ng rate in the dorsal raphe nucleus, this prevented endogenous 5-HT acting tonically at the somato-dendritic 5-HT1A autoreceptors. From the description here it can be deduced that the agonists of 5-HT1A have a dual effect on the 5-HT1A dependant mechanisms, these are inhibition of serotoninergic neurone firing and transmission via the somato-dendritic autoreceptors and stimulation serotoninergic neurotransmission due to the activation on post synaptic targets. Experiments conducted on rats show that the significant inhibition of serotoninergic neurotransmission via stimulation of the somato-dendritic autoreceptors in the anterior raphe nuclei stimulates food consumption, similar effects to this can be achieved by post synaptic blockade of 5 –HT2C receptors located on satiety mediating hypothalmic neurones) using cyproheptadine (KENNET 1999). Figure 22 (left) a resting potential (right) depolarization occuring on the post synaptic neuronLTP was first observed in mid 1970’s, it is a form of synaptic plasticity and is considered to be linked with learning and memory in the mammalian central nervous system. It displays the integration of glutamate receptor subtypes in the initiation of long term potentiation. LTP is achieved when glutamate released from a presynaptic terminal binds to two types of glutamate receptor NMDA and AMPA subtypes. The molecular basis of this achievement is explained using the biophysical properties of NMDA receptor and AMPA receptor subtypes. The key elements of this mechanism are the voltage gated blockade of NMDA receptor channel by magnesium ions, and the unusual permeability of calcium ions through the depolarised NMDA channel.In low frequency synaptic transmission, glutamate is released from axon terminals and binds to both NMDA and AMPA receptor subtypes. NMDA channels are blocked by a magnesium ion at negative membrane potentials therefore the current produced from the low frequency transmission ...
