scholarly journals Modulation of Synaptic Transmission by Dopamine and Norepinephrine in Ventral but not Dorsal Striatum

1998 ◽  
Vol 79 (4) ◽  
pp. 1768-1776 ◽  
Author(s):  
Saleem M. Nicola ◽  
Robert C. Malenka
Keyword(s):  
Synaptic Transmission ◽  
Adrenergic Receptor ◽  
Dorsal Striatum ◽  
Normal Functioning ◽  
Postsynaptic Potentials ◽  
Functional Roles ◽  
Inhibitory Synaptic Transmission ◽  
Excitatory Transmission ◽  
Inhibitory Postsynaptic Potentials ◽  
Dependent Mechanism

Nicola, Saleem M. and Robert C. Malenka. Modulation of synaptic transmission by dopamine and norepinephrine in ventral but not dorsal striatum. J. Neurophysiol. 79: 1768–1776, 1998. Although the ventral striatum (nucleus accumbens; NAc) and dorsal striatum are associated with different behaviors, these structures are anatomically and physiologically similar. In particular, dopaminergic afferents from the midbrain appear to be essential for the normal functioning of both nuclei. Although a number of studies have examined the effects of dopamine on the physiology of NAc or striatal cells, results have varied, and few studies have compared directly the actions of dopamine on both of these nuclei. Here we use slice preparations of the NAc and dorsal striatum to compare how synaptic transmission in these nuclei is modulated by catecholamines. As previously reported, dopamine depressed excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs) in the NAc. Surprisingly, however, neither EPSPs nor IPSPs in the dorsal striatum were affected by dopamine. Similarly, norepinephrine depressed excitatory synaptic transmission in the NAc by an α-adrenergic receptor-dependent mechanism but was without effect on excitatory transmission in the dorsal striatum. Inhibitory synaptic transmission was not affected by norepinephrine in either structure. These results suggest that the functional roles of dopamine and norepinephrine are not the same in the dorsal striatum and the NAc.

Synaptic Connectivity of Distinct Hilar Interneuron Subpopulations

1998 ◽  
Vol 79 (6) ◽  
pp. 3229-3237 ◽  
Author(s):  
Matteo Forti ◽  
Hillary B. Michelson
Keyword(s):  
Morphological Characteristics ◽  
Pyramidal Cells ◽  
Synaptic Connectivity ◽  
Postsynaptic Potentials ◽  
Functional Roles ◽  
Inhibitory Postsynaptic Potentials ◽  
Projection Properties ◽  
Inhibitory Circuit ◽  
Ca3 Pyramidal Cells ◽  
Dentate Hilus

Forti, Matteo and Hillary B. Michelson. Synaptic connectivity of distinct hilar interneuron subpopulations. J. Neurophysiol. 79: 3229–3237, 1998. Dual intracellular recordings of hilar interneurons and CA3 pyramidal cells were performed in transverse slices of guinea pig hippocampus in the presence of the convulsant compound 4-aminopyridine (4-AP) and ionotropic glutamate receptor antagonists. Under these conditions, interneurons burst fire synchronously, producing synchronized inhibitory postsynaptic potentials (sIPSPs) in pyramidal cells. Three different hilar interneuron subpopulations that contributed to the sIPSP were identified based on their projection properties and morphology. These three types were pyramidal-like stellate interneurons, spheroid interneurons, and oviform interneurons. Physiologically, pyramidal-like stellate interneurons could be differentiated from the other interneuron subpopulations because they generated short synchronized bursts of action potentials coincident with the hyperpolarizing and depolarizing γ-aminobutyric acid-A (GABAA)-mediated inhibitory postsynaptic potentials (IPSPs) recorded in pyramidal cells. The bursts in pyramidal-like stellate cells were abolished by theGABAA-receptor blocker, bicuculline. In contrast, spheroid interneurons of the dentate-hilus (D-H) border and oviform hilar interneurons exhibited prolonged bicuculline-resistant bursts that occurred coincident with the GABAB pyramidal cell sIPSPs. Pyramidal-like stellate interneurons likely did not contribute to the generation of synchronized GABAB responses in hippocampal pyramidal cells. Spheroid interneurons were unique among these subpopulations of interneurons in that the bicuculline-resistant bursts in spheroid interneurons were sustained by a synaptic depolarization that persisted in the presence of antagonists of ionotropic glutamate, GABAA and GABAB receptors [6-cyano-7-nitroquinoxaline-2,3-dione, 20 μM; 3-3(2-carboxipiperazine-4-yl)propyl-1-phosphonate, 20 μM; bicuculline, 10–15 μM; CGP 55845A, 20 μM]. This novel depolarizing potential reversed between −30 and 0 mV. No noticeable synaptic depolarization sustaining burst firing could be isolated in oviform interneurons, suggesting that firing in this interneuron subpopulation was synchronized by nonsynaptic mechanisms. The results of the present study indicate that the hilar inhibitory circuit is composed of at least three different subpopulations of interneurons, distinguishable by their morphological characteristics and synaptic inputs and outputs. These findings give further support to the hypothesis that there are distinct populations of interneurons producing GABAA and GABAB responses with defined functional roles within the hippocampal inhibitory circuit. Notably, we found that spheroid interneurons were unique among the hilar interneurons studied, in that the synchronized bursts observed in these cells are sustained by a novel ionotropic glutamate and GABA receptor-independent synaptic depolarization.

scholarly journals Functional roles and circuitry in an inhibitory pathway to feeding command neurones in Pleurobranchaea

1984 ◽  
Vol 113 (1) ◽  
pp. 423-446
Author(s):  
J. A. London ◽  
R. Gillette
Keyword(s):  
Motor Activity ◽  
Soap Solution ◽  
Inhibitory Pathway ◽  
Postsynaptic Potentials ◽  
Functional Roles ◽  
Rhythmic Motor ◽  
Pleurobranchaea Californica ◽  
Inhibitory Postsynaptic Potentials ◽  
Animal Preparation ◽  
The Brain

The paracerebral neurones (PCNs) of the brain of Pleurobranchaea californica serve a command role in the initiation of feeding behaviour (Gillette, Kovac & Davis, 1978). The PCNs are synaptically excited by food stimuli applied to the oral veil of hungry, naive animals. In food avoidance-conditioned animals, the PCNs are inhibited by a barrage of inhibitory postsynaptic potentials concomitant with the suppression of feeding (Davis & Gillette, 1978). In this paper, an interneuronal pathway is described which causes inhibition of the PCNs and potentially mediates the effects of learning. The inhibitory pathway consists of three serially connected interneurones. One population, designated the Interneurone 1s (Int-1s), monosynaptically inhibits the PCNs. A second population, the Interneurone 2s (Int-2s), excites the Int-1 population. They also excite other neurones of the brain including the metacerebral giant neurones. A third population, the Interneurone 3s (Int-3s), monosynaptically excites the Interneurone 2 population. Dual intracellular recordings and current injection show that ipsilateral members of the Int-2 population are electrically coupled via a nonrectifying connection. Contralateral members of the Int-2 population are excitatorily coupled via a polysynaptic pathway. The Int-1 population is phasically active during the rhythmic motor activity that underlies feeding. In the isolated nervous system Int-1 activity is phase-locked with rhythmic PCN activity; Int-1 activity occurs maximally at the end of a PCN burst, during the retraction phase of the cycle. Int-2 activity also occurs during the retraction phase. During actual feeding in the whole animal preparation, the Int-2s are also phasically active; maximal excitation occurs during buccal mass retraction and maximal inhibition during protraction and the bite. Stimulated activity in a single Int-2 can entirely suppress the rhythmic motor activity of the feeding network evoked by electrical stimulation of the stomatogastric nerve. The suppressant effects of Int-2 activity must be mediated widely within the feeding network because the rhythmic motor output so driven is not dependent on PCN spiking. Application of an appetitive chemosensory stimulus to whole and semi-intact animal preparations initiated feeding and elicited excitation of the Int-1 and Int-2 populations. Noxious chemosensory stimuli, such as a dilute soap solution or ethanol, elicited oral veil withdrawal and inhibition of the Int-2s by multiple inhibitory postsynaptic potentials.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Modulation of Inhibitory Synaptic Potentials in the Piriform Cortex

1999 ◽  
Vol 81 (5) ◽  
pp. 2103-2118 ◽  
Author(s):  
Madhvi M. Patil ◽  
Michael E. Hasselmo
Keyword(s):  
Synaptic Transmission ◽  
Associative Memory ◽  
Pyramidal Neurons ◽  
Piriform Cortex ◽  
Neuronal Firing ◽  
Physiological Data ◽  
Postsynaptic Potentials ◽  
Inhibitory Synaptic Transmission ◽  
Synaptic Potentials ◽  
Stimulation Of

Modulation of inhibitory synaptic potentials in the piriform cortex. Intracellular recordings from pyramidal neurons in brain slice preparations of the piriform cortex were used to test results from a computational model about the effects of cholinergic agonists on inhibitory synaptic potentials induced by stimulation of afferent fibers in layer Ia and association/intrinsic fibers in layer Ib. A simple model of piriform cortex as an associative memory was used to analyze how suppression of inhibitory synaptic transmission influenced performance of the network. Levels of suppression of excitatory synaptic transmission were set at levels determined in previous experimental work. Levels of suppression of inhibitory synaptic transmission were then systematically varied within the model. This modeling work demonstrated that suppression of inhibitory synaptic transmission in layer Ib should be stronger than suppression of inhibitory synaptic transmission in layer Ia to keep activity levels high enough for effective storage. Experimental data showed that perfusion of the cholinergic agonist carbachol caused a significant suppression of inhibitory postsynaptic potentials (IPSPs) in the pyramidal neurons that were induced by stimulation of layer Ib, with a weaker effect on IPSPs induced by stimulation of layer Ia. As previously described, carbachol also selectively suppressed excitatory postsynaptic potentials (EPSPs) elicited by intrinsic but not afferent fiber stimulation. The decrease in amplitude of IPSPs induced by layer Ib stimulation did not appear to be directly related to the decrease in EPSP amplitude induced by layer Ib stimulation. The stimulation necessary to induce neuronal firing with layer Ia stimulation was reduced in the presence of carbachol, whereas that necessary to induce neuronal firing with layer Ib stimulation was increased, despite the depolarization of resting membrane potential. Thus physiological data on cholinergic modulation of inhibitory synaptic potentials in the piriform cortex is compatible with the functional requirements determined from computational models of piriform cortex associative memory function.

scholarly journals Input-selective adenosine A1 receptor-mediated synaptic depression of excitatory transmission in dorsal striatum

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Brandon M. Fritz ◽  
Fuqin Yin ◽  
Brady K. Atwood
Keyword(s):  
Dorsal Striatum ◽  
Synaptic Depression ◽  
Potential Contribution ◽  
Functional Roles ◽  
Excitatory Transmission ◽  
Whole Cell Patch Clamp ◽  
Neuropsychiatric Diseases ◽  
Compulsive Behaviors ◽  
And Function

AbstractThe medial (DMS) and lateral (DLS) dorsal striatum differentially drive goal-directed and habitual/compulsive behaviors, respectively, and are implicated in a variety of neuropsychiatric disorders. These subregions receive distinct inputs from cortical and thalamic regions which uniquely determine dorsal striatal activity and function. Adenosine A1 receptors (A1Rs) are prolific within striatum and regulate excitatory glutamate transmission. Thus, A1Rs may have regionally-specific effects on neuroadaptive processes which may ultimately influence striatally-mediated behaviors. The occurrence of A1R-driven plasticity at specific excitatory inputs to dorsal striatum is currently unknown. To better understand how A1Rs may influence these behaviors, we first sought to understand how A1Rs modulate these distinct inputs. We evaluated A1R-mediated inhibition of cortico- and thalamostriatal transmission using in vitro whole-cell, patch clamp slice electrophysiology recordings in medium spiny neurons from both the DLS and DMS of C57BL/6J mice in conjunction with optogenetic approaches. In addition, conditional A1R KO mice lacking A1Rs at specific striatal inputs to DMS and DLS were generated to directly determine the role of these presynaptic A1Rs on the measured electrophysiological responses. Activation of presynaptic A1Rs produced significant and prolonged synaptic depression (A1R-SD) of excitatory transmission in the both the DLS and DMS of male and female animals. Our findings indicate that A1R-SD at corticostriatal and thalamostriatal inputs to DLS can be additive and that A1R-SD in DMS occurs primarily at thalamostriatal inputs. These findings advance the field’s understanding of the functional roles of A1Rs in striatum and implicate their potential contribution to neuropsychiatric diseases.

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