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Results for “Picrotoxin”

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At least 37 records · Page 2Linked to original sources

PubMed1979

Turning behaviour induced by injection of muscimol or picrotoxin into the substantia nigra demonstrates dual GABA components.

Injection of the GABA agonist muscimol into rat caudal substantia nigra caused contralateral turning, whereas injection into the rostral substantia nigra caused ipsilateral turning. The GABA antagonist picrotoxin had the opposite effect. These findings support the hypothesis that GABA has dual actions in the substantia nigra. Ipsilateral turning induced by injection of muscimol into rostral nigra was abolished by haloperidol pretreatment, indicating the involvement of dopaminergic mechanisms. Haloperidol pre-treatment did not prevent turning induced by muscimol injected into the caudal nigra, supporting the existence of a non-dopaminergic nigral output system.

Animals↗

PubMed1979

Effects of picrotoxin and strychnine on fish retinal S-potentials: evidence for inhibitory control of depolarizing responses.

Simultaneous recording of the light evoked electrical signals from different classes of slow(S)-potential unit in the isolated fish retina established that picrotoxin, an antagonist of GABA, selectively suppresses the depolarizing component of C-type S-potentials. In contrast, equivalent concentrations of strychnine have no effect on S-potentials, but suppress a component of transient amacrine cell responses. On the basis of these and other experimental data [3,4] we propose a network diagram for the C-type S-potential units in the cyprinid fish retina. This network includes a GABA-ergic feed-back loop and is essentially similar to that proposed by Fuortes and Simon [5].

Animals↗

PubMed1979

The effect of strychnine, bicuculline, and picrotoxin on X and Y cells in the cat retina.

The effect of intravenous strychnine and the GABA antagonists picrotoxin and bicuculline upon the discharge pattern of center-surround-organized cat retinal ganglion cells of X and Y type were studied. Stimuli (mostly scotopic, and some photopic) were selected such that responses from both on and off-center cells were either due to the center, due to the surround, or clearly mixed. Pre-drug control responses were obtained, and their behavior following administration of the antagonists was observed for periods up to several hours. X-cell responses were affected in a consistent manner by strychnine while being unaffected by GABA antagonists. All observed changes following strychnine were consistent with a shift in center-surround balance of X cells in favor of the center. For Y-cell responses to flashing annuli following strychnine, there was either no shift or a relatively small shift in center-surround balance. Compared to X-cell responses to flashing lights, those of Y cells were very little affected by strychnine and in most cases were unaffected. It thus appears that glycine plays a similar role in receptive field organization of X cells as does GABA in Y cells (Kirby and Enroth-Cugell, 1976. J. Gen. Physiol. 68:465-484).

Action Potentials↗

PubMed1978

Comparative effects of centrophenoxine on the picrotoxin convulsive-seizure threshold in non-irradiated and irradiated mice.

A comparative study is made of the effect of centrophenoxine (CP) on the picrotoxin convulsive-seizure threshold (PCST) in non-irradiated and irradiated 3 and 7 days previously male mice. It is found that the CP appliked intracerebroventricularly in doses of 200 and 400 micrograms/mouse (weight 18-22 g), increases PCST. In non-irradiated mice the PCST-increasing effect of CP occurs rapidly (5 min) and it is brief (it can be observed until the 15th min). When the irradiation is performed three days previously, the PCST-increasing effect of CP is prolonged (it is observed until the 6th hour after its application). When the irradiation is performed seven days previously the characteristic features of the PCST-increasing effect of CP are similar to those in the early stage (3 days), the only difference being that the duration of the effect is prolonged to 120 min. Generally, these specificities of the CP effect are valid for all three phases of the convulsive seizure (general excitation, clonic convulsive seizure and tonic convulsive seizure.

Animals↗

PubMed1979

Facilitation of bicuculline- and picrotoxin-induced seizures by sodium valproate in rats.

Paralysed rats anaesthetized with urethane or halothane were injected with bicuculline or picrotoxin at doses which induced seizure activity in the EEG. Sodium valproate (50--1200 mg/kg) or saline was injected i.p. and its effect on the amplitude and duration of the seizures was measured. The seizures induced by either convulsant were increased significantly by doses of valproate greater than or equal to 200 mg/kg. The sites of action of the drugs in the brain, and the possible transmitter mechanisms involved, are discussed.

Animals↗

PubMed1977

[Behavior modifications induced by unilateral administration of picrotoxin into rat substantia nigra].

Intranigral injection of picrotoxin in Rats induced contralateral rotation and stereotyped behaviour. These responses were significantly altered following neuroleptic treatment (haloperiod, pimozide) or ipsilateral striatal electrolytic destruction. The present results provide behavioural evidence for gamma-aminobutyric acid-mediated inhibition of the dopaminergic nigrostriatal pathway.

Animals↗

PubMed1979

Hypersynchronisation and sedation produced by GABA-transaminase inhibitors and picrotoxin: does GABA participate in sleep control?

Systemic administration of GABA-transaminase inhibitors, gamma-acetylenic GABA (100 mg/kg) or gamma-vanylic GABA (1200 mg/kg) produces behavioral picture of somnolence accompanied by EEG hypersynchronisation reminiscent of electrographic signs of petit mal epilepsy. Similarly, systemic administration of GABA antagonist, Picrotoxin (3--4 mg/kg) produces a short lasting period of sedation preceding the development of myoclonic jerks which is also accompanied by Wave-spike discharges. The role of GABA in sleep control is discussed. Although the area is not ready for firm conclusions, the results suggest that hyperactivity of GABA-ergic system as well as its hypoactivity could mediate pathological somnolence associated with different forms of epilepsy.

4-Aminobutyrate Transaminase↗

PubMed1978