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T Schallert

Publications and source records attributed to T Schallert.

At least 91 records · Page 5Linked to original sources
PubMed1980

Muscarinic receptor binding and behavioral effects of atropoine following chronic catecholamine depletion or acetylcholinesterase inhibition in rats.

Rats were subjected to one of two experimental treatments: (1) intraventricular infusion of the catecholamine neurotoxin 6-hydroxydopamine (6-OHDA), known to permanently reduce brain dopamine and norepinephrine levels, or (2) chronic administration of the irreversible acetylcholinesterase inhibitor diisopropylfluorophosphate (DFP). Both treatments are believed to produce relative overactivity of cholinergic systems and to suppress forward locomotion. The anticholinergic agent atropine sulfate yielded excessive forward walking in otherwise chronically akinetic 6-OHDA-treated rats, whereas atropoine slightly decreased locomotion in controls. The hypothesis that such supersensitivity to atropine may be related to a reduction in the density of muscarinic cholinergic receptors was not supported: First, 3H-quinuclidinyl benzilate (QNB) binding to membrane preparations was not decreased in the 6-OHDA-treated rats; secondly, atropine did not induce excessive forward locomotion in the DFP-treated rats in which 3H-QNB binding was decreased. There were other changes in the DFP-treated rats consistent with muscarinic receptor alteration, including tolerance to the locomotor suppressive effects of DFP, cross tolerance to the cholinergic agonist pilocarpine, and exaggerated atropine-induced increases in core temperature and stereotypy. It is concluded that 6-OHDA and DFP produce different long-term changes in cholinergic brain systems and atropine-sensitive behaviors.

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PubMed1980

Atropine stereotypy as a behavioral trap: a movement subsystem and electroencephalographic analysis.

An analysis was made of the movement subsystems involved in the stereotyped behaviors and electroencephalographic (EEG) activity that appear in rats given the anticholinergic drug atropine sulfate (50-75 mg/kg). One form of stereotypy occurred when the drugged faced the closed end of an alleyway. Instead of scanning briefly and then turning around to face the open end, as undrugged rats do, they typically "trapped", i.e., they continued to engage in rapid, repetitive scanning by the snout up and down or side to side along the surfaces of the closed end for long periods of time. Atropine appears to produce an exaggerated snout thigmotaxis. Accordingly, the behavioral pattern can be manipulated simply by changing the configuration of the environment, which alters sensory input to the snout. Therefore, such stereotyped behavior is not a motor automatism but rather a circular chain of reflexive reactions to surfaces which trap the animal. During rapid shifts in direction of movement in undrugged rats, there were often extremely brief periods of hippocampal theta that could be blocked by atropine. The presence of theta during such shifts might be important for normal behavioral sequencing. This could partially account for the fact that atropine-treated rats failed to change from their initial reactions in the alleyway to more adaptive behaviors. When a low roof was placed over the alleway, head scanning was greatly limited, and immobility in a lying posture rapidly became the more frequent behavior. This immobility was accompanied by a sleeplike (synchronized) neocortical EEG pattern rather than the activated (desynchronized) neocortical pattern that occurs during repetitive thigmotactic scanning. It is hypothesized that scanning stereotypy and activated EEG are maintained through movement-concurrent positive feedback.

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PubMed1979

Inhibition of in vivo 3H-spiperone binding by the proposed antipsychotic Des-Tyr1-gamma-endorphin.

The proposed antipsychotic neuropeptide des-tyrosine1-gamma-endorphin (DT gamma E, beta LPH62,77) inhibits in vivo 3H-spiperone binding in the hypothalamus, corpus striatum and mesolimbic areas of rat brain. The neuroleptic drug haloperidol produces similar effects in these areas as well as in frontal cortex, but is considerably more potent than DT gamma E. Correspondingly, haloperidol produces postural and motor abnormalities not seen with DY gamma E. These data together with the results from previous in vitro studies suggest DT gamma E might act indirectly, having a selective neuroleptic-like action at 3H-spiperone binding sites.

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PubMed1978

Compulsive, abnormal walking caused by anticholinergics in akinetic, 6-hydroxydopamine-treated rats.

In otherwise profoundly akinetic rats that had been severely depleted of brain catecholamines, anticholinergic drugs caused excessive walking. The effect did not appear until 10 days after surgery and then increased with time, suggesting that a phenomenon analogous to denervation supersensitivity may be involved. If the animals walked into corners, they were unable to turn around or back out. Their gait (extremely short steps) was reminiscent of that of patients with Parkinson's disease. The results are consistent with a mutually antagonistic interaction between cholinergic and dopaminergic brain systems and emphasize certain complexities in this interaction.

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PubMed1978

Two types of aphagia and two types of sensorimotor impairment after lateral hypothalamic lesions: observations in normal weight, dieted, and fattened rats.

In two experiments, reactions to food and to tactile stimuli were examined in rats whose body weights were normal, reduced by restricted feeding (dieted), or raised by having access to palatable foods (fattened) prior to receiving bilateral lesions in the lateral hypothalamic (LH) area. Postoperative aphagia and sensorimotor impairments were less prolonged than normal in the dieted rats and more prolonged than normal in the fattened rats. The LH lesions produced a transient hyperthermia which was attenuated by dieting and facilitated by fattening. Certain motor impairments (which accompanied more posterior lesion placements), hypokinesia, and a lesion-induced exaggerated aphagia to novel foods were relatively unaffected by preoperative body weight. Depending importantly upon lesion placement, there appeared to be at least two types of aphagia and two types of sensorimotor impairment. Animals with more posterior LH lesions displayed a passive kind of aphagia and sensory neglect. These animals did not react to food or to sensory stimuli presented externally, but they chewed and appeared to swallow food placed in the mouth. Animals with more anterior LH lesions displayed an active kind of aphagia and sensory rejection. These latter animals briskly turned their heads toward food or a light touch; however, they also showed simple stereotyped withdrawal or reactions of aversion to the food, to a light touch, and to a variety of sensory stimuli. Animals with intermediately placed lesions showed symptoms common to passive and active aphagia and to sensory neglect and sensory rejection. The effects of preoperative weight manipulation on the specific types of aphagia and sensorimotor impairments are discussed.

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PubMed1977

Hippocampal RSA (theta), apnea, bradycardia and effects of atropine during underwater swimming in the rat.

Hippocampal RSA (theta), neocortical EEG, and heart rate were recorded during surface and underwater swimming in the rat. RSA was present with slightly reduced frequency during the apnea, bradycardia, and vibrissae arrest associated with under water swimming. Atropine sulfate (50 mg/kg) blocked bradycardia did not affect RSA. Contrary to previous suggestions, no causal relation was found between RSA and respiration, heart rate, or vibrissae movement. The study supports the view that RSA is related to the neural control of voluntary movement. It is suggested that the slight reduction in RSA frequency during underwater swimming may be part of an oxygen conservation process.

Animals↗
PubMed1977

Aphagia, behavior sequencing and body weight set point following orbital frontal lesions in rats.

Discrete lesions were made in the orbital frontal neocortex of rats and eating, drinking, sensorimotor responsiveness, and sequencing of motor acts were studied. Duration of aphagia was related to palatability/texture of food. Rats were aphagic for a mean of two days to palatable cookie mash presented on a spatula, six days to a high fat diet mash presented in a 4 cm high dish and for seven days to dry laboratory food. Water drinking was resumed with injestion of dry food. Rats presurgically fattened to 120% of body weight appeared stuporous and akinetic for 2-3 postoperative days, and the period for acceptance of food in tall tests was protracted. Rats presurgically dieted to 80% of normal body weight did not show accelerated recovery of feeding. Preoperatively normal, fattened and dieted rats assumed a chronic postoperative body weight level 25% lower than control rats. Rats with lesions showed sensorimotor neglect when tested on an open table top, but did not show neglect when tested in their home cages. In grooming tests, rats with lesions showed all of the components of normal grooming, but failed to exhibit the long chains of grooming characteristics of control rats. They also showed attenuated tongue extension and had difficulty manipulating food with the forepaws. The experiments suggest that following orbital frontal lesions, motor impairments, motor sequencing dysfunctions, change in body weight set point, and depending upon the test situation, sensorimotor neglect, may all be contributing factors to aphagia. The orbital frontal cortex may influence feeding and other behaviors via descending neural projections to the hypothalamus and branistem.

Animals↗
PubMed1977

Gastric pathology and feeding deficits induced by hypothalamic damage in rats: effects of lesion type, size, and placement.

Three doses each of cathodal or anodal direct current were delivered to coagulate lateral hypothalamic tissue bilaterally in rats. Increases in hypothalamic tissue damage were associated with more instances of aphagia, greater amounts of glandular, but not rumenal, gastric pathology, and greater weight loss. Both anodal and cathodal lesions produced aphagia and similar amounts of gastric pathology, but anodal lesions also appeared to facilitate weight loss independently of the tissue damage. Extensive chromatolysis surrounding anodal lesion cavities may be importantly related to the postoperative effects. In additional experiments, anodal electrolytic lesions or cortical suction ablations were used to vary the location of neural damage. Fedding deficits and gastric pathology resulted from the destruction of several brain areas. In particular, eating of dry food in the presence of high gastric pathology was observed in rats with lesions ventral and medial to an area in the dorsolateral hypothalamus that was associated with aphagia. When aphagia was accompained by severe gastric pathology, the brain lesions typically encroached extensively on more ventromedial areas. Moreover, aphagia sometimes was observed with only negligible gastric pathology. It is suggested that gastric pathology is not primary to the expression of the aphagia that follows lateral hypothalamic damage.

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PubMed1976

Intraventricular anti-cholinergics do not block cholinergic hippocampal RSA or neocortical desynchronization in the rabbit or rat.

Electroencephalographic (EEG) electrodes and ventricular cannulae were implanted in 8 rabbits and 12 rats. Two anti-cholinergic agents, atropine sulfate and scopolamine hydrobromide, were given systemically (1-50 mg/kg) and intraventricularly (5-800 mug). Systemic but not intraventricular injections blocked sensory stimulation-induced or eserine-induced neocortical desynchronization and hippocampal RSA in rats and rabbits which were immobile and either undrugged or ethanol intoxicated. Systemic injections also blocked hippocampal RSA but not neocortical desynchronization in rats given sensory stimulation under urethane anaesthesia, while intraventricular injections only reduced RSA amplitude. Neither systemic nor intraventricular injections blocked neocortical desynchronization or hippocampal RSA recorded from animals when they walked in a motor driven wheel. These experiments support the hypothesis that there are two types of neocortical desynchronization and hippocampal RSA, one cholinergic and one non-cholinergic. They also suggest that atropine and scopolamine pass more readily to the neural system responsible for cholinergic EEG activity from the capillary bed than from the ventricular fluid.

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