Pharmacological Aspects of Parkinsonism

Comparison of the Electroencephalographic and Motor Effects of Orphenadrine, an Antiparkinson Agent

“…On the other hand, such signs of the behavioral sedation associated with the depression of the tegmental motor response were not observed in the animals that received orphenadrine, atropine or scopolamine . The depression of the head turning reported to be produced by 2.5 mg/kg of chlorpromazine in the cat (10) was also confirmed in the rabbit which received 1 to 2 mg/kg. 2.…”

“…Such an effect has been utilized for the evaluation of the antiparkinson agents (10,12). In the present experiments the effects of various agents including orphenadrine were ob served on the arousal responses of the cortical EEG and on the motor responses such as the head turning and neck tremor caused by electrical stimulation of the midbrain tegmentum.…”

Comparison of the Electroencephalographic and Motor Effects of Orphenadrine, an Antiparkinson Agent

“…On the other hand, such signs of the behavioral sedation associated with the depression of the tegmental motor response were not observed in the animals that received orphenadrine, atropine or scopolamine . The depression of the head turning reported to be produced by 2.5 mg/kg of chlorpromazine in the cat (10) was also confirmed in the rabbit which received 1 to 2 mg/kg. 2.…”

“…Such an effect has been utilized for the evaluation of the antiparkinson agents (10,12). In the present experiments the effects of various agents including orphenadrine were ob served on the arousal responses of the cortical EEG and on the motor responses such as the head turning and neck tremor caused by electrical stimulation of the midbrain tegmentum.…”

Rat brain amines, blood histamine and glucose levels in relationship to circadian changes in sleep induced by pentobarbitone sodium

“…The significant decrease in 5-HT levels during the light phase of the illumination cycle following pretreatment with pentobarbitone sodium suggests either an increase in utilization of 5-HT during barbiturate sleep and/or a net decrease in 5-HT synthesis. The latter might be due to a decrease in body temperature resulting in a slowing of the circulatory processes and enzymic activity (Friedman & Everett, 1964). The average difference in rectal temperature between control and treated rats observed during the dark phase of the illumination cycle was 2.54°, whilst the average difference noted during the light phase was only 0.780 C. The decrease in body temperature in the pentobarbitone treated animal is in part the result of decreased motor activity and depressed metabolic activity.…”

ANTI‐TREMOR ACTION OF C10DICHOL, A PERIPHERAL ACETYLCHOLINE SYNTHESIS INHIBITOR

“…This conclusion is based on the observations that CloDichol, which impairs the synthesis of ACh and does not pass the blood brain barrier (see Introduction), is able to inhibit tremor induced by Oxo-T, physostigmine and nicotine and affords partial protection against physostigmine-induced lethality in mice (see Results). These tests are widely recognised as useful screening procedures for evaluation of anti-Parkinson drugs (Friedman & Everett, 1964;Jenden, 1968;Nase & Kojima, 1970) Peripheral skeletomotor involvement in the 'Oxo-T model' of Parkinsonism and a presynaptic muscarinic-dopaminergic link in the motor nerve endings have been demonstrated in recent years (for references, see Introduction). Like Oxo-T, the presynaptic effects of nicotine and physostigmine on motor nerve terminals mediated through excess ACh are well documented (Barstad, 1962;Randic & Straughan, 1964;Chiou & Long, 1969;Chiou, 1973).…”

“…Of these agents, the muscarinic agonist oxotremorine (Oxo-T), is unique in producing the typical features of Parkinson's disease (Friedman & Everett, 1964;Jenden, 1968). This effect of Oxo-T is mediated at least in part through a presynaptic cholinergic CH3 dominance at the myoneural junction resulting from activation of presynaptic muscarinic receptors on the motor nerve endings (Das et al, 1978;Ganguly & Das, 1979).…”

Comparison of the Electroencephalographic and Motor Effects of Orphenadrine, an Antiparkinson Agent

“…On the other hand, such signs of the behavioral sedation associated with the depression of the tegmental motor response were not observed in the animals that received orphenadrine, atropine or scopolamine . The depression of the head turning reported to be produced by 2.5 mg/kg of chlorpromazine in the cat (10) was also confirmed in the rabbit which received 1 to 2 mg/kg. 2.…”

“…Such an effect has been utilized for the evaluation of the antiparkinson agents (10,12). In the present experiments the effects of various agents including orphenadrine were ob served on the arousal responses of the cortical EEG and on the motor responses such as the head turning and neck tremor caused by electrical stimulation of the midbrain tegmentum.…”

Rat brain amines, blood histamine and glucose levels in relationship to circadian changes in sleep induced by pentobarbitone sodium

“…The significant decrease in 5-HT levels during the light phase of the illumination cycle following pretreatment with pentobarbitone sodium suggests either an increase in utilization of 5-HT during barbiturate sleep and/or a net decrease in 5-HT synthesis. The latter might be due to a decrease in body temperature resulting in a slowing of the circulatory processes and enzymic activity (Friedman & Everett, 1964). The average difference in rectal temperature between control and treated rats observed during the dark phase of the illumination cycle was 2.54°, whilst the average difference noted during the light phase was only 0.780 C. The decrease in body temperature in the pentobarbitone treated animal is in part the result of decreased motor activity and depressed metabolic activity.…”

ANTI‐TREMOR ACTION OF C10DICHOL, A PERIPHERAL ACETYLCHOLINE SYNTHESIS INHIBITOR

“…This conclusion is based on the observations that CloDichol, which impairs the synthesis of ACh and does not pass the blood brain barrier (see Introduction), is able to inhibit tremor induced by Oxo-T, physostigmine and nicotine and affords partial protection against physostigmine-induced lethality in mice (see Results). These tests are widely recognised as useful screening procedures for evaluation of anti-Parkinson drugs (Friedman & Everett, 1964;Jenden, 1968;Nase & Kojima, 1970) Peripheral skeletomotor involvement in the 'Oxo-T model' of Parkinsonism and a presynaptic muscarinic-dopaminergic link in the motor nerve endings have been demonstrated in recent years (for references, see Introduction). Like Oxo-T, the presynaptic effects of nicotine and physostigmine on motor nerve terminals mediated through excess ACh are well documented (Barstad, 1962;Randic & Straughan, 1964;Chiou & Long, 1969;Chiou, 1973).…”

“…Of these agents, the muscarinic agonist oxotremorine (Oxo-T), is unique in producing the typical features of Parkinson's disease (Friedman & Everett, 1964;Jenden, 1968). This effect of Oxo-T is mediated at least in part through a presynaptic cholinergic CH3 dominance at the myoneural junction resulting from activation of presynaptic muscarinic receptors on the motor nerve endings (Das et al, 1978;Ganguly & Das, 1979).…”

Comparison of the Electroencephalographic and Motor Effects of Orphenadrine, an Antiparkinson Agent

“…On the other hand, such signs of the behavioral sedation associated with the depression of the tegmental motor response were not observed in the animals that received orphenadrine, atropine or scopolamine . The depression of the head turning reported to be produced by 2.5 mg/kg of chlorpromazine in the cat (10) was also confirmed in the rabbit which received 1 to 2 mg/kg. 2.…”

“…Such an effect has been utilized for the evaluation of the antiparkinson agents (10,12). In the present experiments the effects of various agents including orphenadrine were ob served on the arousal responses of the cortical EEG and on the motor responses such as the head turning and neck tremor caused by electrical stimulation of the midbrain tegmentum.…”

Rat brain amines, blood histamine and glucose levels in relationship to circadian changes in sleep induced by pentobarbitone sodium

“…The significant decrease in 5-HT levels during the light phase of the illumination cycle following pretreatment with pentobarbitone sodium suggests either an increase in utilization of 5-HT during barbiturate sleep and/or a net decrease in 5-HT synthesis. The latter might be due to a decrease in body temperature resulting in a slowing of the circulatory processes and enzymic activity (Friedman & Everett, 1964). The average difference in rectal temperature between control and treated rats observed during the dark phase of the illumination cycle was 2.54°, whilst the average difference noted during the light phase was only 0.780 C. The decrease in body temperature in the pentobarbitone treated animal is in part the result of decreased motor activity and depressed metabolic activity.…”

ANTI‐TREMOR ACTION OF C10DICHOL, A PERIPHERAL ACETYLCHOLINE SYNTHESIS INHIBITOR

“…This conclusion is based on the observations that CloDichol, which impairs the synthesis of ACh and does not pass the blood brain barrier (see Introduction), is able to inhibit tremor induced by Oxo-T, physostigmine and nicotine and affords partial protection against physostigmine-induced lethality in mice (see Results). These tests are widely recognised as useful screening procedures for evaluation of anti-Parkinson drugs (Friedman & Everett, 1964;Jenden, 1968;Nase & Kojima, 1970) Peripheral skeletomotor involvement in the 'Oxo-T model' of Parkinsonism and a presynaptic muscarinic-dopaminergic link in the motor nerve endings have been demonstrated in recent years (for references, see Introduction). Like Oxo-T, the presynaptic effects of nicotine and physostigmine on motor nerve terminals mediated through excess ACh are well documented (Barstad, 1962;Randic & Straughan, 1964;Chiou & Long, 1969;Chiou, 1973).…”

“…Of these agents, the muscarinic agonist oxotremorine (Oxo-T), is unique in producing the typical features of Parkinson's disease (Friedman & Everett, 1964;Jenden, 1968). This effect of Oxo-T is mediated at least in part through a presynaptic cholinergic CH3 dominance at the myoneural junction resulting from activation of presynaptic muscarinic receptors on the motor nerve endings (Das et al, 1978;Ganguly & Das, 1979).…”