic antagonists atropine and scopolamine and the nicotinic antagonist mecamylamine failed to block reticular facilitation and sometimes even enhanced the effects of reticular stimulation. However, when administered in combination muscarinic and nicotinic antagonists eliminated or significantly reduced the facilitation. This was even true when the two antagonists were administered with a time lag of several hours. These results support the notion that reticular facilitation of cortical responses is mediated by cholinergic mechanisms and suggest that this effect is mediated either by a receptor with a mixed pharmacological property or by two independent pathways acting via nicotinic and muscarinic receptors. This hypothesis is discussed in the context of recent evidence on cholinergic transmission and earlier data on the pharmacology of reticular arousal.

Animals↗

Structures mediating cholinergic reticular facilitation of cortical responses in the cat: effects of lesions in immunocytochemically characterized projections.

Cholinergic afferents to the neocortex controlled by the mesencephalic reticular formation (MRF) are known to transiently facilitate cortical excitability. In an attempt to identify the pathway mediating this effect in the cat visual cortex we combined retrograde tracing techniques with immunocytochemical methods to visualize the acetylcholine-synthesizing enzyme choline acetyltransferase (ChAT). In addition we examined, in acute electrophysiological experiments, whether local neurotoxin injections into nuclei of the basal forebrain interfered with the reticular facilitation of cortical evoked potentials. Cholinergic projections to area 17 originate from different centers in the homolateral substantia innominata/internal capsule, the septal nuclei, and the nuclei of the diagonal band of Broca. No direct cholinergic projection from the MRF to the visual cortex was observed. Retrogradely labelled cells intermingled with ChAT-positive neurons in the brainstem generally revealed immunopositivity for catecholaminergic markers. Local injections of neurotoxins in the substantia innominata blocked reticular facilitation, whereas local lesions of the septal nuclei and the nuclei of the diagonal band had no effect on MRF-induced facilitation. The blockage of the reticular facilitation of cortical evoked responses after unilateral lesions of the substantia innominata was bilateral, suggesting a cooperative interaction between basal forebrain structures of the two hemispheres. The anatomical and physiological data are discussed with respect to possible mechanisms of transient brainstem influences on cortical excitability.

Animals↗

Seasonal variations in the circadian activity of AChE in the brain stem reticular formation of mice under normal and constant light regimens.

AChE activity in mouse brain stem reticular formation was studied at 4 hr intervals for 48 hr at 4 different times of the year under normal (LD 12/12) and constant light (LL) regimens. Under both illumination regimens, a significant ultradian rhythm of AChE activity was observed. In the investigated seasons of the year, changes in AChE behaviour were limited to mean activity of the enzyme (median) as well as to the amplitude and acrophase of the rhythm.

Acetylcholinesterase↗

Effect of lithium on circadian activity of AChE (EC 3.1.1.7) in the reticular formation of mouse brain stem under LD 12:12.

The investigation was carried out on male mice 6-8 weeks old. Control animals were fed standard chow without lithium, while the experimental ones received on additional 10 mmol LiCl/kg of chow. After 30 days feeding, 7 mice at a time were killed every 4h. The activity of free AChE was assessed in the brain stem reticular formation according to the method of Ellman. The results were statistically analyzed using Student's t-test and Fisher test. Parameters of periodic function were then applied to the means obtained by the method of least-squares. In both the control and experimental groups diel changes in the AChE activity were observed. Acrophase activity occurred in the control group at 1956. In the experimental group lithium caused a shift in acrophase to 0551. It may therefore be supposed that lithium not only affects the duration of the rhythm period but also shifts its phase by 1800. This could be relevant to the therapeutic use of lithium in manic-depressive patients who may present advancing phase of circadian rhythms.

Acetylcholinesterase↗