title: Electrophysiological investigation of thalamic neuronal mechanisms of motor disorders in parkinsonism: an influence of D2ergic transmission blockade on excitation and inhibition of relay neurons in motor thalamic nuclei of cat.
abstract: In acute experiments on cats anaesthetized with ketamine (25 mg/kg, i.m.) and immobilized with myorelaxine (2 mg/kg, i.v.) the activity of two groups of motor thalamic (nucleus ventralis anterior thalami-nucleus ventralis lateralis thalami) relay neurons was studied. The neurons (n = 7) receiving afferents from deep cerebellar nuclei and projecting to the motor area 4 gamma were included in the first group, and those (n = 12) receiving afferents from nucleus entopeduncularis and projecting to the supplementary motor area 6 were included in the second one. All changes in the background activity and reactions to cerebellothalamic or nucleus entopeduncularis stimulation developing under the influence of D2 receptor antagonist haloperidol (1.5-1.7 mg/kg, i.v.) have been studied in the same cell. Under haloperidol influence both groups of neurons showed a reliable decrease of background activity and generation of high frequency discharges accompanied by a shift in the mode of interspike interval histograms. A regular decrease of probability and increase of response latencies after stimulation of afferent input were observed in neurons receiving afferents from the cerebellum. In nucleus ventralis anterior thalami-nucleus ventralis lateralis thalami neurons with an inhibitory input from nucleus entopeduncularis, a shortening of inhibition from 17.5 +/- 3.6 to 9.1 +/- 1.8 ms (P < 0.05) under the haloperidol influence was evident. If the inhibition evoked by nucleus entopeduncularis stimulation consisted of two phases separated by a period of excitation (n = 4), the duration of the second phase of inhibition after haloperidol injection regularly increased and the excitation separating the phase of inhibition after haloperidol injection regularly increased and the excitation separating the phases of inhibition became more prominent. Observation on the spontaneous activity and reactions of the same neuron for 2 h or more showed a gradual moderation of the changes evoked by haloperidol. On the basis of data obtained it is concluded that the blockade of D2 receptors is followed by the increase of inhibitory processes in the relay neurons of motor thalamic nuclei. The suggestion is discussed that during the blockade of D2 receptors afferent impulsation to the motor cortex is being restricted and its influence on segmental apparatus of the spinal cord decreases. These conditions are beneficial for the development of spasticity (rigidity). At the same time, hyperpolarization of the relay neurons promotes the development of oscillatory processes at least in part of them and creates conditions for forming of tremor generators.
authors.affiliation: Department of Physiology of Cerebral Cortex and Subcortical Structures, A. A. Bogomoletz Institute of Physiology, Kiev, Ukraine.
authors.lastname: Voloshin MYu
authors.forename: E P
authors.initials: EP
authors.lastname: Lukhanina
authors.forename: B P
authors.initials: BP
authors.lastname: Kolomietz
authors.forename: V F
authors.initials: VF
authors.lastname: Prokopenko
authors.forename: V A
authors.initials: VA
authors.lastname: Rodionov
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D002415:Cats; D002531:Cerebellum / Q000502:physiology*; D004298:Dopamine / Q000502:physiology*; D065127:Dopamine D2 Receptor Antagonists; D006220:Haloperidol / Q000494:pharmacology*; D008297:Male; D009043:Motor Activity / Q000502:physiology*; D009044:Motor Cortex / Q000502:physiology*; D009127:Muscle Rigidity / Q000503:physiopathology; D009128:Muscle Spasticity / Q000503:physiopathology; D009474:Neurons / Q000502:physiology; D010300:Parkinson Disease / Q000503:physiopathology*; D011930:Reaction Time / Q000187:drug effects; D017448:Receptors, Dopamine D2 / Q000502:physiology; D013787:Thalamic Nuclei / Q000502:physiology*
chemical_list: D065127:Dopamine D2 Receptor Antagonists; D017448:Receptors, Dopamine D2; D006220:Haloperidol; D004298:Dopamine