Amphetamine elicited potential changes in vertebrate and invertebrate central neurons

The effects of amphetamine on potential changes in both vertebrate and invertebrate central neurons and factors affecting the potential changes were tested. The animals studied included mice, newborn rat and African snail. Seizure was elicited after lethal doses of d-amphetamine (75 mg/kg, i.p.) administration in mice. Repetitive firing of the action potentials were elicited after d-amphetamine (1-30 microM) administration in thin thalamic brain slices of newborn rat. Bursting firing of action potentials in the giant African central RP4 neuron were also elicited after d-amphetamine or l-amphetamine (0.27 mM) administration. The amphetamine elicited bursting firing of action potentials was not blocked even after high concentrations of d-tubocurarine, atropine, haloperidol, hexamethonium administration. Therefore, the amphetamine elicited potential changes may not be directly related to the activation of the receptors of the neuron. The bursting firing of action potentials elicited by amphetamine occurred 20-30 min after amphetamine administration extracellularly, even after high concentrations of d-amphetamine administration (0.27, 1 mM). However, the bursting firing of potentials occurred immediately if amphetamine was administrated intracellularly at lower concentration. Extracellular application of ruthenium red, the calcium antagonist, abolished the amphetamine elicited bursting firing of action potentials. If intracellular injection of EGTA, a calcium ion chelator, or injection with high concentrations of magnesium, the bursting firing of potentials were immediately abolished. These results suggested that the active site of amphetamine may be inside of the neuron and the calcium ion in the neuron played an important role on the bursting of potentials. In two-electrode voltage clamped RP4 neuron, amphetamine, at 0.27 mM, decreased the total inward and steady outward currents of the RP4 neuron. d-Amphetamine also decreased the calcium, Ia and the steady-state outward currents of the RP4 neuron. Besides, amphetamine elicited a negative slope resistance (NSR) if membrane potential was in the range of -50 to -10 mV. The NSR was decreased in cobalt substituted calcium free and sodium free solution. The effects of secondary messengers on the amphetamine elicited potential changes were tested. The bursting firing of action potentials elicited by amphetamine in central snail neurons decreased following extracellular application of H8 (N-(2-methyl-amino) ethyl-3-isoquinoline sulphonamide dihydrochloride), a specific protein kinase A inhibitor and anisomycin, a protein synthesis inhibitor. However, the bursting firing of action potentials were not affected after extracellular application of H7 (1,(5-isoquinolinesulphonyl)-2-methylpiperasine dihydrochloride), a specific protein kinase C (PKC) inhibitor, or intracellular application of GDPbetaS, a G protein inhibitor. The oscillation of membrane potential of the bursting activity was blocked after intracellular injection of 3'-deoxyadenosine, an adenylyl-cyclase inhibitor. These results suggested that the bursting firing of action potentials elicited by d-amphetamine in snail neuron may be associated with the cyclic AMP second messenger system; on the other hand, it may not be associated with the G protein and protein kinase C activity. It is concluded that amphetamine elicited potential changes in both vertebrate and invertebrate central neurons. The changes are closely related to the ionic currents and second messengers of the neurons.     

Conditioned reactions of hippocampal neurons during amphetamine poisoning and its counteraction with haloperidol

Activity of 144 neurones of the dorsal part of the rabbits hippocamp was recorded during elaboration of motor conditioned reflex to time. Chronic amphetamine intoxication lowered the ability of hippocampal neurones to form conditioned reactions in response to pairings of sound stimuli with electrocutaneous reinforcement and fully suppressed mechanisms of reproduction by cells of engrams of previous pairings in series of their omissions Single administration of haloperidol to intact animals somewhat increased the number of neurones reacting to the pairing and their omissions in conditioned reflex to time without significantly influencing the intensity and dynamics of reproduction of endogenous cellular reactions in the series of consecutive omissions of pairing. Haloperidol administration during amphetamine intoxication elicited shifts towards normalization of conditioned activity of neurones, eliminating the suppressing action of amphetamine on mechanisms of reproduction of engrams of combined stimuli. Such "therapeutic" effect of haloperidol in many cases did not depend on the character of its psychotropic action. The properties of amphetamine and haloperidol action on the cells of the hippocamp are discussed as compared to their action on the neurones of other brain structures, previously studied in an analogous experimental situation.     

Changes in trace reactions of sensorimotor cortex and putamen neurons as affected by haloperidol

Experiments on conscious rabbits were made to elaborate motor conditioned reflexes through pairing stimuli with electrocutaneous reinforcement applied every 30 s. Neuronal activity in the sensorimotor cortex and putamen was recorded during formation and reproduction of the conditioned reflexes before and after haloperidol injection (0.2 mg/kg i. v.). In the putamen, haloperidol increased the number of neurons exhibiting trace conditioned activity and made the intensity and duration of these processes rise. The changes seen in the sensorimotor cortex were opposite in nature. Inhibition of trace conditioned activity in the sensorimotor cortex depended mainly on the decreased amplitude of the reaction conditioned component. The role of the dopaminergic system in the interaction of the neostriatum and sensorimotor cortex and in formation and reproduction of trace conditioned activity of both the structures is discussed.     

Zooplankton community structure driven by vertebrate and invertebrate predators

Summary A zooplankton community was established in outdoor experimental ponds, into which a vertebrate predator (topmouth gudgeon: Pseudorasbora parva) and/or an invertebrate predator (phantom midge larva: Chaoborus flavicans) were introduced and their predation effects on the zooplankton community structure were evaluated. In the ponds which had Chaoborus but not fish, small- and medium-sized cladocerans and calanoid copepods were eliminated while rotifers became abundant. A large-sized cladoceran Daphnia longispina, whose juveniles had high helmets and long tailspines as anti-predator devices, escaped from Chaoborus predation and increased. In the ponds which had fish but not Chaoborus, the large-sized Daphnia was selectively predated by the fish while small-and medium-sized cladocerans and calanoid copepods predominated. In the ponds containing both Chaoborus and fish, the fish reduced the late instar larvae (III and IV) of Chaoborus but increased the early instar larvae (I and II). Small- and large-sized cladocerans were scarcely found. The former might have been eliminated by predation of the early instar larvae of Chaoborus, while the latter was probably predated by fish. Consequently, the medium-sized cladocerans, which may have succeeded in escaping from both types of predator, appeared abundantly. The results suggest that various combinations of vertebrate and invertebrate predators are able to drive various kinds of zooplankton community structure.     

Modulation of vertebrate and invertebrate neuromuscular junctions

Advances in our understanding of how the neuromuscular junction is modulated include an expanded appreciation of the many different types of modulatory influences, from soluble factors to second-messenger systems, to specific proteins in nerve and muscle. Recent studies indicate that modulation of neuromuscular function is effected on both the presynaptic and postsynaptic sides of the neuromuscular junction.     

Hexamethonium increases the excitability of sympathetic neurons by the blockade of the Ca2+-activated K+ channels

Effects of hexamethonium (C6) on the excitability of sympathetic ganglion cells were examined by means of intracellular recording. When DC currents were injected, high concentrations of C6 significantly augmented the repetitive firing of the cells without any change in threshold voltage for initiation of the spike. The Ca2+-sensitive component of the after-hyperpolarization following a spike was reduced by C6 in a dose-dependent fashion (0.3 to 10 mM). C6 slightly affected parameters for the spike but neither the resting membrane potential nor the input membrane resistance. The amplitude of the Ca2+ spike (in the presence of 1 microM tetrodotoxin and 10 mM tetraethylammonium) was not affected even by 30 mM C6. Bee venom (0.3 micrograms/ml) which contains apamin showed similar effects. These results suggest that C6 blocks the Ca2+-activated K+ channels, resulting in an increase in excitability of the cells.     

Adrenergic receptor homologies in vertebrate and invertebrate species examined by DNA hybridization

The deduced protein sequences of the mammalian adrenergic receptors (ARs) suggest that these proteins have evolved by several ancient gene duplication events. To investigate in what species these events may have occurred DNA fragments encoding the family of adrenergic receptors from human (beta 1AR and alpha 2AR) and hamster (beta 2AR and alpha 1AR) were used to detect homologous sequences in other vertebrates, invertebrates and unicellular organisms by Southern blot hybridization analysis. Sequences homologous to hamster beta 2AR were detected in lower vertebrates, invertebrates and Dictyostelium, but not in yeast or bacteria. Within vertebrates, sequences strongly homologous to human beta 1AR and human platelet alpha 2AR were confined to the higher vertebrates only. In the invertebrates, only Drosophila contained sequences homologous to hamster alpha 1AR. Our results suggest that non-mammalian species may contain receptors homologous to the mammalian adrenergic receptors and that the sequences homologous to human beta 2AR have been the most strongly conserved.     

Substitution of the dental root by aquatic invertebrate skeletons in animals and man

The biocompatibility of mammal bone with aragonite and calcite skeletons of aquatic invertebrates (Corals, Molluscs) led us, after animal experimentation, to implant in humans artificial dental roots derived from such invertebrates. These roots, incorporated but not resorbed, serve as supports for a prosthetic crown; they are equipped to isolate the root from the buccal cavity and to ensure shock absorbtion during mastication. The greater ease of implanting artificial teeth and their excellent acceptance will in many cases modify the strategy of current dental treatment.     

Molecular biology of the invertebrate dopamine receptors

Dopamine is found in the nervous systems of both vertebrates and invertebrates. However, the specific actions of dopamine depend on the dopamine receptor type that is expressed in the target cell. As in mammals, different subtypes of dopamine receptors have been cloned and characterized from invertebrates, and these receptor subtypes have different structural and functional properties. Understanding how these receptors respond to dopamine and in which cells each receptor type is expressed is key to our understanding of the role of dopamine signaling. Comparison of the amino acid sequences and experimentally determined functional properties suggest that there are at least three distinct types of dopamine receptors in invertebrates. This review focuses on invertebrate dopamine receptors for which the genes have been isolated and identified, and examines our current knowledge of the functional and structural properties of these receptors, and their pharmacology and expression.     

Comparison of the effects of chronic haloperidol treatment on A9 and A10 dopamine neurons in the rat

The effects of chronic haloperidol (CHAL) treatment on A9 and A10 dopamine (DA) neurons were compared using extracellular single cell recording techniques. CHAL caused a time-dependent reduction in the number of spontaneously active A9 and A10 DA cells and induced an irregular firing pattern in many of the DA cells that remained active. Both of these effects occurred earlier and to a greater extent in A10 than in A9. Intravenous injection of the DA agonist apomorphine reversed both the reduction of active DA neurons and the irregular discharge pattern, suggesting that both effects were due to the process of depolarization inactivation. Lesions of the nucleus accumbens (NAc) produced by ibotenic acid prevented the development of depolarization inactivation of A10 DA neurons, indicating that this process is mediated primarily by NAc — A10 feedback pathways. The results suggest that the slow development of depolarization inactivation of DA cells produced by CHAL may contribute to the delayed onset of the clinical effects of long-term treatment with antipsychotic drugs.