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Biomedical subjects

C H Vanderwolf

Publications and source records attributed to C H Vanderwolf.

At least 91 records · Page 5Linked to original sources
PubMed1984

Cholinergic activation of the electrocorticogram: role of the substantia innominata and effects of atropine and quinuclidinyl benzilate.

Systemic injection of quinuclidinyl benzilate partially abolished low voltage fast activity (LVFA) in the neocortex of waking rats, resulting in the appearance of large irregular slow waves during Type 2 behaviors (e.g. immobility, sniffing without head movement, face washing). These slow waves did not occur during Type 1 behavior (e.g. walking, head movement). Atropine sulfate produced a similar effect but it was less potent by a factor of about 12. Injection of kainic acid into the substantia innominata: (a) destroyed local cells which contain acetylcholinesterase (AChE) and reduced AChE staining in the ipsilateral neocortex; and (b) produced large slow waves in the ipsilateral neocortex during Type 2 behavior but not during Type 1 behavior. These slow waves were abolished by systemic injection of pilocarpine. Kainic acid injection into the thalamus produced extensive local cell loss but failed to produce slow waves in the neocortex. The data suggest that the LVFA which is normally present in the neocortex during waking Type 2 behavior is dependent on a cholinergic input to the neocortex from the substantia innominata. The relevance of these findings to Alzheimer's disease is discussed.

Animals↗
PubMed1984

Hypothalamic self-stimulation: the role of dopamine and possible relations to neocortical slow wave activity.

Reserpine abolishes self-stimulation in rats but the behavior can be restored temporarily by treatment with D-amphetamine or L-DOPA. Apomorphine does not restore self-stimulation even though it restores spontaneous motor activity in reserpinized rats. The data indicate that dopamine plays a role in reinforcement as well as in motor function. The ability of D-amphetamine to restore self-stimulation in reserpinized rats is eliminated by concurrent treatment with atropine or scopolamine. This effect may be related to the presence of continuous large amplitude slow wave activity in the neocortex under these conditions.

Animals↗
PubMed1983

Cellular bases of hippocampal EEG in the behaving rat.

Rats implanted with recording and stimulating electrodes were trained to run in an activity wheel for a water reward. Unitary discharges and slow activity were recorded by a movable tungsten microelectrode and by fixed electrodes. Single cells were classified according to their spontaneous and evoked response properties as pyramidal cells, granule cells and interneurons. Unit activity, EEG and their interrelations were studied by spectral and spike-triggered averaging methods. Gradual phase-shifts of RSA were observed both in CA1 and the dentate gyrus. Movement-related RSA was correlated with a decrease in firing rate of pyramidal cells and an increase in the firing of both interneurons and granule cells. In the CA1 region pyramidal cells and interneurons fired preferentially on the negative and positive phases of the locally derived RSA, respectively. In the dentate gyrus both granule cells and interneurons discharged mainly on the positive portion of the local RSA waves, about 90 degrees before the CA1 pyramidal cells. Fourier analysis of the spike trains of interneurons and granule cells showed high power at RSA frequency, coherent with the concurrent EEG. Phase relations between discharges of interneurons and RSA remained unchanged following urethane anesthesia. In waking rats, atropine administration resulted in a decreased discharge of interneurons at RSA frequency, and reduced coherence with RSA. Lesions of the septum or the fimbria-fornix abolished RSA and the rhythmic discharges of the interneurons. Isolation of the entorhinal cortex (EC) from its cortical inputs did not change either EEG or neuronal firing. However, in such a preparation atropine completely abolished RSA and related rhythmicity of interneurons. During drinking and immobility but not during walking, sharp waves (SPW) of about 40-100 ms duration appeared in the EEG. SPWs were invariably accompanied by synchronous discharges of several pyramidal cells and interneurons. CA3 pyramidal cells also discharged in synchronous bursts but without local SPWs. Laminar profiles of SPWs and the field potentials evoked by stimulation of Schaffer collaterals were essentially identical. The behavior-dependent occurrence of SPWs was retained following atropine administration, septal lesion or EC isolation but was lost after fimbria-fornix-neocortex lesion or following atropine administration in EC isolated rats. In addition to relations to RSA and SPWs, interneurons were phase-locked to the fast EEG pattern (25-70 Hz). This relationship was preserved following lesions of the septum or the fimbria-fornix complex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1980

Monoamine replacement after reserpine: catecholaminergic agonists restore motor activity but phenylethylamine restores atropine-resistant neocortical low voltage fast activity.

A large dose of reserpine abolishes an atropine-resistant form of neocortical low voltage fast activity (LVFA) which normally accompanies certain patterns of motor activity in rats. An attempt was made to reverse this effect by replacement of specific monoamines or by injection of suitable agonists in rats pretreated with reserpine (10 mg/kg). The following compounds, alone or in various combinations, failed to restore atropine-resistant LVFA in reserpinized rats even though spontaneous motor activity was restored in many cases: L-DOPA (150-300 mg/kg) after pretreatment with an inhibitor of peripheral L-aromatic amino acid decarboxylase; 5-hydroxytryptophan (100-200 mg/kg); D-amphetamine (1-2 mg/kg); apomorphine (0.25-2.5 mg/kg); lysergic acid diethylamide (100-300 microgram/kg); and clonidine (0.5-1.0 mg/kg). In contrast beta-phenylethylamine was quite effective in restoring atropine-resistant LVFA and its effects were not diminished by pretreatment with alpha-methyl-p-tyrosine (400 mg/kg), chlorpromazine (15 mg/kg). It is suggested that a trace amine plays an essential role in the production of atropine-resistant LVFA independent of catecholamines.

5-Hydroxytryptophan↗
PubMed1980

Reserpine abolishes movement-correlated atropine-resistant neocortical low voltage fast activity.

Following a large dose of atropine, rats display large amplitude slow waves in the neocortex during immobility, tremor, tooth-chattering and face-washing (Type II behavior) but display low voltage fast activity (LVFA) during walking, struggling, postural changes and head movement (Type I behavior). Rats treated with a large dose of reserpine usually continue to display LVFA during immobility as well as during movement although large amplitude slow waves are present more frequently than normal. A combination of reserpine and atropine abolishes all LVFA even during intense sensory stimulation or electrical stimulation of the reticular formation. Chlorpromazine, lysergic acid diethylamide, methysergide, phenoxybenzamine, pimozide, promethazine, propranolol and trifluoperazine do not have this effect when combined with atropine. In rats treated with nialamide prior to reserpine and atropine, LVFA continues to occur in association with Type I behavior just as in rats given atropine alone. It is proposed that the occurrence of LVFA in the neocortex is determined by two distinct reticulocortical systems. A cholinergic system produces all LVFA occurring during Type II behavior and a second system, dependent on a monoamine, produces LVFA in association with Type I behavior. The view that LVFA is a correlation of arousal or the sleep-waking cycle is criticized.

Animals↗
PubMed1980

Behavior-dependent evoked potentials in the hippocampal CA1 region of the rat. II. Effect of eserine, atropine, ether and pentobarbital.

The correlations of the rat's behaviors and the hippocampal EEG with the averaged evoked potentials (AEPs) evoked by the Schaffer collaterals in the hippocampal CA1 region of the rat were studied after intraperitoneal injections of several drugs known to affect hippocampal EEG. Ether and eserine induced continuous train of rhythmical slow activity (RSA) of 5-6/sec in the hippocampal EEG, during which the AEPs showed waveforms intermediate between those elicited during large irregular activity (LIA) in the awake, immobile control and those elicited during walking in the control. Low dose nembutal and atropine induced high amplitude LIA during immobility, resembling EEG during slow-wave sleep (SWS). The AEPs during these LIA states, and that during LIA of wake-immobility were of similar waveforms. The AEP waveforms are proposed to form a continuum which corresponds to the continuum of EEG from high amplitude LIA to RSA of increasing frequency. AEP waveforms do not depend only on walking or similar movements which correlate with high frequency RSA. Atropine sulfate (25-50 mg/kg i.p.) severely dampened the oscillations in the AEPs of rats during walking or similar movements, even though the high frequency RSA was essentially unaffected. The difference between AEPs during immobility and those during walking was markedly reduced after atropine, even though the EEG-behavior relationship persisted. The effect of atropine on AEPs may be interpreted as a direct effect on the hippocampus which is apparently inconsistent with present knowledge. If the effect was on inputs from the brain stem or the septum to the hippocampus, the hypothesis that there are two pharmacological types of RSA (atropine-sensitive and -resistant) requires re-definition and re-examination.

Animals↗
PubMed1980

Frequency-specific RSA-like hippocampal patterns elicited by septal, hypothalamic, and brain stem electrical stimulation.

Hippocampal electrographic patterns comprised of specific frequencies of slow waves electrographically similar to the waves comprising normal hippocampal rhythmical slow activity (RSA, theta) may be generated by appropriate electrical stimulation of specific septal, hypothalamic, and brain stem sites. The waves elicited from some but not all sites are further similar to normal RSA patterns in that they may be differentiated into atropine-sensitive (immobility-related) and atropine-resistant (movement-related) types by the same criteria used to define atropine-sensitive and atropine-resistant RSA. The high degree of behavioral, pharmacological, and electrographic similarity between the electrically elicited hippocampal activity and normal hippocampal RSA would seem to warrant further use of the present technique in the investigation of hippocampal function.

Animals↗
PubMed1978

Behavior of the rat after removal of the neocortex and hippocampal formation.

After surgical removal of the neocortex and hippocampal formation, rats retained most of the movement patterns of locomotion, climbing, grooming, feeding, and fighting. However, forepaw immobility during swimming was abolished. Feeding behavior was suppressed temporarily but recovered partially. The distinctive postures of sleep and walking and a circadian rhythm of motor activity were retained. However, behaviors were often not performed at the appropriate time and place. The normal sequence of grooming behavior was disrupted; food hoarding and social behavior were essentially abolished. Removal of the neocortex alone had much the same effect as removal of neocortex and hippocampus together. Removal of hippocampus alone produced only a mild disruption of behavior. It is suggested that ascending nonspecific projections to the cerebral cortex play an important role in the moment-to-moment control of behavior but are not essential for the sleep-waking cycle.

Aggression↗
PubMed1977

Are the dorsal noradrenergic bundle projections from the locus coeruleus important for neocortical or hippocampal activation?

Three different methods were used to examine the importance of the dorsal noradrenergic bundle projections from the locus coeruleus (LC) in activation of the neocortex and hippocampus in freely moving rats. (1) After cerebral norepinephrine (NE) was depleted by systemic neonatal injections of 6-hydroxydopamine (6-OHDA) both atropine-resistant and atropine-sensitive forms of hippocampal rhythmical slow activity (RSA; theta) and neocortical low voltage fast activity (LVFA) remained intact. Compared to controls the adult rats treated with 6-OHDA in infancy reared less in a 24 h time sample of behavior and ran less in running wheels. (2) Brain dopamine and NE were also depleted by systemic injections of alpha-methyl-p-tyrosine. Following this treatment rats were very inactive behaviorally. However, normal activation of the hippocampus and neocortex was still present. (3) In normal rats, electrical stimulation of the LC was relatively ineffective, compared to stimulation of nucleus reticularis pontis caudalis, in producing behavioral changes (especially locomotion) or either atropine-resistant or atropine-sensitive hippocampal RSA or neocortical LVFA. It is concluded that the locus coeruleus is not important for cerebral activation, and that mechanisms for cerebral activation are probably diffusely represented in the reticular core. The data also show that when attempting to assess the effect of experimental manipulations on brain activity it is essential to control for the possible effects of changes in behavior.

Animals↗
PubMed1977

Hippocampal electrical activity during waking behaviour and sleep: analyses using centrally acting drugs.

Rhythmical slow activity (RSA) occurs in the hippocampus under many conditions including waking behaviour, active sleep and surgical anaesthesia. Under all these conditions RSA, apparently, is produced by the coupled operation of CA1 and dentate gyrus generators. Two ascending brainstem systems appear capable of initiating activity in these coupled generators. One system, ascending via the diagonal band and medial septal nucleus, may contain cholinergic synapses since it is blocked by atropine and stimulated by eserine. The RSA produced by this system usually has a frequency of 4--7 Hz and can occur during total immobility during the waking state, active sleep or anaesthesia. A second ascending system produces RSA of higher frequency (usually 7--12 Hz) and is active during waking if, and only if, movements such as walking occur. During active sleep this system is active only during phasic muscular twitches. Anaesthetics (ether, urethane) and morphine abolish activity in this second system but it is resistant to atropinic and nicotinic drugs. Amphetamine stimulates, and major tranquillizers depress the atropine-resistant system but these drugs do not abolish its normal relation to behaviour. Neocortical activity appears to be controlled by two ascending systems which parallel closely those ascending to the hippocampus.

Anesthesia, General↗
PubMed1975

Neocortical and hippocampal activation relation to behavior: effects of atropine, eserine, phenothiazines, and amphetamine.

Evidence is presented to suggest that the hippocampus receives 2 nonspecific inputs from the brainstem, each capable of producing rhythmical slow activity. The neocortex appears to receive 2 similar inputs, each capable of producing low voltage fast activity. One input to both hippocampus and neocortex is blocked by atropine and stimulated by eserine, and is essentially unrelated to concurrent motor activity. A second input to both hippocampus and neocortex is resistant to atropine, is depressed by phenothiazines, and is activated by d-amphetamine. Activity in this system is closely related to concurrent "voluntary" movement.

Animals↗