Neurons postsynaptic responses

Figure 2.12 From voltage-clamp to current-clamp micro-electrode recordings of synaptic current (/, lower trace) and synaptic potential with superimposed action potential (V, upper trace) from a neuron in an isolated rat superior cervical sympathetic ganglion following a single stimulus (S) applied to the preganglionic nerve trunk. The interval between the stimulus and the postsynaptic response includes the conduction time along the unmyelinated axons of the preganglionic nerve trunk. (SJ Marsh and DA Brown, unpublished)...

Daniel H, Rancillac A, Crepel F (2004) Mechanisms underlying cannabinoid inhibition of presynaptic Ca2+ influx at parallel fibre synapses of the rat cerebellum. J Physiol 557 159-74 Davies CH, Davies SN, Coflingridge GL (1990) Paired-pulse depression of monosynaptic GABA-mediated inhibitory postsynaptic responses in rat hippocampus. J Physiol 424 513-31 De Camilli P, Greengard P (1986a) Synapsin I a synaptic vesicle-associated neuronal phospho-protein. Biochem Pharmacol 35 4349-57... 

Both oci and (3 adrenoceptors are postsynaptic excitatory heteroreceptors. Their action is mediated via the activation of Ca2+ current. However, different mechanisms are involved Gq-mediated phospholipase C (PLC) activation and Gs-mediated AC stimulation, respectively (Kandel et al., 2000). When they present on glutamate pyramidal neurons, (3-adrenoceptors receptors decrease the Ca2+-activated after-hyperpolarization K+ influx, making the neurons more responsive for excitatory inputs. The a] adrenoceptors, however, increase membrane conductance and make the pyramidal cells less excitable (Devilbiss and Waterhouse 2000). 

Postsynaptic responses to neurotransmitters are invariably initiated by the binding of the transmitter to a specific recognition site, or receptor. This finding is true both for interneuronal communications and the transmission of signals from neurons to effector cells. Perhaps the only known exception to this observation is the presumed communication in the central nervous system between electrotonic synapses, a topic beyond the scope of this chapter [see Weight (1971) and Schmitt et al. (1976) for further details]. 

The postsynaptic response to a chemical messenger appears to occur at postsynaptic active zones, which can be recognized morphologically at sites where nerve terminals make contact with other neurons or effector cells such as striated muscle. They consist of a pronounced density of intra-membranous particles as viewed under electron microscopy. These particles are at least 100-fold more enriched in active zones when compared to the remainder of the membrane. At the cholinergic nerve-muscle junction, evidence exists to suggest that these intramembranous particles are in fact ion channel—receptor complexes. Portions of the particles, thought to be the receptors, turn over with a time course of days, but the overall integrity of the active zones remains intact. In the cerebral cortex of the central nervous system, dendritic spines of neurons have been shown to be concentrated with active zones. These active zones appear to be intimately associated with portions of the neuronal cytoskeleton, since the cytoplasmic portion of the active zone displays a prominent band of fuzzy material, which, in turn, makes contact with microfilaments. 

The elucidation of synaptic mechanisms involving endocannabinoids has revealed some surprises. Indeed, endocannabinoids are released in the extracellular space from postsynaptic neurons in response to a rise in intracellular Ca. Then, endocannabinoid neurotransmitters travel backward across synapses, and eventually stimulate CBl receptor on the presynaptic neuron. The main effect of endocannabinoids on presynaptic neurons is to decrease the release of either the inhibitory y-aminobutyric acid (GABA) or the excitatory glutamate neurotransmitters, resulting in a control of a broad range of physiological functions including food intake, fear,and anxiety. ... 

Nicotine is the main psychoactive ingredient of tobacco and is responsible for the stimulant effects and abuse/ addiction that may result form tobacco use. Cigarette smoking rapidly (in about 3 sec ) delivers pulses of nicotine into the bloodstream. Its initial effects are caused by its activation of nicotinic acetylcholine (nACh) receptors. nACh receptors are ligand-gated ion-channels and pre- and postsynaptically located. Reinforcement depends on an intact mesolimbic dopamine system (VTA). nACh receptors on VTA dopamine neurons are normally activated by cholinergic innervation from the laterodorsal tegmental nucleus or the pedunculopontine nucleus. 

Several findings support this model. For instance, an early report suggested that there is a positive correlation between the density of (postsynaptic) jS-adrenoceptors in rat cortex and behavioural resistance to a mild environmental stress (novelty and frustration) but a negative correlation between these parameters when the stress is intensified (Stanford and Salmon 1992). More recently, it has been proposed that the phasic response of neurons in the locus coeruleus (which governs attentiveness ) depends on their tonic activity (which determines arousal). Evidence suggests that the relationship between these two parameters is described by a bell-shaped curve and so an optimal phasic response is manifest only at intermediate levels of tonic activity (Rajkowski et al. 1998). 

Figure 11.5 Chloride distribution and the GABAa response. The change in membrane voltage (Fm) that results from an increase in chloride conductance following activation of GABAa receptors is determined by the resting membrane potential and the chloride equilibrium potential (Fci)- (a) Immature neurons accumulate CF via NKCC, while mature neurons possess a Cl -extruding transporter (KCC2). (b) In immature neurons GABAa receptor activation leads to CF exit and membrane depolarisation while in mature neurons the principal response is CF entry and h5q)erpolarisation. This is the classic inhibitory postsynaptic potential (IPSP)...

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